The ketogenic diet (KD) is a high-fat, adequate-protein, and low-carbohydrate diet that leads to nutritional ketosis and weight loss. It is known to induce ketosis but is not an established cause of clinically significant ketoacidosis. Lactation ketoacidosis is well established in bovine literature but remains a rare phenomenon in humans. Here we present a life-threatening case of severe ketoacidosis in a nondiabetic lactating mother on a strict ketogenic diet. We review the available case reports of lactation ketoacidosis in humans and the mechanisms thereof. Although ketogenic diet has been shown to be safe in nonpregnant individuals, the safety of this diet in lactating mothers is not known. Health professionals and mothers should be made aware of the potential risk associated with a strict ketogenic diet when combined with lactation. Prompt diagnosis and immediate treatment cannot be overemphasized. To our knowledge, this is the first reported case of life-threatening lactation ketoacidosis associated with ketogenic diet while consuming an adequate number of calories per day.
Ketogenic diet is a high-fat, adequate-protein, and low-carbohydrate diet that leads to nutritional ketosis and weight loss. Although ketogenic diet is safe in nonpregnant individuals, its safety in lactating mothers is unknown. This case report aims to increase the awareness to healthcare professionals, mothers, and dietitians on the potential risk associated with a strict ketogenic diet when combined with lactation.
A healthy nondiabetic 24-year-old 18 weeks postpartum woman presented to the emergency department with severe nausea, vomiting, and several episodes of diarrhea of 9-hour duration. While in the emergency department, she developed abdominal pain, low back cramps, and malaise. The patient reported adhering to a strict ketogenic diet as a health-conscious life style modification since the recent birth of her 18-week-old son. She had continued to provide her son an exclusively breastfed diet since birth. She reported an intentional 25-pound weight loss in the 18-week postpartum period. She had an unremarkable prenatal care and delivered a healthy baby boy at 40 weeks of gestation by spontaneous vaginal delivery. Her puerperium was otherwise uneventful. She denied smoking and use of alcohol. Dietary review revealed a typical breakfast consisting of egg and bacon; lunch usually consisted of some variation of vegetable salad with cheese, and a dinner consisted of vegetables and meat. Typical food items include vegetables such as peppers, spinach, broccoli, cheese, and carrot soups. For protein, she consumed mostly chicken, salmon, and other white fish. She avoided nuts or shellfish but would have 1-2 tablespoons of peanut butter per day. She eliminated all other forms of carbohydrate including wheat, pasta, bread, or any grain products. She denied any restriction in her daily caloric intake, stating that she consistently tracked her macronutrients at an average of 2200 Kcals per day.
On presentation to the emergency department, her blood pressure was 117/82 mmHg, heart rate of 103 beats/min, respiratory rate of 18 cycles/min, a temperature of 98.1°C, and oxygen saturation 98% on room air. Physical examination was remarkable for dry mucous membranes, comfortable resting tachypnea though she was breathing more deeply, mild epigastric/right upper quadrant tenderness, but was otherwise unremarkable.
Laboratory studies revealed a chemistry panel with sodium of 138 meq/L; potassium, 4.3 meq/L; chloride, 109 meq/L; urea, 10 mg/dl; creatinine, 0.84 mg/dl; bicarbonate, 6 meq/L; glucose 68mg/dl; calculated anion gap of 27.3 meq/L; phosphorus of 2.3meq/L; calcium of 9.7mg/dl; and venous lactate of 1.3 mmol/L. Hematologic indices were grossly unremarkable with hemoglobin of 14.4 g/dl; white blood cells at 9.4; and neutrophils, 7.8. Her beta-hydroxybutyric acid level was initially markedly elevated at 109.5mg/dl (Figure
Trend of serum beta-hydroxybutyric acid level during hospitalization.
She was initially managed with a combination of IV fluids including NS, Isotonic Bicarbonate, and D5W. A repeat arterial blood gas in six hours showed improved pH- 7.28; partial pressure of carbon dioxide, 15.8 mmHg; bicarbonate (HCO3), 7.8 mmol/L; base excess, -16.9 mmol/L. She was immediately restarted on oral carbohydrate diet. She was allowed to continue to breastfeed her infant as she preferred. She received insulin with glucose supplementation as part of the treatment of nondiabetic ketoacidosis. Insulin levels measured at different times during hospitalization showed appropriate response to blood glucose levels ruling out euglycemic diabetic ketoacidosis. During her treatment, she developed significant metabolic derangements including worsening hypophosphatemia down to 1.0, hypokalemia to a nadir of 2.6, and hypocalcemia down to 7.3. These were closely monitored and were repleted accordingly. She experienced associated symptoms of digital tingling, perioral anesthesia, and trousseau syndrome which gradually improved with therapy. Interestingly, she did not develop respiratory failure associated with severe hypophosphatemia.
