Background: Plasmalyte A, a balanced solution is reported to be associated with a reduced incidence of hyperchloremia and metabolic acidosis when compared with 0.9% NaCl among adults. Considering the paucity of evidence in the pediatric population, the present study was conducted with an objective to compare the efficacy and safety of plasmalyte and normal saline as intravenous fluid bolus therapy in children with shock in terms of Electrolytes and Acid-base balance at admission and at 6 h. Subjects and Methods: This double-blinded, randomized controlled trial was conducted in the pediatric emergency department (ED) of a tertiary care hospital among children aged 1 month to 14 years who presented to the ED with shock. A total of 400 children were randomized to receive either plasmalyte or 0.9% saline solution as intravenous fluid bolus therapy. Changes in laboratory parameters including pH, serum bicarbonate levels, serum lactate level, and serum electrolytes-sodium, potassium, chloride levels from baseline (hour 0) to hour 6 were compared in both groups. Secondary outcomes included the need for vasopressors, duration of hospital stay, and in-hospital mortality. Results: The two groups were similar in terms of baseline clinical characteristics. Patients receiving plasmalyte demonstrated significantly greater improvement in the pH (P = 0.001), bicarbonate (P = 0.001) and lactate levels (P = 0.03) compared with patients receiving normal saline. In addition, normal saline group patients had a higher rise in sodium (P = 0.11) and chloride levels (P = 0.02) as compared to the plasmalyte group. The children who received plasmalyte had a significantly lesser need for vasopressors (P = 0.04), shorter mean duration of hospital stay (P = 0.01), and lower mortality (P = 0.03). Conclusion: Plasmalyte was superior to Normal saline when used as a resuscitation fluid in children with shock, in terms of better improvement of acid-base balance after fluid bolus therapy, a lower rise in serum chloride level at 6 h from baseline, shorter hospital stay, lesser need for vasoactive drugs and lower mortality.

No abstract

Atlantoaxial dislocation (AAD) occurs secondary to joint laxity between C1 and C2 vertebrae, resulting in loss of normal articulation and movement. Etiology of AAD could be genetic, inflammatory, or rarely traumatic. Majority of children with AAD are syndromic (such as Down syndrome) or genetic (such as Ehler–Danlos syndrome or Marfan syndrome). To the best of literature search, there were no reports of AAD among children with congenital hypothyroidism. This case highlights an uncommon association of AAD presenting with features of compressive myelopathy in a child with congenital hypothyroidism. Early detection and neurosurgical intervention could possibly avert this irreversible neurological damage.