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Growth and breakup of ligaments in unsteady fragmentation

Published online by Cambridge University Press:  18 January 2021

Y. Wang
Affiliation:
The Fluid Dynamics of Disease Transmission Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
L. Bourouiba*
Affiliation:
The Fluid Dynamics of Disease Transmission Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
*
†Email address for correspondence: lbouro@mit.edu

Abstract

We elucidate the physics underlying the birth, evolution and breakup of ligaments on a rim bounding an unsteady liquid sheet. This rim destabilizes into corrugations that can grow into ligaments, which in turn, break into secondary droplets via end-pinching. Combining experiments and theory, we show that not all corrugations can grow into ligaments. The number of corrugations is captured by linear instability coupled with nonlinear rim thickness self-adjustment ($\text {Bond number} = 1 \text { criterion}$, Wang et al. (Phys. Rev. Lett., vol. 120, 2018, 204503)) and scales as $N_c \sim We^{3/4}$ with Weber number, $We$. The number of ligaments scales as $N_{\ell } \sim We^{3/8}$. The growth of a ligament is governed by the competition between the constraint imposed by the geometry of the local rim–ligament junction; the local force balance including the fictitious force from the continuously decelerating rim; and the global rim mass conservation constraint. The temporal evolution of the average width of ligaments is predicted. Key to understanding the ligament population, a minimum distance between two corrugations is required to enable their actual transition into ligaments. By predicting this minimal distance, we derive the evolution of the number of ligaments. We show that droplets are shed, one at a time, following a chaotic dripping end-pinching regime independent of $We$. Finally, the number of droplets shed per unit of time decreases over time and scales as $S_d \sim We^{3/4}$; while the volume shed per unit of time increases over time and is independent of $We$. Theoretical predictions are validated without fitting parameters.

Information

Type
JFM Papers
Copyright
© The Author(s), 2021. Published by Cambridge University Press
Figure 0

Figure 1. ($a$) Schematic diagram of canonical unsteady fragmentation upon drop impact on a surface of comparable size, $d_r$, to that of the impacting drop, $d_0$. ($b$) Unsteady fluid fragmentation is described in four steps: (i) sheet evolution; (ii) rim destabilization; (iii) corrugation to ligament transition; (iv) ligament end-pinching and droplet ejection. Key physical quantities for each step of the fragmentation are listed on the right and labelled in the diagram.

Figure 1

Table 1. Summary of the experimental conditions used for water drop impacts on a rod, including the impact drop diameter, $d_0$, impacting speed, $u_0$, and associated $We = \rho u_0^2 d_0/\sigma$ and $Re= u_0d_0/\nu$, where $\rho = 1.0\times 10^3\ \textrm {kg}\,\textrm {m}^{-3}$, $\nu = 1.0\times 10^{-6}\ \textrm {m}^{2}\,\textrm {s}^{-1}$ and $\sigma = 72\ \textrm {mN}\,\textrm {m}^{-1}$, are the density, kinematic viscosity, and surface tension of the water drop, respectively. $N_{exp}$ is the number of experiments carried out for each group. $d_r$ is the diameter of the impact rod. $\eta$ is the ratio of the diameter of the surface, $d_r$, with that of the impact drop, $d_0$.

Figure 2

Figure 2. Key steps of our AIP algorithms: ($a$) detection of inner and outer contours of the rim–ligament system; ($b$) morphological analysis of the rim–ligament system and the separation of the ligaments from the rim. The inset illustrates the high accuracy of the automatic separation between the rim and the ligaments conducted; ($c$) the ligament-tracking algorithm links the ligaments detected at different frames to form their trajectories.

Figure 3

Figure 3. Illustration of the algorithms detecting the local protrusions and corrugations on the rim. ($a$) Inner and outer contours are detected. The local distance between two contours is calculated from the difference in radial positions of the inner and outer contours. The circle dots correspond to the local maxima of distances detected. ($b$) The detected local maxima capture the local protrusions on the rim.

Figure 4

Figure 4. ($a$) Time evolution of the ratio, $\kappa (t)$, of the sheet thickness at the rim, $h(r_s,t)$, with the rim thickness $b(t)$ for impact $We = 679$ and rod-to-drop size ratio $\eta = 1.45$, showing that $\kappa (t) \ll 1$ during the entire sheet evolution. ($b$) Time evolution of the instability time scale, $\tau _{is}$, of the fastest-growing mode of the coupled RP–RT instability of the rim, compared with the rim thickening time scale, $\tau _h$, based on both the volume influx entering the rim and the stretching of the rim length (sheet perimeter) for the same experimental condition as ($a$). It shows that the instability time scale is much slower than the actual thickening.

