Case Report: Lactation Ketoacidosis Can Complicate the Ketogenic Diet



 

Michelle C Liu RD, BS; Ruth Ann Bertsch MD, PhD, FACP

Perm J 2021;25:20.162 [Full Citation]

https://doi.org/10.7812/TPP/20.162
E-pub: 01/06/2021Full Citation

Introduction: Ketoacidosis is a metabolic condition caused by the buildup of ketone bodies. The most common causes are diabetes, alcoholism, and starvation. This is a case of a lactating mother on a ketogenic diet who developed a community-acquired pneumonia and then went into life-threatening ketoacidosis.

Case Presentation: A 32-year-old, lactating, 8-week-postpartum woman presented to the hospital complaining of nausea, vomiting, rhinorrhea, and cough. She had no history of diabetes or of alcohol or drug use but reported following a ketogenic diet and was found to have a pneumonia. The pneumonia was treated with antibiotics, and the acidosis resolved with a dextrose solution.

Conclusion: We report the case of a mother who, while lactating and losing weight on a ketogenic diet, developed a pneumonia and then went into ketoacidosis. Physicians should be aware that patients on the ketogenic diet are at risk for life-threatening acidosis, especially if they develop a second and/or third stressor or energy requirement on top of the low-carbohydrate diet. This case and those reviewed in the literature indicate that ketogenic diets may not be safe during lactation and could be associated with increased morbidity.

Keywords: Atkins diet, ketoacidosis, ketogenic diet, ketosis, lactating, lactation, Paleo diet

INTRODUCTION

Ketoacidosis is a metabolic condition caused by the buildup of ketone bodies.1 Although most ketoacidosis is caused by diabetes, alcoholism, and starvation, lactation ketoacidosis is a rare subtype of starvation ketoacidosis.2 We present a case of ketoacidosis in a woman who was simultaneously experiencing 3 metabolic stressors: strict adherence to a ketogenic diet, lactating a growing infant, and fighting a pneumonia.

CASE PRESENTATION

A 32-year old gravida 2, para 2, 8-weeks-postpartum lactating woman presented to the hospital with the chief complaint of 1 day of nausea, vomiting, and rigors and 1 week of upper respiratory infectious symptoms including rhinorrhea and cough. She had an insignificant past medical history other than hypertension and had no history of diabetes. The patient reported starting the ketogenic diet nearly 1-2 months prior to her admission, following the birth of her daughter, and was limiting her carbohydrate intake to 25 g/d. She did so by eliminating all grains and concentrated sweets and by consuming only low-carbohydrate fruits (specifically strawberries and blackberries). Her main motivation for the diet change was weight loss following her pregnancy-associated weight gain and having seen her sister successfully lose weight following this diet. While on this diet, the patient breast fed on average 8-10 times per day and continued to take her prenatal vitamins. She denied alcohol and other substance use.

In the emergency department, her vital signs included: temperature of 97.9°F, respiratory rate of 20, heart rate of 126, and blood pressure of 146/103. On physical examination, the patient was alert and oriented; her abdomen was soft and nondistended. Serum labs (Table 1) included a bicarbonate of 8 mEq/L, an anion gap of 26, glucose of 89 mg/dL, and a lactic acid of 1.2 mmol/L. A urinalysis showed 80 mg/dL of ketones (reference range = 0-4 mg/dL) and no leukouria. A complete blood count showed a leukocytosis of 18 k/µL, 90% neutrophils, 1% immature granulocytes, and a hemoglobin of 16.5. She was administered 2.7 L of normal saline, and subsequent blood gas analysis in the emergency department showed a pH of 7.16 and calculated bicarbonate of 5.2 mmol/L (Table 1). Also, a computerized tomography scan of the abdomen was obtained to assess her vomiting and subjective abdominal pain. The imaging revealed a very small (6 mL) left lower lobe consolidation, likely the sequelae of her cold-like symptoms of coughing and rhinorrhea.

