Lactation Ketoacidosis in a COVID-19 patient: A Case Report

Introduction

Metabolic acidosis is a potentially life-threatening medical problem characterized by low blood pH and a low serum bicarbonate concentration [1]. Metabolic acidosis may occur as a result of high anion gap metabolic acidosis (HAGMA) or loss of bicarbonate from the gastrointestinal tract or kidneys. HAGMA is commonly caused by diabetic ketoacidosis (DKA), lactic acidosis, renal insufficiency, and intoxications (e.g., methanol, ethanol, and salicylate) [2].

Lactation ketoacidosis and isolated starvation ketoacidosis are rare causes of HAGMA with only a few reported cases. Common underlying factors exacerbating HAGMA include intensive exercise, change in diet, skipping meals, or un- derlying illness. Meanwhile, a recent retrospective study had shown that COVID-19 might cause ketosis, ketoacidosis and diabetic ketoacidosis (DKA) [3]. The authors in that study hypothesized that COVID-19 might increase fat breakdown and thereby inducing ketosis and ketoacidosis.

Ketoacidosis in the lactating woman is rapidly reversible with appropriate treatment; hence, detailed medical history and clinical presentation assessment in addition to blood investigations are essential to identify the underlying cause of HAGMA and providing the appropriate treatment.

Until recently, no cases of either isolated starvation ketoaci- dosis nor lactation ketoacidosis were reported in association with COVID-19.

Areej AlMweisheer, Aisha AlAtawi are with Department of Emer- gency Medicine, King Fahad Medical City, Saudi Arabia, e-mail: areej.almweisheer@hotmail.com, e-mail: aalatawi@kfmc.med.sa

Areej AlMweisheer is the corresponding author.

Patient: A Case Report

Here, we report on a young, four months’ postpartum lady with HAGMA despite no history of diabetes. She had been diagnosed with COVID-19 and showed gastrointestinal disturbances and abdominal pain.

CASE PRESENTATION A 22-year-old lady, 4-month postpartum, presented to the emergency department (ED) with five days’ history of non- specific symptoms, including mild fever that is responding to antipyretics, nausea, vomiting, and abdominal pain. She had been diagnosed with COVID-19 five days before her presentation. Due to her worsened condition, she had been unable to tolerate any food intake in the preceding five days. She denied any change in bowel habits, jaundice, shortness of breath, chest pain, syncope, neurological manifestations, or skin changes. She did not have a history of diabetes, alcohol drink, or drug abuse.

On Arrival to ED, her vital signs revealed a blood pres- sure of 122/95 mmHg, a heart rate of 154 beats/min, a temperature of 37.8 degrees Celsius, and a respiratory rate of 22 breaths/min, and point of care random blood sugar 2.8 mmol/L. The clinical examination revealed an anxious- ill appearing woman and dry oral mucous membranes, with the rest of the physical examination being normal. Bedsides, abdominal ultrasound did not reveal any remarkable findings suggestive of abdominal pain.

Venous blood gas was taken, and revealed severe metabolic acidosis with PH: 7.06, partial pressure of carbon dioxide (PCO2): 18.2 kPa, bicarbonate (HCO3): 8.7 mmol/L, lactate: 1.4 mmol/l. A urine dipstick analysis revealed ketonuria (+3). Moreover, her hemoglobin was 14.20 g/dl, leukocyte count 7.67 10e9/l, serum creatinine 81 umol/l, potassium 4.8 mmol/l, chloride 111 mmol/l, sodium 139 mmol/l, and bicarbonate < 5.0 mmol/l. She had high anion gap metabolic acidosis (HAGMA) with anion gap: 27.8 mmol/l, enzymes revealed as- partate aminotransferase: 39 units/l, alanine aminotransferase: 62 units/l, and alkaline phosphatase 46 units/l. Additionally, her blood glucose level was 3.2 mmol/L. On admission, chest X-ray did not show any signs of acute cardiopulmonary problems and a 12-lead electrocardiogram showed sinus tachy- cardia. Her serum albumin on admission was 52 g/L, and serum lactate was 0.80 mmol/L. Besides, the blood alcohol level was negative. (references range for laboratory findings are included in table 1)

Based on the initial evaluation, she received in the ED 2 litres of normal saline, 50 ml of 50% dextrose, 10 mg of metoclopramide, and 1 gr of paracetamol.

Differential diagnoses of HAGMA were taken into con- sideration including environmental causes, toxicology causes,

Discussion

Ketoacidosis is a severe metabolic disorder characterized by the accumulation of ketone bodies and acidosis, is mostly seen in people with diabetes, and is rarely induced by other pathological conditions [4]. However, lactation ketoacidosis is a rare cause of HAGMA affecting breastfeeding mothers. Ketoacidosis has been reported to be induced by a low carbo- hydrate diet [5]. A negative energy balance due to any stressor exacerbates ketogenesis; thus, a stressor such as breastfeeding can produce lactation ketoacidosis [6].

In our case, a non-diabetic lactating woman presented with ketoacidosis. The patient had been diagnosed with COVID- 19 5-days before her presentation to the ED. Her nonspecific presenting symptoms were similar to those of lactation ke- toacidosis, which could result from metabolic acidosis and hypoglycaemia. Due to her worsened condition, she had been unable to tolerate any food intake in the preceding five days. In light of a recent study which reported that COVID-19 might increase fat breakdown and induce ketosis which leads to ketoacidosis, it stands to reason that lactating women infected with COVID-19 should have a high carbohydrate diet to reduce the risk of ketoacidosis.

The mechanism of COVID-19-induced lactation ketoacido- sis needs further research. However, a recent study showed that

Acknowledgements

The authors would like to express their very great appreciation to the patient for her contribution to this paper and would also like to show their appreciation for Mr Isamme AlFayyad – the clinical research specialist- for his valuable and constructive suggestions during the planning and development of this paper.

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