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Severe Ketoacidosis in a Patient with an Eating DisorderEun Hui Bae

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141

Letters to the Editor

www.cmj.ac.kr

http://dx.doi.org/10.4068/cmj.2016.52.2.141

Chonnam Medical Journal, 2016 Chonnam Med J 2016;52:141-142

Corresponding Author:

Hyoung Lho

Department of Emergency Medicine, North York General Hospital 4001 Leslie St, Toronto, ON M2K 1E1, Canada Tel: +1-416-756-6882, Fax: +1-416-756-6793, E-mail: hyoung.lho@utoronto.ca

Article History:

Received March 8, 2016 Revised March 22, 2016 Accepted March 25, 2016 TABLE 1. Biochemical markers

Blood (normal range) Urine

Venous pH 6.96 (7.32-7.42) 5.0

HCO3 (mmoL/L) 5 (23-31)

PCO2 (mmHg) 22 (40-50)

Base deficit 27 (0-2)

Homoglobin 136 (120-150)

Hematocrit (%) 42.1 (34-48)

MCV (fl.) 118 (84-95)

Glucose (mmoL/L) 4.9 (3.8-7.8)

Urea (mmoL/L) 2.5 (2.0-8.0)

Creatinine (mmoL/L) 90 (44-100)

Serum osmolarity 290 (275-295)

Sodium (mmoL/L) 131 (133-145)

Potassium (mmoL/L) 3.9 (3.3-4.5) Chloride (mmoL/L) 105 (95-107) Calcium (mmoL/L) 1.86 (2.15-2.55) Phosphate (mmoL/L) 0.98 (0.8-1.5)

Albumin (g/L) 39 (34-50)

Alkaline phosphatase (U/L) 153 (35-104)

AST (U/L) 46 (0-37)

ALT (U/L) 51 (0-41)

Lactate (mmoL/L) 1.1 (0.5-2.2)

Ketones + (neg) 1+

Severe Ketoacidosis in a Patient with an Eating Disorder

Eun Hui Bae1 and Hyoung Lho2,*

1Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea, 2Department of Emergency Medicine, North York General Hospital, Toronto, Ontario, Canada

Severe ketoacidosis with a blood pH below 7.0 is only rarely seen in other diseases except type 1 diabetes. This paper reports a case of severe ketoacidosis secondary to an eating disorder.

A 46-year-old woman presented to the emergency depart- ment with an acute onset of shortness of breath. She has a history of an eating disorder, an anxiety disorder, and hypothyroidism. Her body mass index was 19. Examination of the initial vital signs revealed the following: pulse, 91 beats/min; body temperature, 34.9oC; respiratory rate, 35 breaths/min; oxygen saturation, 100% on room air; and blood pressure, 130/70 mmHg. Urinalysis revealed specific gravity of >1.030, pH of 5.5, negative results for glucose, and positive results for ketone bodies (>150 mg/dL). Her serum glucose level was 4.9 mmol/L. Venous blood gas anal- ysis revealed the following: pH, 6.96; HCO3, 5 mmol/L, pCO2, 22 mmHg; base deficit, 27 and anion gap, 21. the pa- tient showed a high anion gap metabolic acidosis with prop- er respiratory compensation. Results of the blood analysis are shown in Table 1. The osmolar gap was 20, which sug- gested unmeasured anions. However, tests for ethanol, sal- icylate, ethylene glycol, and methanol levels were negative.

The serum ketone test was positive. These laboratory pa- rameters made us rule out diabetic ketoacidosis and alco- holic ketoacidosis as the cause of the metabolic acidosis.

Initially, the patient received a 5% dextrose solution in nor- mal saline (D5W NS). After 12 hours of hospitalization on D5W NS, venous blood gas analysis revealed improved re- sults: pH, 7.18; HCO3, 5 mmol/L; and pCO2, 13 mmHg, with a base deficit of 23.

Initially, the family and the patient told us that the pa- tient had been doing much better in the last 2 weeks regard- ing her eating habits. We asked her repeatedly and she fi- nally admitted to giving her food to her dog underneath the table. Moreover, she had been taking stool laxatives.

In a patient with ketonemia, low glucose levels excluded diabetic ketoacidosis as the cause of severe metabolic acidosis.1 Negative results for laboratory tests for toxicol- ogy and toxic alcohol levels led us to consider starvation as the etiology of the acid-base imbalance.2 Ketoacidosis sec-

ondary to starvation is due to diminished insulin secretion that leads to an increase in lipolysis and ketogenesis.3

Eating disorders not otherwise specified are a category of eating disorder that includes patients with early aber- rant eating patterns and weight management habits who do not meet the criteria for anorexia or bulimia nervosa.4 It occurs in approximately 3-5% of women aged between 15 and 30 years in Western countries.5 Patients with bulimia ten to abuse laxatives. It prevents the absorption of calo- ries, which may aggravate starvation ketoacidosis.6

In conclusion, starvation should be considered as one of the causes of severe ketoacidosis in individuals with an eat- ing disorder, even when the patient denies diet restriction.

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142

Starvation Ketoacidosis

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/

by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

CONFLICT OF INTEREST STATEMENT None declared.

REFERENCES

1. Shah P, Isley WL. Ketoacidosis during a low-carbohydrate diet.

N Engl J Med 2006;354:97-8.

2. Cahill GF Jr. Fuel metabolism in starvation. Annu Rev Nutr 2006;26:1-22.

3. Chalasani S, Fischer J. South beach diet associated ketoacidosis:

a case report. J Med Case Rep 2008;2:45.

4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Arlington:American Psychi- atric Association, 2013.

5. Putukian M. The female triad. Eating disorders, amenorrhea, and osteoporosis. Med Clin North Am 1994;78:345-56.

6. Mitchell JE, Hatsukami D, Pyle RL, Eckert ED, Boutacoff LI.

Metabolic acidosis as a marker for laxative abuse in patients with bulimia. Int J Eat Disord 1987;6:557-60.

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