Severe acute malnutrition (SAM) remains as one of the leading causes of mortality for children under five years. SAM can be clinically categorized into either severe wasting (MRM), characterized by extreme muscle loss; or oedematous malnutrition (KWK), a phenotypically entirely different form of SAM characterized by oedema, fatty liver, hair depigmentation, desquamating skin lesions and behavioural changes; some children have both phenotypes. The pathophysiology and etiology of KWK remains enigmatic and mainly descriptive. This gap in the literature is not just an academic puzzle as KWK children are notoriously difficult to manage leading to higher mortality. Several hypotheses on the cause of KWK have been proposed but none have been substantiated by strong clinical and/or pre-clinical evidence. Hence, we performed a pilot study employing proteomics and targeted metabolomics techniques to potentially elucidate the pathophysiology of KWK. This proposal is built upon the results of the preliminary investigation and is aimed at validating and exploring the roles of the eicosanoid pathway in KWK development and plasma lipidome differences compared to MRM. Despite the fact that KWK and MRM are different both in their clinical manifestation and mortality rates, treatment protocols are globally the same for both phenotypes. Hence, a deeper understanding of KWK at the molecular level may lead to more targeted strategies to decrease the mortality rates of children with KWK.