With the initiation of carbohydrates and dextrose her blood B-hydroxybutyric acid normalized and her anion gap closed in less than 24 hours of hospitalization. She was successfully discharged on day 4 of hospitalization (Table
There are several established causes of ketoacidosis including diabetic ketoacidosis, starvation ketoacidosis, alcoholic ketoacidosis, and some inborn errors of metabolism including succinyl CoA:3 ketoacid CoA transferase deficiency, mitochondrial 2-methylacetoacetyl CoA thiolase deficiency, and methylmalonyl-CoA mutase deficiency [
Literature review of existing case reports and their precipitating factor.
Case Report | Precipitating Factor |
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A case of lactation “bovine” ketoacidosis [ | Breastfeeding twins in the setting of a “selected diet” |
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A severe case of iatrogenic lactation ketoacidosis [ | Nil per oral for 3 days to treat a bowel obstruction |
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“Bovine ketosis” in a nondiabetic postpartum woman [ | Urinary tract infection in the setting of a weight reduction diet |
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Severe spontaneous “bovine” ketoacidosis in a lactating woman [ | Urinary tract infection in the setting of a high protein, carbohydrate-free reduction diet |
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A case of bovine ketoacidosis in a lactating woman [ | 2-day nausea & vomiting in the setting of several small high-protein carbohydrate-free meals |
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Ketoacidosis associated with low-carbohydrate diet in a non-diabetic lactating woman [ | Low carbohydrate, high fat diet for 10 days |
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Starvation ketosis in a breastfeeding woman [ | Bariatric surgery during lactation |
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Severe ketoacidosis in breastfeeding woman with low energy and carbohydrate intake [ | Illness while on a low carbohydrate diet |
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Ketoacidosis in a non-diabetic woman who was fasting during lactation [ | Starvation during lactation due to abdominal pain |
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Lactation ketoacidosis: an unusual entity and a review of the literature [ | No precipitating factor except for lactation |
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Life-threatening lactation or Bovine ketoacidosis [ | Frequent skipping of meals while on a high protein, low carbohydrate diet |
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A rare cause of metabolic acidosis: ketoacidosis in a non-diabetic lactating woman [ | Gastroenteritis in the setting of a low carbohydrate diet |
Table demonstrating serial pertinent laboratory values during hospitalization and after discharge.
On admission, June | June | June | June | On discharge, June | 1 week after discharge, June | |
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Serum bicarbonate (meq/L) | 6 | 10 | 24 | 30 | 29 | 23 |
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Glucose (mg/dl) | 50 | 124 | 112 | 105 | 99 | 77 |
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Insulin level (uiu/ml) | 3.4 | 11.1 | ||||
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Phosphorous (mg/dl) | 2.3 | 1.4 | 1.0 | 2.4 | 3.3 | 3.9 |
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Potassium (meq/l) | 4.2 | 3.0 | 2.6 | 3.1 | 4.3 | 4.0 |
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Calcium (mg/dl) | 7.3 | 7.9 | 8.8 | 8.6 | 9.2 | 8.8 |
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Urine Ketone | 4+ | |||||
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pH ABG | 7.11 | 7.28 | ||||
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pCO2 ABG | 17.0 | 15.8 | ||||
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Bicarbonate ABG | 5.3 | 7.3 |
ABG: arterial blood gas.
Ketogenic diet (KD) is described as a high-fat, adequate-protein, and low-carbohydrate diet (<50g/day) [
We came across few studies that evaluated the acid-base safety of patients on ketogenic diet, one showed that majority had a ketone level less than 54mg/dl and none was greater than 106 mg/dl while the other study reported patients had a mild compensated metabolic acidosis with no significant metabolic derangement [
Postpartum mothers are at an increased pressure to lose weight gained during pregnancy and may resort to this proven efficacious method of rapid weight loss. The increased energy demands of lactation which results in increased glucose utilization may lead to a dysregulation of the compensatory mechanism regulating normal ketone levels in lactating women on ketogenic diet [
Existing case reports like ours demonstrated complete resolution of symptoms, ketoacidosis, and laboratory derangements with rehydration and restarting normal diet.
Although ketogenic diet is being considered a safe nutritional intervention for weight loss and has grown to be a popular implementation for successful weight loss in the medical literature, social media, and fitness blogs, the index case may provide caution in lactating mothers on/or considering a ketogenic diet. It is important for clinicians to educate lactating mothers interested in weight.
The case submitted in this paper was also accepted as an abstract case at the American Society of Nutrition (ASN) conference on June
The authors declare that they have no conflicts of interest.