A lipemic blood sample in the paediatric critical care unit

A 5-year-old girl was admitted to our paediatric critical care unit with a first presentation of severe diabetic ketoacidosis (DKA). Initial bloodwork demonstrated: blood glucose 35.1 mmol/L, venous pH < 6.9, pCO2 21 mmHg and HCO3 3.9 mmol/L. Her vital signs were: heart rate 150 bpm, respiratory rate 45/minute, blood pressure 113/70 mmHg, oxygen saturations 98% on room air, temperature 36.5°C and GCS 14. Her electrolytes were: sodium 140 mmol/L, potassium 3.4 mmol/L and chloride 120 mmol/L. Her corrected sodium when triglycerides (TG) peaked was 151 mmol/L. Her BMI was 21.9 (99th percentile). Her hemoglobin A1C was 11.8% (normal < 6.0%). DKA management was initiated with intravenous (IV) fluids and an insulin infusion at 0.1 units/kg/hour. Based on various factors, she was diagnosed with type 1 diabetes mellitus (T1D). Her past medical history was significant for prematurity (born at 29 weeks gestation), grade 4 interventricular hemorrhage, right hemiplegic cerebral palsy, mild developmental delay and complex partial seizures, controlled on carbamazepine. Twelve hours after admission, the laboratory was unable to reliably report bloodwork results as her blood was too lipemic. Subsequently, her blood became visibly lipemic on repeat sampling. Her lipid profile peaked with TGs of 62 mmol/L (normal <1.69 mmol/L), total cholesterol of 28.91 mmol/L (normal <5.2 mmol/L) and high-density lipoprotein of 2.53 mmol/L (normal >1.30 mmol/L). Her pancreatic and renal function were normal. Paediatric endocrinology was consulted and recommended to continue with routine DKA management. Her DKA resolved within 24 hours and at discharge 5 days later her TG level was 8.35 mmol/L. At a clinic visit 5 months later her TGs and cholesterol had normalized and she never required maintenance therapy. Diagnosis: Severe hypertriglyceridemia (HT) in DKA Severe HT is a TG level greater than 11.3 mmol/L. Patients with DKA are at risk for severe HT because of insulin deficiency, which promotes lipolysis in adipose tissue resulting in the release of free fatty acids. This leads to increased production of very low-density lipoprotein which, coupled with the inhibition of lipoprotein lipase, results in HT (1). In adults, the incidence of severe HT in patients with DKA is 8 to 11% (1,2), however the incidence in children is unknown and there are only nine case reports in the literature (3–5). In these cases, peak TG levels ranged from 11.5 mmol/L to 163.4 mmol/L and all patients had T1D. Four children were suspected of having cerebral edema and six patients developed acute pancreatitis (AP) (3,4). All but one patient was managed conservatively with insulin and IV fluid infusions. One patient received fenofibrate and plasmapheresis, and she had the highest TG level, as well as AP and renal dysfunction (6). In all patients, their TG levels normalized within 2 weeks. In adults, the risk factors associated with the development of severe HT in patients with DKA include T1D, male gender, first presentation of diabetes and higher serum pH (2). The majority of adult patients had normalization of their TG levels with improved glycemic control, and did not require TG lowering agents (2). The risk factors in paediatrics are unknown. Our patient is the only one with any significant past medical history and the only one prescribed carbamazepine; of note, carbamazepine is not a risk factor for other causes of secondary HT in children (7). The main complication of severe HT is AP, which is seen in 50% of adult patients (1) and 55% (five of nine) of paediatric cases (3,4). Pancreatitis in adult patients with DKA is associated with a more severe clinical course (1). The relationship between severe HT and cerebral edema is not well understood, however 44% (four of nine) of the paediatric cases had suspected cerebral edema, which is higher than the baseline risk of 0.5 to 1% (8). It is hypothesized that severe HT could predispose to cerebral edema because it results in increased viscosity and decreased cerebral blood flow (3). Finally, severe HT can result in spurious laboratory results including pseudohyponatremia, pseudohypokalemia and pseudohypochloremia (5). Management does not differ from routine DKA treatment with IV fluids and insulin, as the major mechanism is insulin deficiency. In all except one of the paediatric cases, the patients received routine DKA management and demonstrated a full recovery in their TG levels. One patient with very high levels of TGs and end-organ dysfunction required fenofibrate and plasmapheresis (9). Plasmapheresis has been used in adult patients with severe HT and has been associated with decreased length-of-stay and hospital admissions (10). In summary, severe TG is a rare complication of paediatric DKA. Management generally does not differ from routine DKA treatment, and all paediatric patients’ TG levels normalized without long-term therapy. We have received consent from the parents for this case

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