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Diabetic ketoacidosis mimicking hyperemesis gravidarum: case report / Hiperemezis Gravidarumu Taklit Eden Diyabetik Ketoasidoz: Olgu Sunumu.


Diabetic ketoacidosis (DKA) characterized by hyperglycemia, ketosis and acidosis is a serious metabolic decompensation of diabetes mellitus (DM). It is a medical emergency that can occur in type 1, type 2 and gestational diabetes. Polyuria, polydipsia, nausea, vomiting, weakness, weight loss are the symptoms of DKA. Acidemia, hyperglycemia, increased anion gap, ketonemia, ketonuria are the laboratory findings. DKA can cause fetal and maternal mortality during pregnancy and usually occurs in the second and third trimester due to increased insulin resistance (1). Infections, emesis, non-compliance, insulin pump failure, drugs such as corticosteroids and [beta]-sympa-thetomimetic agents, undiagnosed pregnancy are the precipitating factors. Maternal acidosis, hyperglycemia, volume depletion, electrolyte imbalance may effect the fetus. Aggressive fluid replacement, insulin infusion, as well as searching, correcting and treating the precipitating factors and electrolyte imbalance are the treatment modalities (1), (2).

Nausea and vomiting accompany 50-90% of all pregnancies (3). It is mostly self-limiting and peaks at 9 weeks of gestation. The most severe degree of vomiting during pregnancy is hyperemesis gravidarum (HG). It is characterized by persistent vomiting, weight loss, ketonuria, electrolyte abnormalities, and dehydration (4).

Metabolic acidosis and ketonaemia may occur both in HG and DKA. Metabolic disorders such as DKA, gastrointestinal conditions, pyelonephritis, neurological causes and vestibular disorders should be considered in the differential diagnosis of HG (3), (4).

In this report, we describe a case of type 1 DM with fulminant course which occurred in the second trimester of pregnancy mimicking HG and resulted in fetal loss.

Case Report

A 30-year-old woman, nullipara-nulligravida, was admitted to a private clinic at 13 weeks of gestation with nausea, vomiting, poor appetite, shortness of breath, weakness and fatigue. She had polyuria, polydipsia and nocturia since the beginning of her pregnancy. In the first thirteen weeks of gestation, her physical findings and fetal growth had been normal. Nausea, vomiting and presence of ketonuria (+1) in urinary analysis were diagnosed as HG. Plasma glucose levels were not checked in the first trimester, but her pre-pregnancy blood chemistry was completely normal. After a short period of admission to private clinic, she developed incontinence, hypothermia, tachypnea, and stupor. Arterial blood gas analysis revealed severe metabolic acidosis (Table 1). Her blood glucose was extremely high with a level of 1800 mg/dL. Sodium level was 147 mmol/L (the corrected sodium level according to the plasma glucose level was 175 mmol/L) and potassium level was 2 mmol/L. Urine analysis demonstrated ketonuria 3+ and glucosuria. There was no elevation in pancreatic enzymes. Thyroid function tests were normal. She had massive vaginal bleeding, and a stillborn was delivered. The patient was transported to our intensive care unit with an admitting diagnosis of coma and DKA complicated with pneumonia. She was treated with intravenous insulin (75-100 U/day), saline and appropriate antibiotic therapy. Antiglutamic acid decarboxylase (GAD), islet cell antibodies (ICA) and insulin auto antibodies (IAA) were negative. Fasting serum C-peptide was 0.319 (0.9-4.3 ng/mL) and HbA1c was 9.1%. Urinary organic acid analysis was negative. The genotype of human leukocyte antigens (HLA) of the patient was DRB1*04 and DRB1*09. Based on her clinical and laboratory findings, she was diagnosed as type 1 DM with fulminant course. After the treatment, the plasma glucose level was lowered to < 180 mg/dL and ketonuria disappeared. She reported bilateral leg pain as burning, pins and needles, tingling, aching that was worse during the night. Cranial magnetic resonance imaging (MRI) revealed hypointense areas in the pons (figure 1). Peroneal nerve response amplitudes were decreased in electromyography. She was discharged with prandial and basal insulin for diabetes control.

Table 1. Admission biochemical data of the patient
Analysis Normal range
Glucose 1800 mg/dL 0-160
HBA1C 9.1% 4.8-6
Serum C-peptide 0.319 ng/mL 0.9-4.3 ng/mL
BUN 11 mg/L 7-17
Creatinine 0.8 mg/dL 0.6-1.1
Sodium 147 mmol/L 135-145
Potassium 2 mmol/L 3.5-5.3
Amylase 42 U/L 28-100
AST 15 U/L 0-36
ALT 13 U/L 0-52
TSH 1.03 uIU/mL 0.47-4.64
FT4 0.8 ng/mL 0.71-1.85
Hematocrit 40% 34-47
Urine ketones positive (+++) Negative
Arterial blood gas
Anion GAP -30
Arterial pH 6.85
Bicarbonate 2.7
Effective Serum 398 mOsm/kg 285-295 mOsm/kg
Osmolality [H.sub.2]O [H.sub.2]O


Nausea and vomiting can accompany pregnancy. The most severe form of vomiting in pregnancy is HG and the incidence of HG is 0.5-2% of all live births. Diagnosis of HG should be made following the exclusion of other causes including DKA. Laboratory analysis should include haematocrit, electrolytes, transaminases, bilirubin, plasma glucose level, urinary status and thyroid function tests (3).