Table 1. Laboratory values during hospitalization

Timeline Day 0 2000 h 2050 2103 2330 Day 1 0100 0430 0830 1240
Intervention   NS bolus started       D5-1/2 NS started at 100 mL/h    
Chemistry
 Na (mEq/L) 134     136     139 137
 K (mEq/L) 4.2   4.0   3.5 3.3
 Cl (mEq/L) 100   107   110 108
 Bicarbonate (mEq/L) 8   8   11 14
 BUN (mg/dL) 20   16   10 11
 Creatinine (mg/dL) 1.1   0.8   0.8 0.7
 Glucose (mg/dL) 89   73   77 107
 Anion gap 26   21   18 14
 AST (U/L) 11          
 ALT (U/L) 11          
 ALKP (U/L) 177          
 Bilirubin (mg/dL) 0.4          
 Lipase (U/L) 51          
 Serum lactase (mEq/L)   1.2        
 Albumin     3.9      
Arterial blood gas
 pH         7.16 7.2    
 pCo2 (mmHg)       15 19    
 Bicarbonate (mmol/L)       5.2 7.1    
Urinalysis
 Ketones (mg/dL) 80              
 Leukocyte (Leu/µL) Negative          
 Glucose Negative          
 Specific gravity 1.019          
 WBC (HPF) 13          
 Squamous cells (LPF) 70          

ALKP = alkaline phosphatase; ALT = alanine aminotransferase; AST = aspartate aminotransferase; BUN = blood urea nitrogen; HPF = high-power field; LPF = low-power field; NS = normal saline; WBC = white blood cell. Bold numbers signify those outside the reference range, i.e. abnormal values.

From her labs and symptoms, she was diagnosed with a metabolic acidosis from ketogenesis. Other causes of ketoacidosis were ruled out because she was not a diabetic and her history and toxicology were negative for ethanol.

The patient was treated with D5-1/2 normal saline at 100 mL/h gtt, and within 11 hours her anion gap had closed at 15 and the bicarbonate had increased to 14 mmol/L. (We suspect the last blood gas was actually drawn at least 10 minutes before the D5-1/2 normal saline was started.) She was also given extensive nutritional education regarding sufficient energy intake for breast-feeding and was ultimately discharged tolerating a regular diet. Also due to the findings on her computerized tomography scan, the patient was given a 5-day course of antibiotics for pneumonia. She was discharged on hospital day 1 with follow-up with her regular physician in 10 days (Figure 1).

tpj20162f1

Figure 1. Timeline of case events.

Patient Perspective

Staying within my BMI has always been a challenge for me. I tried exercising and diet pills, but nothing seemed to last. At first, I wasn’t interested in the keto diet or lifestyle change to help me shed those pounds. I have a sweet tooth; I didn’t want to give up that good stuff. My curiosity spiked when I noticed my sister, who also found it difficult to lose weight, thinning out. She encouraged me to change my lifestyle with keto but to start after giving birth to my second daughter.

Approximately a month after giving birth, I jumped into the keto diet. I was excited to see the pounds shed quickly. Within the first week I had the keto flu. It was hard on my body. I remember waking up in the middle of the night to vomit. I kept up with the diet thinking all is normal. Besides the keto flu, I was happy with the lifestyle change. This was the lightest I’ve been in years. I was also nursing during this time. Within 3-4 weeks of the diet, I began getting really fatigued and tired. One day I couldn’t keep any food or drink down and I kept vomiting brown liquid. I waited until my husband came home from work, which was 8-9 hours later. We knew we had to go to the ER. I recall abdominal pain, shortness of breath, and symptoms of a fever.

My body nutrients and electrolytes were replenished at the hospital. I was thankful for the turnaround because it could have been worse. After leaving the hospital, I realized that my priorities should be reviewed. I wanted my newborn to have a good milk supply so I stopped the keto diet.

DISCUSSION

Low Carbohydrate Diets

The Atkins Diet

The ketogenic (i.e., very low carbohydrate) diet has gained popularity due to the rapid weight loss many achieve. Although previously the diet had been used mostly for epileptic patients, Dr. Atkins popularized low-carbohydrate diets for weight loss in the 1970s.3 There are multiple varieties of the Atkins diet. In the Atkins 20, people limit their carbohydrate intake to 20 g and slowly increase their intake over 4 phases. In the Atkins 40, people limit their carbohydrate intake to 40 g/d and gradually increase their intake over a period of time as well.4

