Abstract: SUN 048

A Case Report of Persistent Hypomagnesemia Delaying Transition to Subcutaneous Insulin in a Patient with DKA

Presenter: Amit Lahoti


Melissa Shenep1 and Amit Lahoti*2
1University of Tennessee Health Science Center, Memphis, TN, 2University of Tennessee Health Science Center, Le Bonheur Children's Hospital, Memphis, TN

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Melissa Shenep1 and Amit Lahoti*2
1University of Tennessee Health Science Center, Memphis, TN, 2University of Tennessee Health Science Center, Le Bonheur Children's Hospital, Memphis, TN

Background: The prevalence of hypomagnesemia in pediatric patients with DKA ranges from 15% to 62.4%. Hypomagnesemia can cause nausea and delay correction of other electrolyte imbalances during DKA.
Clinical case: A 15-year-old previously healthy female presented with 1-month history of classical symptoms of diabetes and 1-day history of vomiting. Laboratory testing confirmed new onset diabetes mellitus (likely type 1 based on her body habitus and absence of acanthosis) and severe DKA with a pH of 6.8 and bicarbonate of 4 mmol/L (ref. range 20-31) on venous blood gas. On physical exam, she was tachycardic, hypertensive, and appeared mottled and dehydrated with Kussmaul breathing. After fluid resuscitation, she was started on an insulin drip at 0.1 U/kg/hr, given a subcutaneous dose of glargine and IV fluids containing potassium phosphate and potassium acetate (total 40 mEq of K+) with an estimated 8.5% fluid dehydration. 2-bag IV fluid system was used to maintain glucose in 150-250 range until bicarbonate rose above 16. Her acidosis resolved on day#2 of hospitalization, and she was given a dose of subcutaneous Lispro in preparation for transitioning off insulin drip, but she failed to consume enough carbohydrates due to her nausea. Thus, she was restarted on IV fluids per the 2-bag system and insulin drip. On hospital day#3, IV insulin drip and IV fluids were discontinued, and she was started on daily glargine with q3-4 hour correction with Lispro. She tolerated PO fluids, but continued to complain of nausea and poor appetite. Her serum potassium ranged between 2.5-3 mEq/L (ref. range 3.7-5.6 mEq/L) requiring multiple IV and oral potassium supplemental doses. Her serum Mg2+ was noted to be low at 1 mEq/L (ref. range 1.6 to 2.6 mEq/L). On hospital day#4, her calcium was noted to be low, in addition to her potassium and magnesium, thus she was started on PO calcium and potassium supplements and she was given a bolus of IV Magnesium sulfate. She developed epigastric pain; amylase and lipase were normal. The patient was started on IV ranitidine and ondansetron. In the evening, her Mg2+ was noted to be critically low at <0.7 mEq/L and another IV MgSO4 bolus was given. On hospital day#5, she was given another Mg bolus and her Mg level gradually improved to 2.6 and potassium normalized. Patient’s appetite improved. On hospital day#6, all electrolytes remained in normal range, The patient tolerated breakfast and was successfully transitioned to subQ Lispro by sliding scale with meals. She was discharged home on a 14-day course of oral PPI and daily basal-bolus insulin therapy.

Conclusion: This case highlights the importance of timely identification and management of hypomagnesemia in patient recovery after severe DKA.

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