Root Cause Analysis of Gaps in Non-communicable Disease Monitoring in a Sub-district Hospital, Tamil Nadu: A Quality Improvement Initiative.

Introduction Non-communicable diseases (NCDs) present a significant public health challenge globally, and India is deeply affected. With the largest population in the world, India struggles with a high burden of NCDs, encompassing cardiovascular diseases, diabetes, cancer, and chronic respiratory conditions. These ailments contribute substantially to morbidity and mortality, placing a strain on healthcare systems. Despite efforts through public health initiatives, NCD monitoring and management remain deficient, especially at grassroots levels. Methods At a sub-district hospital in Tamil Nadu, India, a quality improvement initiative targeted diabetes and hypertension, prevalent NCDs. Utilizing Fishbone analysis and process flow diagrams, we identified gaps in NCD monitoring. Employing the Plan-Do-Study-Act model and reorienting the patient flow, we enhanced NCD monitoring by optimizing patient health record maintenance within the hospital. Results Root cause analysis identified a lack of patient record protocols and patient loss of records as key hindrances in NCD monitoring. We revamped patient flow and implemented a robust record-keeping system, boosting access to patient health records. This initiative was embraced by healthcare providers, enhancing NCD management. Leveraging these records, we assessed control rates of diabetes and hypertension patients effectively. Conclusion The research underscores the importance of maintaining comprehensive patient health records in healthcare centers for enhancing NCD monitoring. These records serve as valuable tools for healthcare providers, aiding in the monitoring and treatment of patients with diabetes and hypertension. By leveraging these records, healthcare providers can achieve better disease control outcomes, thereby improving the overall management of NCDs.

In utero depletion of fetal hematopoietic stem cells improves engraftment after neonatal transplantation in mice.

Although in utero hematopoietic cell transplantation is a promising strategy to treat congenital hematopoietic disorders, levels of engraftment have not been therapeutic for diseases in which donor cells have no survival advantage. We used an antibody against the murine c-Kit receptor (ACK2) to deplete fetal host hematopoietic stem cells (HSCs) and increase space within the hematopoietic niche for donor cell engraftment. Fetal mice were injected with ACK2 on embryonic days 13.5 to 14.5 and surviving pups were transplanted with congenic hematopoietic cells on day of life 1. Low-dose ACK2 treatment effectively depleted HSCs within the bone marrow with minimal toxicity and the antibody was cleared from the serum before the neonatal transplantation. Chimerism levels were significantly higher in treated pups than in controls; both myeloid and lymphoid cell chimerism increased because of higher engraftment of HSCs in the bone marrow. To test the strategy of repeated HSC depletion and transplantation, some mice were treated with ACK2 postnatally, but the increase in engraftment was lower than that seen with prenatal treatment. We demonstrate a successful fetal conditioning strategy associated with minimal toxicity. Such strategies could be used to achieve clinically relevant levels of engraftment to treat congenital stem cell disorders.