The Ketogenic Diet is Very Popular for Good Reason

In the last few years, the ketogenic diet, which does not increase carbohydrates every week like the Akins diet, has become one of the more popular diets. This version of a low-carbohydrate diet is trendy not only due to rapid weight loss but also due to the common experience that ketones suppress appetite. Anorexia increases and falls in proportion to the degree of ketonemia. Research subjects consumed a ketone ester drink that increased the concentration of ketone body β-hydroxybuturate in the blood.5 Subsequently, in proportion to the rise in serum β-hydroxybuturate, one of the ketone bodies involved in ketosis, the subjects experienced increased satiety and decreased appetite when compared with an isocaloric dextrose drink. In addition, the concentration of ghrelin, the hormone associated with the feeling of hunger, decreased as β-hydroxybuturate increased.6

Typically the ketogenic diet reduces total carbohydrate intake to between 20 and 50 grams/d (dependent on individual energy requirements), which is roughly equivalent to 1-2 bananas or 2-3 slices of Wonder Bread. Generally, the ketogenic diet derives 70%-80% of its calories from fat, 10%-20% from protein, and 5%-10% from carbohydrate.3 This is unlike other low-carbohydrate diets, such as the paleo diet, which recommends more protein and carbohydrate (30% of calories from both) and only 40% of calories from fat7 (Table 2).8 The ketogenic diet emphasizes moderate protein because too much protein intake can prevent ketosis by allowing the body to utilize amino acids for gluconeogenesis.3

Table 2. Comparison of common low-carbohydrate diets

Diet Atkins 20 Atkins 40 Paleo Ketogenic
Carbohydrate (% of total calories) 5%-10% 10%-15% 30% 5%-10%
Grams carbohydrates in a 200 cal diet 25-50 50-75 150 25-50
Protein (% of total calories) 20%-30% 20%-30% 30% 10%-20%
Grams protein in a 200 cal diet 100-150 100-150 150 50-100
Fat (% of total calories) 60%-70% 55%-65% 40% 70%-80%
Grams fat in a 200 cal diet 135-155 120-145 90 155-175

Compositions of low carbohydrate diets, specifically the paleo diet, the ketogenic diet, and phase 1 of both the Atkins 20 and Atkins 40 diet. Also included is an example of total grams of each macronutrient in a 2000 cal/d diet.8 .

Example of the Ketogenic Diet in Action: Our Patient

Based on our patient’s weight history and other information obtained during her nutrition interview, she was found to have had 8.1% (10 lb) weight loss in less than 1 month and an overall 19.2% (27 lbs) weight loss from her pregravid weight. Both degrees of weight loss were considered severe per evidence-based ASPEN (American Society for Parenteral and Enteral Nutrition) criteria, despite her relatively normal admission body mass index of 24.45 kg/m2. Her food intake was inadequate, consisting of mostly salads, bacon, and chicken. In summary, she met criteria for moderate protein calorie malnutrition per the ASPEN definition. Such malnutrition puts people at risk for deficiencies of protein, minerals, vitamins, and other micronutrients. This puts people at higher risk for infection and a variety of other organ dysfunctions.9

The Physiology of Energy Mobilization in Starvation and Ketogenic Diets in Nonlactating, Nonpregnant Healthy Adults

In the setting of low glucose consumption, glycogen stored in the liver is the primary source of glucose. However, a prolonged low-carbohydrate diet depletes the hepatic glycogen stores. This depletion can happen within 24 hours of fasting or restricting carbohydrate intake.10 After 1 or several days,11 fat becomes the main energy source for nearly all tissues due to the decrease in glucose availability, the subsequent decrease in circulating insulin, and a higher concentration of glucagon.10 The scarcity of insulin increases lipolysis from adipose tissue and consequently increases free fatty acids in the serum.12 Tissues convert the fatty acids into energy by oxidizing them into acetyl-CoA molecules and then running those through the citric acid (Krebs) cycle.13

Insulin and glucagon are not the only hormones involved in shifting the metabolism from burning glucose to burning fat. Catecholamines, released during stresses like dehydration and infection, increase lipolysis.14 When the body is stressed for more than a few days, cortisol also increases fatty acid release while reducing insulin action.1,15 Glucagon, the catecholamines, and cortisol all effectively push substrate into the hepatic gluconeogenic pathways.14

The Physiology of Lactation during Ketosis

Milk production uses an additional 300-500 kcal/d above the metabolic requirements of a nonlactating woman.16 The mammary glands rely on glucose absorption from the blood.17 When the mother eats an adequate amount of carbohydrates, they get converted into glucose via hepatic gluconeogenesis pathways,13 and the mother can supply the mammary glands adequately for milk production.17,18 However, in the setting of inadequate carbohydrate intake, the liver increases gluconeogenesis, and the minimally available amounts of glucose go mainly to the mammary glands.19 In addition, more free fatty acids are released, and ketogenesis is increased in order to feed the rest of the body.19

