The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2018

A curious case of ketoacidosis (#257)

Brendan J Nolan 1 , Marina Lee 1 , Suresh Varadarajan 1
  1. Endocrinology, Northern Health, Melbourne, VIC, Australia

Lactation ketoacidosis is a rare but serious complication of carbohydrate restriction in breastfeeding women. We report the case of an otherwise well 26-year-old Caucasian female, 8 weeks post-partum, who presented to the Emergency Department with a four-day history of abdominal pain and progressive shortness of breath.  Initial investigations revealed a severe high anion gap metabolic acidosis (pH 6.97, HCO3- 5, pCO2 22, anion gap 27, base excess -25.5, glucose 4.0).  Capillary ketones were elevated at 6.3 mmol/L.

 In an attempt to assist weight loss post-partum, she had commenced a low carbohydrate diet (<50 grams/day) 17 days prior, with 7 kg weight loss.  There was a further reduction in oral intake in the days prior to presentation to ED.  She had been exclusively breastfeeding since delivery. 

Following recognition of ketoacidosis, the patient was commenced on an insulin and dextrose infusion and transferred to ICU.  Other causes of high anion gap metabolic acidosis were excluded.  Lactate was 1.0 mmol/L.  Serum ketones normalised 25 hours after presentation.  She was advised to cease breastfeeding during the acute admission but was given advice to increase her carbohydrate intake and continued breastfeeding post-discharge.

 

Discussion

Lactation ketoacidosis is a rare condition, with twelve reported cases published in the medical literature (1-12).  Most cases have been reported in first three months post-partum.  Symptoms are usually non-specific, with nausea, vomiting, malaise and abdominal discomfort.  Low carbohydrate intake, either intentionally or through fasting, is a common precipitant.  Treatment incorporates intravenous dextrose and resumption of carbohydrate intake.  

Lactation ketoacidosis results when energy intake and hepatic gluconeogenesis are unable to match the increased energy requirement of lactation.  If sufficient energy intake is not maintained, a hypoglycaemic, hypoinsulinaemic state results, resulting in adipose tissue breakdown, and ketone body formation.

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