## 1 Introduction
In this study, we focus on the feasibility of deploying a cutting-edge microfluidic lab-on-chip device in a low-resource setting to measure prognosis and guide the clinical management of SCD using results of morphological and rheological properties of red blood cells as they traverse the microvasculature under the effect of clinical stress conditions. Our lab-on-chip device, called the microfluidic microcirculation mimetic (MMM), [10; 11; 12; 13; 14] mimics both the pulmonary and peripheral microcirculatory environments, measures cell transit times and deformability and assesses the obstructive effects of constrictions on the cells. These measurements and assessments constitute readouts of the mechanical or rheological characteristics of the cells, which, in a broader context, have been shown to have important physiological roles [15; 16; 17] and are in the diagnostic focus for characterizing pathologies [18; 19; 20]. The main objective of this study was to show the feasibility of using an advanced lab-on-chip microfluidic platform (here, MMM) to unravel the contributions of morpho-mechanical properties of single RBCs to a vaso-occlusive crisis, VOC, to characterize and advance clinical management of SCD complications in individual patients, even in a resource-poor setting. Furthermore, this study points out that it is also possible to use the MMM technique to assess the effects of novel interventions, which are under development, on the microcirculatory vasculature. Of course, this possibility fits with the knowledge that SCD is not merely a monogenic hemoglobin disorder resulting in increased RBC stiffness which leads to VOC but is also a vasculopathic disease. Our work is a necessary preparation for the introduction of more lab-on-chip platforms that will address several old and new questions about SCD complications such as the role of adhesion versus stiffness of cells [21]. The real-time deformability cytometer (RT-DC) [22] and the integrated automated particle-tracking microfluidic [23] platforms are among those whose utility thepresent feasibility report assesses for future work. The scientific reasons for an amplified armamentarium emerge from the pathophysiology of SCD and current treatment strategies. Thus, we have established a multinational collaboration involving researchers based in the USA and Germany, who developed advanced cutting-edge tools to directly address clinical questions around SCD management, and clinical researchers in sub-Saharan Africa where SCD burden is the highest for the quick deployment of diagnostic tools with an effective synergy in bench-to-bedside translational research. Sickling of RBC in the human vascular beds can result in ischemic tissue injury with organ dysfunction and early death [9]. Patients with SCD can develop very painful, life-threatening complications, including extensive organ damage, which can reduce their quality of life and life expectancy. Chronic organ damage involving the central nervous system, the heart, the lungs and the kidneys has also been observed to be part of SCD complications. The complications that follow an acute sickle cell crisis are often infarction or thromboembolic events in any of the organs. Other complications include sensory-neural hearing loss and proliferative and non-proliferative retinopathy [24]. Yet, other complications include splenic fibrosis, autosplenectomy from the repeated episodes of infarction and consecutive immunosuppression. Priapism and chronic leg ulcers are common complications among adolescents, especially those with homozyggote sickle cell disease. Still, other complications are nephrotic syndrome, gnathopathy, avascular necrosis of the head of the femur, septic arthritis and osteomyelitisitis [25]. Patients with SCD have a markedly decreased life expectancy, and their quality of life is greatly compromised by frequent hospitalization caused by the disease [12; 21].