Figure 5

Figure 5. ($a$) Time evolution of the number of corrugations, including ligaments, on the rim, compared with the prediction (4.1) from the wavelength of the fastest-growing mode of the Rayleigh–Plateau instability for different Weber numbers. ($b$) Time evolution of the measured number of ligaments, compared with the measured number of corrugations as shown in ($a$) for $We = 679$. The number of ligament is systematically smaller than that of the corrugation, indicating, at each time, that not all corrugations can grow into ligaments. Error bars indicate the standard deviation from 28 experiments for each condition (table 1).

Figure 6

Figure 6. ($a$) Schematic diagram of corrugation growth based on linear stability analysis. The corrugation width is half of the wavelength of the fastest-growing mode of the linear instability, and the length is the amplitude of the perturbation, following an exponential growth. ($b$) Time evolution of the measured population mean width of a single ligament for impact $We = 693$, compared with the prediction (4.3a,b). ($c$) Time evolution of the measured population average length of ligaments for $We = 693$, compared with prediction (4.3a,b). The ligament length is normalized by the initial measured length of the ligament $\ell _0$, which can be considered as the initial amplitude of the rim's perturbation. Time is non-dimensionalized by the local capillary time, $\tau _b = \sqrt {\rho b^3/8\sigma }$, based on the local rim thickness around the ligament.

Figure 7

Figure 7. ($a$) Schematic diagram of a jet emanating from an orifice. ($b$) Schematic diagram for a classic ligament analysis, selecting a control volume at the tip of the ligament (§ 5.1).

Figure 8

Figure 8. ($a$) Sequence illustrating the growth of a ligament from initial perturbation to a corrugation that is finally pulled away from the rim to form a long ligament in the reference frame of the rim. Time increment between images is 0.5 ms. Scale bar is 0.5 mm. ($b$) Schematic diagram of the model of ligament growth from corrugation without solid-boundary constraints at its root (§ 5.2.2). ($c$) Schematic diagram of the reduced model of ligament dynamics (§ 5.2.3).

Figure 9

Figure 9. ($a$) Time evolution of the measured and predicted dimensionless rim deceleration $\ddot {-R_s}$ throughout the sheet evolution. The deceleration is non-dimensionalized by $d_0/\tau _{cap}^2$, where $d_0$ is the impacting drop diameter and $\tau _{cap}$ is the capillary time. $We = \rho u_0^2 d_0/\sigma$ is the impact Weber number. The time window shown is that over which the ligament shown in ($b$,$c$,$d$) elongates. The inset illustrates the experimental measurement of the ligament length and average width. ($b$) Time evolution of the measured volume of one ligament based on our AIP algorithms. $t_1$ is the time of onset of corrugation growth. $t_2$ is the time of ligament breakup into a secondary droplet. ($c$,$d$) Time evolution of the measured length ($c$) and average width ($d$) of the ligament, compared with our predictions using the measured volume rate, $q_{\ell }$, from ($b$), which captures the data of both ligament length and width very well, showing the ability of our reduced model, (5.19), to capture the ligament dynamics very well.

Figure 10

Figure 10. ($a$–$c$) Time evolution of the measured volume of various ligaments for different impact $We$. The other two rows show the time evolution of the ligament length ($d$–$f$) and width ($g$–$i$) for the corresponding single ligament volume evolution shown in ($a$–$c$). Based on the measured injection volume rate, $q_{\ell }$, for each ligament, the predictions of the ligament width, $w$, and length, $\ell$, are in very good agreement with the data. This confirms the ability of the reduced model (5.19) to capture the geometrical evolution of ligament growth on unsteady rims. $(a{,}d{,}g)\, We = 484,\, (b{,}e{,}h)\, We = 679 \,\,{\rm and}\,\, (c,f{,}i)\, We = 963.$

Figure 11

Figure 11. ($a$) Schematic diagram of the ligament's root where the curvature is associated with suction of fluid emanating from the rim into the ligament. ($b$) Experimental observations of the roots of different ligaments growing on the same rim at the same time, for different impact $We$. The circles fit the curvature of the roots set by the width of the ligaments. Scale bar is 0.5 mm.

Figure 12

Figure 12. Time evolution of the measured volume influx speed into various ligaments, compared with prediction (5.38a,b). The prediction captures the data very well for each ligament and for all $We$. $(a)\,\, We = 484,\, (b)\,\, We = 679\,\, {\rm and}\,\, (c)\,\, We = 963.$

Figure 13

Figure 13. Time evolution of the measured ligament width ($a$–$c$) and length ($d$–$f$), compared with our predictions derived from (5.39). Our predictions are in excellent agreement with the data. $(a{,}d)\,\, We = 484,\, (b{,}e)\,\, We = 679\,\, {\rm and}\,\, (c,f) We = 963.$

Figure 14

Figure 14. ($a$) Measured time evolution of the ratio of the ligament's population average width $w$ with the rim thickness $b$, which is independent of the impact $We$ and increases over time. The dashed line shows that the prediction from mass conservation (6.2) captures the order of magnitude of $w/b$, but misses its temporal evolution. The solid line shows that the prediction (6.15) involving the rim stretching and contraction captures the data very well. The inset shows the time evolution of $w$, compared with $b$ for $We = 693$. ($b$) Measured time evolution of the population average width $\langle W \rangle$ of ligaments on the rim, normalized by $We^{-1/4}$, compared with the prediction (6.17), which captures the data very well. The inset shows the non-normalized evolution of $\langle W \rangle$. Error bars indicate the standard deviation of 28 experiments for each condition (table 1).

