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Endocrine Abstracts (2019) 62 P27 | DOI: 10.1530/endoabs.62.P27

1Homerton University Hospital, London, UK; 2The Royal (Dick) School of Veterinary Studies and The Roslin Institute, Edinburgh, UK.


Case history: A 27-year-old woman presented with a 48 hour history of lethargy, nausea and myalgia. Twelve days earlier she had given birth to her first child. Her daughter was born at term following an uncomplicated pregnancy. She had no abdominal pain or vaginal discharge and her episiotomy wound was well healed. She had no significant past medical history, took no regular medications and did not drink alcohol. There was no significant family history. On arrival in the emergency department, she was tachycardic (119 bpm) and tachypnoeic (28 breaths per minute) with a normal temperature, blood pressure and oxygen saturations.

Investigations: She underwent detailed biochemical assessment including arterial blood gas analysis.

Results and treatment: Arterial blood gas analysis revealed a severe metabolic acidosis (pH 6.99, bicarbonate 2.2 mmol/L) with partial respiratory compensation (PaCO2 1.2kPa). The anion gap was raised at 30.5 (sodium 139 mmol/L, potassium 4.7 mmol/L, chloride 111 mmol/L). Causes of a raised anion gap metabolic acidosis were considered. She denied ethanol or other toxin ingestion and blood alcohol, paracetamol and salicylate levels were undetectable. Renal function was normal (urea 4.9 mmol/L) as were lactate (1. 2 mmol/L) and glucose (4.4 mmol/L). There was, however, significant ketonuria (4+ on dipstick) and ketonaemia (capillary beta-hydroxybutyrate 6.6 mmol/L). On direct questioning, it transpired that she had adopted a diet virtually absent in carbohydrates since delivery and her infant was exclusively breastfed. A diagnosis of starvation and lactation-induced ketoacidosis was made. Given the severity of her acidosis, she was admitted to the intensive care unit for invasive monitoring and received parenteral B vitamins, glucose and 8.4% sodium bicarbonate. Breastfeeding was temporarily discontinued and a dietician review was obtained. The acidosis resolved within 24 hours and she was discharged 48 hours later. Her acid-base status remained normal in convalescence and she was able to continue breastfeeding whilst adhering to an unrestricted diet. Urinary organic acid analysis confirmed the diagnosis with elevations of 3-hydroxybutyric acid and acetoacetic acid only.

Conclusions and points for discussion: Ketoacidosis associated with lactation is a common occurrence in dairy cattle (incidence exceeding 10%) but has been described in only a handful of human cases, almost exclusively in association with a low carbohydrate diet. Years of selective breeding to maximise milk yields, necessitating ambitious feed intakes, explains its increased prevalence in cattle and provides an excellent opportunity to discuss peri-partum comparative physiology.

Volume 62

Society for Endocrinology Endocrine Update 2019

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