The Pathogenesis of Ketosis

When the demand for fuel increases further, fatty acid oxidation rates accelerate, and acetyl-CoA production can exceed the capacity of the citric acid cycle to burn the acetyls all the way to carbon dioxide. Thus, acetyl-CoAs are diverted into the ketogenesis pathway instead.13 This produces 3 major ketone bodies: acetoacetate, β-hydroxybutyrate, and acetone. The production of large amounts of ketone bodies is associated with the production of acid.20

Under most circumstances, a fasting person who is not exercising strenuously can maintain ketosis comfortably. A well individual on a ketogenic diet has multiple mechanisms for keeping acid within an acceptable range. End organs, such as the brain, start absorbing ketone bodies.1 Ketone bodies themselves inhibit lipolysis and stimulate insulin.1,21 For example, the minimal amount of insulin circulating is often sufficient to decrease fatty acid mobilization and to inhibit ketogenesis and, thus, inhibit acid production.22,23 The ketone bodies make the adipose tissue more sensitive to insulin.21 Also, the kidney excretes nitrogen in the form of the ammonia cation instead of as the uncharged urea molecule.22

Normally a nonpregnant, nonlactating adult following a very-low-carbohydrate diet does not develop a metabolic acidosis from ketogenesis.24,25 In fact, the ketogenic diet has been used for decades for epilepsy in children often without causing nausea, vomiting, abdominal pain, or other symptoms of ketoacidosis.26,27

The Pathogenesis of Ketoacidosis

When the drive for energy increases further, more ketone bodies accumulate, the pH of the blood drops, and acidosis, specifically ketoacidosis, arises. What would push the hormones to overstimulate ketone production beyond ketosis into ketoacidosis? Starvation plus third-trimester pregnancy has caused ketoacidosis in at least several other patients.28 Often, lactating mothers following the ketogenic diet had to experience a third stressor before going into ketoacidosis.29-36 Often the mother had been vomiting for several days, suggesting the vomiting may have started before the acidosis worsened it.31,32 In other reports, lactating mothers present with an infection, such as a urinary tract infection31 or, in our case, pneumonia. Our patient’s pneumonia may have contributed to her metabolic acidosis due to the effect of stress response hormones on glucose metabolism.

The Treatment Shuts Down Acid Production

The treatment for diet- and stress-induced ketoacidosis is simple and similar to that for alcoholic ketoacidosis. Infusing dextrose stimulates the pancreas to secrete insulin. The extra insulin significantly increases the insulin/glucagon ratio, impeding ketogenesis. The insulin reduces the production of free fatty acids and inhibits the hepatic synthesis of ketone bodies1 and thus reduces acid production. In our case, the addition of the antibiotics helped resolve the third stressor—her pneumonia.

CONCLUSION

We report the case of a mother who, while lactating and losing weight on a ketogenic diet, developed a minuscule pneumonia and then went into ketoacidosis. Physicians should be aware that patients on the ketogenic diet are at risk for life-threatening acidosis, especially if they develop a second and/or third stressor or energy requirement on top of the low-carbohydrate diet. This case and those reviewed in the literature indicate that ketogenic diets may not be safe during lactation and could be associated with increased morbidity.

Disclosure Statement

The author(s) have no conflicts of interest to disclose.

Acknowledgments

Kathleen Louden, ELS, of Louden Health Communications performed a primary copy edit.

Author Affiliations

The Permanente Medical Group Inc, Sacramento, CA

Corresponding Author

Ruth Ann Bertsch, MD, PhD, FACP ()

Author Contributions

Michelle C Liu, RD, BS, counseled the patient in the case report, followed her up, researched the background, wrote the first draft of the report, drafted the tables and figures, and participated in the rewriting process and further research with the corresponding author. Ruth Ann Bertsch, MD, PhD, FACP participated in the rewriting process and further research with the first author.

How to Cite this Article

Liu MC, Bertsch RA. Case report: Lactation ketoacidosis can complicate the ketogenic diet. Perm J 2021;25:20.162. DOI: 10.7812/TPP/20.162

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Keywords: 

Atkins diet, ketoacidosis, ketogenic diet, ketosis, lactating, lactation, Paleo diet

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