Figure 15

Figure 15. Schematic diagram of the rim between two adjacent ligaments defined as control volume II (CVII) (grey area). ($a$) Shows the change in control volume II when the rim is stretching, during the phase of sheet expansion. ($b$) Shows the change in control volume II when the rim contracts, during the phase of sheet retraction.

Figure 16

Figure 16. ($a$) Measured time evolution of population average fluid speed, $V_{\ell }$, entering each ligament on the rim for different impact $We$. The solid line shows that our prediction (6.19) captures the data very well. ($b$) Measured time evolution of population average fluid volume, $Q_{\ell }$, entering each ligament on the rim for different impact $We$. Normalized by $We^{-3/8}$, all data collapse on a single curve. The solid line shows that our prediction (6.21) captures the data very well. Error bars indicate the standard deviation of 28 experiments for each condition (table 1).

Figure 17

Figure 17. ($a$) Measured time evolution of the average distance, $\varLambda (T)$, between ligaments on the rim for different impact $We$. Normalized by $We^{1/8}$, all data collapse on a single curve. The solid line shows that the prediction (6.24) of the minimal inter-ligament distance $\varLambda _m$ captures the data very well. ($b$) Measured time evolution of the number of ligaments, $N_{\ell }(T)$ on the rim for different impact $We$. Normalized by $We^{3/8}$, all data collapse on a single curve. The solid line shows that prediction (6.26) captures the data well. Error bars indicate the standard deviation of 28 experiments for each condition (table 1).

Figure 18

Figure 18. ($a$–$c$) Snapshot of ligaments and droplets shed at different times during sheet evolution. ($d$) Comparison of the time evolution of the critical Weber number $We_{\ell }^{(P)}$ (7.5) and the average Weber number, $We_{\ell }$ (7.6), for the fluid entering the ligament throughout the fragmentation. The inset shows the ratio of $We_{\ell }/We_{\ell }^{(P)}$. ($e$) Measured time evolution of the shedding rate, $S_d$, of secondary droplets for $We = 679$, non-dimensionalized by $1/\tau _{cap}$. The prediction (7.7) of the shedding rate is obtained from multiplication of the average shedding rate of each ligament and the number of ligaments. The solid line shows the prediction (7.8) based on the fastest-growing mode of the Rayleigh–Plateau instability, which overestimate the shedding rate. The inset of ($e$) shows that the average length of ligaments on the rim increases over time. $ (a)\,\, t = 0.2 \tau_{cap},\, (b)\,\, t = 0.4 \tau_{cap} \,\,{\rm and}\,\, (c) t = 0.6 \tau_{cap}.$

Figure 19

Figure 19. ($a$) Measured time evolution of the shedding rate $S_d$ of secondary droplets during unsteady fragmentation for different impact $We$. Normalized by $We^{3/4}$, all data collapse on a single curve. The solid line shows that the prediction (7.15) captures the data well, except at the early time when the rim has not destabilized to trigger the shedding of droplets yet. ($b$) Measured time evolution of the cumulative volume partition of secondary droplets shed during fragmentation for different $We$. The volume is normalized by the impacting drop volume $\mathcal {V}_0$. All data collapse onto a single curve, indicating independence from $We$. The inset shows the time evolution of the droplet shedding volume rate $Q_d$. The solid line shows that both predictions (7.17) and (7.21) capture the data well. Error bars indicate the standard deviation of 28 experiments for each condition (table 1).

Figure 20

Table 2. Summary of the property of the other fluid (Dimethyl sulfoxide, DMSO) used in this study, and its initial conditions and associated non-dimensional number. DMSO has a dynamic viscosity close to that of water, while its surface tension is approximately $42\ \textrm {mN}\,\textrm {m}^{-1}$. 30 experiments with the same impact condition are conducted. Impact target diameter is $d_r = 6\ \textrm {mm}$, giving to the drop-to-target size ratio $\eta = 1.6$.

