Case 2: Generalized swelling in a child with newly diagnosed diabetes mellitus

A 14-year-old girl presented with three months of increasing polydipsia and polyuria. Initial investigations revealed a blood glucose level of 28.4 mmol/L, pH 7.19 and large urine ketones. She was diagnosed with new-onset type 1 diabetes mellitus in diabetic ketoacidosis. She was started on subcutaneous insulin and showed clinical improvement. In the following days, her insulin requirement steadily increased. Ten days after diagnosis, she again presented to the emergency department with a six-day history of progressive swelling of her lower limbs, abdominal distention, joint pain and weakness. There was no history of shortness of breath, oliguria, jaundice or abdominal pain. Her weight had increased 10.2 kg since diagnosis. She had facial and sacral edema, and lower extremity pitting edema up to her calves. Her abdomen was distended with dullness to the flanks, and her liver edge was palpable 4 cm below the costal margin. Heart sounds were normal without S3, S4 or murmurs. Lung fields were clear, without crackles. Deep tendon reflexes were decreased and she had distal weakness. A chest x-ray showed no evidence of pleural effusion, and urinalysis showed no proteinuria. Further investigations and evaluation suggested the etiology of her presentation. When the patient was again admitted to the general pediatric ward of the authors'; tertiary care hospital 10 days after starting insulin for type 1 diabetes mellitus, she underwent tests to elucidate the cause of new-onset edema. Echocardiography was normal, an abdominal ultrasound showed normal Doppler flow and renal anatomy, and her serum albumin and renal and liver function tests were normal. A review of the literature was undertaken, which found numerous reports describing a rare complication of a very common treatment: insulin edema. Insulin edema occurs either at initiation of insulin therapy or with escalation in treatment. Of 16 previously published case reports involving children (<18 years of age), seven involved insulin edema in children at the onset of diabetes. All but one of these seven cases occurred in females, with onset of edema one to 10 days after insulin initiation. The children required large daily doses of insulin (0.9 U/kg/day to 2 U/kg/day). Puberty (Tanner stage 2 to 5 in five of seven cases) and ketonuria or ketoacidosis (five of seven cases) were the main risk factors for insulin resistance. These children are typically lean, with no other shared risk factors for insulin resistance such as medication use or ethnicity. Treatment for edema in these children included supportive management in four cases, diuretic therapy in two cases, and both a diuretic and ephedrine in one case. Weight gain ranged from 3.5 kg to 20 kg and weight stabilization occurred in five days to two weeks. Resolution of edema occurred in all cases, taking from seven days to one month. There are several proposed mechanisms by which insulin may cause edema (1,2). First, insulin acts on insulin receptors in the proximal and distal tubules and the loop of Henle to increase sodium reabsorption. Insulin also alters sodium handling by stimulating Na+, K+ ATPase cation transport in the distal tubules. Second, elevated insulin levels increase capillary permeability through expression of vascular growth endothelial factor, stimulation of lymphocytes and alteration in transcellular albumin movement in endothelial cells. Third, insulin leads to vasodilation through β-adrenergic and cholinergic pathways, Ca2+ activated K+ channels, decreased vascular response to vasoconstrictors and stimulation of nitric oxide release. This vasodilation promotes sympathetic activation, further increasing sodium retention and volume expansion. Fourth, insulin is part of a complex hormonal interplay that may promote edema formation. In an insulin-deficient state, glucagon is elevated and has an inhibitory effect on aldosterone. As insulin is replaced, glucagon levels decline, and the inhibition of aldosterone is decreased leading to increased sodium retention. Finally, elevated antidiuretic hormone in the setting of long-standing hyperglycemia may lead to fluid retention in the context of volume repletion. In our case, treatment included dietary salt restriction, modification of injection sites, daily weights, and daily telephone conversations to monitor for symptoms of worsening fluid overload. Sodium was restricted from 3200 g/day to 2300 g/day, and the injection sites were switched from edematous abdominal tissue to her arms. With these measures in place, the patient gradually improved. Her weight stopped increasing six days after presentation with edema. That same day, her insulin requirement peaked at 2 U/kg/day, and subsequently began to decrease. Additionally, her distal weakness was likely related to her degree of edema because the two subsided at the same time. Her edema completely resolved within two weeks. Insulin edema is likely an under-reported condition accounting for mild symptoms of swelling, weight gain and abdominal discomfort in patients with newly diagnosed diabetes. Less commonly, patients may present with frank edema. The edema resolves with time and may not require pharmacological therapy. Insulin edema is a rare and likely under-recognized complication of a very common treatment in general paediatrics. Patients and the families of children receiving insulin should be counselled regarding the possibility of insulin edema to encourage early recognition of symptoms and early presentation to medical attention. Early recognition and assessment before edema becomes severe may allow for a period of close observation with salt restriction before proceeding with more costly and invasive testing if edema worsens.

Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.