ObjectivesAlthough Acute Kidney Injury (AKI) has been described among childhood diabetes ketocidosis (cDKA) there is scarcity of literature on the role of concomitant rhabdomyolysis.MethodA retrospective chart review was undertaken (2014–2018) to identify cDKA who developed AKI and had evidence of rhabdomyolysis defined by serum creatine phosphokinase (CPK) > 5 times upper limit of normal.Result46 cDKA were identified. Ten (22%) developed AKI with 6/10 reaching peak AKI Stage 3 and 8/10 had co-current rhabdomyolysis. In comparison to non rhabdomyolysis group, cDKA with rhabdomyolysis were at presentation significantly more likely to be hypotensive and have higher corrected sodium and calculated osmolality. Subsequently they were more likely to develop lower trough potassium levels during treatment. Five patients, all with rhabdomyolysis, needed dialysis: median duration 9 days (range 4–35). Three children in our cohort died, all from infection complications during treatment, one in AKI only group who did not receive dialysis and two in AKI with rhabdomyolysis on dialysis.ConclusionRhabdomyolysis was common among our cohort of cDKA with AKI and was associated with high morbidity and mortality. Rapid flux in electrolytes and osmolality may be important precipitating factors. We recommend larger prospective studies exploring the importance of rhabdomyolysis among cDKA with AKI.

Secondary erythrocytosis occurs in cyanotic heart disease as a physiological response to chronic hypoxia, and this leads to hyperviscosity and various complications of the same. Microvascular stasis due to hyperviscosity results in symptoms including headache, fatigue, paraesthesia, and loss of vision. An important and dreadful feature of hyperviscosity is overt thrombosis in organ systems, resulting in cerebrovascular accident and myocardial infarction. Limited body iron store in a state of secondary erythrocytosis brings forth iron-deficient microcytic red cells; these being more rigid and less deformable than normocytic cells, further aggravate vascular occlusion. The management of hyperviscosity syndrome starts with intravenous hydration and correction of latent iron deficiency. However, therapeutic phlebotomy may be employed as a rescue measure if symptoms persist despite correction of dehydration and anemia. We present a series of four patients with uncorrected cyanotic congenital heart disease who presented with a spectrum of features of hyperviscosity and discuss pathophysiology, clinical features, and management of hyperviscosity in detail.

i.Objective-To describe epidemiological, clinical, biochemical, and radiological profile of children admitted in PICU of a tertiary care hospital with severe Adenoviral Pneumonia (ADVP) and respiratory sequelae among them. ii. Design-This is a singlecenter, prospective observational study conducted at the Institute of Child Health iii. Settings-The study had been done in

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