Figure 21

Figure 20. ($a$) Snapshot of unsteady sheet fragmentation upon impact of a drop of DMSO and water at the time of maximum sheet radius $T_m$, with no notable difference in fragmentation phenomenology. ($b$–$d$) Measured time evolution of ($b$) number of ligaments $N_{\ell }$, ($c$) population average width of ligaments $\langle W \rangle$ and ($d$) shedding rate $S_d$ of secondary droplets during fragmentation of DMSO, compared with that of water. Normalized by the associated Weber dependence, all data collapse onto a single curve, captured very well by the theoretical prediction, except for the shedding rate at early time. Error bars indicate the standard deviation of all experiments for each condition (tables 1 and 2). ($e$) Distinct from water, the DMSO drop impact consistently generates corona splash at very early time $t < \tau _{imp} = d_0/u_0$ of fragmentation. During corona splash, the initial rim and ligaments growing on it break and detach from the sheet along the edge (see snapshot at $T=0.024$). Meanwhile, a new smooth rim forms around the sheet free of corrugations and ligaments. More time is then needed to re-destabilize this new rim into ligaments and droplets. This explains why the time of regular shedding – not accounting for prompt splash which is another fragmentation mechanism than that considered here – for DMSO in ($d$) is systematically larger than shedding from water impacts. Scale bars are 3 mm.

Figure 22

Figure 21. Time evolution of the measured volume of a single ligament which grows on the rim for a long time. The jump in the volume indicates the time of breakup of the ligament tip to form a secondary droplet. ($b$) Illustration of the advanced image processing algorithm that link the shed droplet with its original ligament at each breakup. ($c$) Time evolution of the modified measured volume of a single ligament, by adding the volume of the droplet shed at each shedding event. A continuous and smooth volume evolution of the ligament is obtained. And a long time evolution of the volume influx from the rim to this ligament can be obtained by taking the derivative of this modified measured volume. ($d$) Time evolution of the measured volume influx speed from the rim to the ligament, compared with the prediction of the influx speed based on the Bernoulli's suction constraint (5.37) and using the radius of curvature as the width of the ligament. Good agreement between the prediction and the experimental data.

Figure 23

Figure 22. ($a$) Full prediction of ligament-to-rim size ratio $\alpha =w/b$ governed by (B 9) for different $We$. For the intermediate-$We$ range $250 of common fragmentation processes (Wang & Bourouiba 2020b), the variation due to the $We$-dependence is only within 5 %. ($b$) Full prediction of $\alpha$ governed by (B 10), compared with the analytic approximate solution expanded to $O(T^2)$ (C 2), which are in good agreement.

Figure 24

Figure 23. ($a$) Full prediction of the time evolution of the normalized population average ligament width $\varPhi (T) = W/We^{-1/4}$ governed by (C 3), compared with the analytic approximate solution expanded to $O(T^4)$ (C 4) and expanded to $O(T^2)$ (C 5), all of which are in good agreement, indicating the expansion to $O(T^2)$ is sufficient. ($b$) Full prediction of the time evolution of the normalized average speed entering single ligaments $\varGamma (T) = V_l/We^{1/8}$, compared with the analytic approximate solution expanded to $O(T^2)$ (C 8) and by taking time average (C 9), which are all in good agreement.

Figure 25

Figure 24. ($a$) Full prediction (C 10) of the time evolution of the normalized population average volume rate $\chi (T) = Q_{\ell }/We^{-3/8}$ entering single ligaments, compared with the analytic approximate solution expanded to $O(T^2)$ (C 12), which are in good agreement. ($b$) Full prediction (C 13) of the time evolution of the normalized number of ligament $\varTheta (T) = N_l/We^{3/8}$, compared with the analytic approximate solution expanded to $O(T^3)$ (C 15) and to $O(T^2)$ (C 15). Only the approximate solution expanded to $O(T^3)$ (C 15) captures the full prediction (C 13).

Figure 26

Figure 25. ($a$) Full prediction (C 16) of the time evolution of the normalized minimal distance separating the growing ligaments on the rim $\xi (T) = \varLambda _m(T)/We^{1/8}$, compared with the analytic approximate solution expanded to $O(T^2)$ (C 18), which are in very good agreement. ($b$) Measured time evolution of the ratio of the minimal distance $\varLambda _m$ with the rim thickness $B$ for different impact $We$. Normalized by $We^{3/8}$, all data collapse on a single curve. The solid line shows that the full prediction (C 19) captures the data well and is approximately constant at first order (C 20).

Figure 27

Figure 26. ($a$) Full prediction (C 21) of the time evolution of the normalized number of droplets shed per unit of time $\zeta = S_d/We^{3/4}$, compared to the analytic approximate solution (C 23). The inset shows that expression $\varrho (T)$ (C 22) remains constant throughout the fragmentation. ($b$) Full prediction of the volume rate, $Q_d$ (C 24) (inset), and the cumulative volume fraction, $\mathcal {V}_d/\mathcal {V}_0$ (C 27), shed in the form of secondary droplets, compared with their approximate analytic solutions (C 26) and (C 28), respectively.