Severe diabetic ketoacidosis in combination with starvation and anorexia nervosa at onset of type 1 diabetes: A case report
A 53-year-old woman with a history of AN since adolescence was admitted to the psychiatric clinic at the Uppsala University Hospital due to psychotic behaviour and inability to take care of herself. There were reports of paranoid schizophrenia and personality disorders, but her contacts with the psychiatric clinic were sparse, and she used no medications. According to her relatives she had isolated herself the last two weeks, and over the last two months she had barely been eating at all. Twenty-four hours after admission to the psychiatric clinic she was admitted to the clinic of internal medicine and presented at the emergency room (ER) in a cachectic state with hypothermia (32.6°C). Her mental status was altered (reaction level scale 2), and she barely responded to questions, being close to stupor. There were clinical signs of severe dehydration and muscle atrophy. Her breathing was shallow with 30 bpm, whereas blood pressure and pulse rate were normal, 110/60 mmHg and 77 bpm (see for a summary of the initial physical examination). She denied alcohol and any substance abuse. An initial arterial blood gas analysis displayed pH 6.895, pCO2 0.93 kPa, pO2 22 kPa, and P-glucose 40.6 mmol/L. There were no signs of infection, and electrolytes were normal (see for a summary of laboratory screening). She was immediately admitted to the intensive care unit (ICU), where rehydration was initiated with warm fluid combined with re-warming with heated blankets. Bicarbonate (100 mL) was administered i.v. in order to reverse acidosis; pH increased to 7.1, and blood glucose decreased to 35 mmol/L. Six hours after ICU admission insulin infusion was started with initially 0.5 IU/h (0.0128 IU/kg) combined with 5 mmol potassium/h. The patient's pH was normalized 15 hours after admission to the ICU, and the blood glucose concentration was kept around 15 mmol until 36 hours after admission. Variations of pH, glucose concentration, and arterial pCO2 and pO2 during the first 24 hours have been displayed in . Laboratory screening at the ICU revealed a P-C-peptide concentration of 0.14 nmol/L (ref. 0.4–1.5 nmol/L), a HbA1c of 151 mmol/mol (ref. <46 mmol/mol), and presence of both glutamic acid decarboxylase (GAD) (74 IE/mL, ref. <5) and insulinoma antigen 2 (IA2) antibodies (69 kE/L, ref. <8).\nDue to the risk of re-feeding syndrome, the intake of calories was restricted to 500 kcal over the first 24 hours and then increased when the patient was able to drink nutritional drinks. The risk of re-feeding syndrome is especially high in patients with a BMI <16, recent weight loss, and electrolyte abnormalities (). In order to prevent re-feeding syndrome, especially carbohydrates should be restricted whereas proteins and fats seem to be less of a threat (). However, in this case administration of i.v. glucose (120 kcal) in the first 24 hours could not be avoided, since plasma glucose concentrations had to be maintained around 15 mmol/L during the insulin infusion in order to prevent the risk of brain oedema. Remaining energy intake was administered per os as nutritional drinks with a balanced protein, fat, and carbohydrate content. A transthoracic echocardiogram was performed in order to exclude ventricular dysfunction and mitralic valve prolapse which can be observed after starvation and can potentially be lethal, especially in combination with re-feeding syndrome (). An expanded health history revealed that the patient had rapidly lost 10 kilograms of weight over the last two weeks and had polydipsia and polyuria. It was noted that her niece had T1D but there was no family history of diabetes.\nAs pH and blood glucose concentrations normalized, the patient improved; she was transferred to an internal medicine ward, and after optimization of the insulin regime she was transferred to the psychiatric clinic for continuous psychiatric care. She is currently on treatment with Insulin Glargine and Insulin Aspart, and on her last clinical control her fasting glucose was 16.1 mmol/L (ref. 4.0–6.0), HbA1c 82 mmol/mol (ref. 31–46), and her P-C-peptide had further decreased to 0.093 nmol/L (ref. 0.4–1.5). There have been no additional episodes of DKA, and her weight has increased to 55 kg with a BMI of 18.2 kg/m2 (ref. 20–25). In , there is a summary of laboratory screening six months post-DKA.