DKA is mentioned in the differential diagnosis of HG. It is an emergency state of inadequate insulin secretion and can be exaggerated in pregnancy. Vomiting, polyuria, dehydration, weakness, hyperventilation, altered mental status are clinical presentations of DKA (5). Montoro et al. reported that 30% of DKA cases occur in pregnant women who have previously undiagnosed diabetes (6). The most common precipitating factor of DKA was emesis in the study by Rodgers et al. (7). Other precipitating factors are infections, poor patient compliance, undiagnosed diabetes, insulin pump failure, drugs and physician management errors. In the literature, maternal mortality is reported as 5 to 15% and fetal mortality is reported as 9-85% in DKA. Fetal hyperglycemia, fetal hyperinsulinemia, as well as decreased 2,3-DPG levels causing an increased affinity of maternal hemoglobin for oxygen can lead to lactic acidosis and hypoxia in the fetus (2),(5).

Nausea and vomiting are usually nonspecific symptoms and can cause dehydration, acidosis due to inadequate nutrition, loss of hydrochloride and hypokalemia by HG. Nausea, vomiting, metabolic ketoacidosis and ketonaemia may occur in both HG and DKA. Metabolic disturbances are considered in the risk factors of HG. So, HG can trigger DKA and DKA can be complicated by HG or vice versa.

Our patient had no significant past medical history, and the course of the pregnancy was uneventful. She had polyuria, polydipsia and nocturia for nearly two months. She suffered from nausea and vomiting for two weeks. At admission, she had a glucose level of 1800 mg/dL and severe acidosis. Such high levels of glucose can be triggered and complicated by DKA and dehydration caused by HG. She was diagnosed with subtype 1B DM, due to absence of ICA, GADAb, IAA, and anti-insulinoma-associated antigen 2 antibody (IA-2Ab) at the time of disease onset. There has been a progressive and rapid loss of pancreatic beta cells.

The treatment involves aggressive fluid treatment, intravenous insulin administration and treatment of precipitating factors. After the acute phase of ketoacidosis, multiple insulin injections should be administered (2).

Our patient suffered from bilateral pain as burning, pins and needles, tingling, aching on her legs that was worse during the night. She had these complaints after aggressive, urgent insulin and fluid treatment. The existing neurological complaints on her legs with EMG findings let us to make the diagnosis of insulin neuritis. Diabetic neuropathy includes symptoms and signs of neuropathy, and the prevalence increases with the duration of DM. This type of neuropathy following rapid improvement in glycaemic control usually manifests in the early course of diabetes with pain that aggravates at night. Ischaemic or metabolic components are implicated in the etiology (8). Cranial MRI showed hypointense areas in the pons. These radiological findings are thought to be caused by hyperglycemia, hyperosmolarity and ketosis.

In conclusion, glucose levels should be monitored regularly during the pregnancy. Physicians should be careful if a pregnant woman shows hyperglycemic symptoms not to overlook the disease. Physicians' management and diagnosis errors, as well as delayed treatment can cause maternal death and fetal demise. The treatment of DKA must be started urgently, once the disease is diagnosed, and should not be discontinue until satisfactory and adequate recovery ensues.


Inform consent was obtained from the patient.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.


(1.) Charfen MA, Fernandez-Frackelton M. Diabetic ketoacidosis. Emerg Med Clin North Am 2005;23:609-28.

(2.) Kamalakannan D, Baskar V, Barton DM, Abdu TA. Diabetic ketoacidosis in pregnancy. Postgrad Med J 2003;79:454-7

(3.) Jueckstock JK, Kaestner R, Mylonas I. Managing hyperemesis gravidarum: a multimodal challenge. BMC Med 2010;8:46.

(4.) Niebyl JR. Clinical practice. Nausea and vomiting in pregnancy. N Engl J Med 2010;363:1544-50.

(5.) Parker JA, Conway DL. Diabetic ketoacidosis in pregnancy. Obstet Gynecol Clin North Am 2007;34:533-43.

(6.) Montoro MN,Myers VP, Mestman JH, et al. Outcome of pregnancy in diabetic ketoacidosis. Am J Perinatol 1993;10:17-20.

(7.) Rodgers BD, Rodgers DE. Clinical variables associated with diabetic ketoacidosis during pregnancy. J Reprod Med 1991;36:797-800.

(8.) Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J 2006;82:95-100.

Zeynep Osar Siva, Ozlem Celik, Deram Buyuktas *, YalIm Dikmen **, Erkan YIlmaz ***

Istanbul University Division of Endocrinology Metabolism and Diabetes, Department of Internal Medicine, Istanbul, Turkey

* Istanbul University Cerrahpasa Medical School, Department of Internal Medicine, Istanbul, Turkey ** Istanbul University Cerrahpasa Medical School, Department of Anaesthesiology, Istanbul, Turkey

*** Istanbul University Cerrahpasa Medical School, Blood Bank, Tissue Typing Laboratory, Istanbul, Turkey
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Title Annotation:Case Report Olgu Sunumu
Author:Siva, Zeynep Osar; Celik, Ozlem; Buyuktas, Deram; Dikmen, YalIm; Yilmaz, Erkan
Publication:Turkish Journal of Endocrinology and Metabolism
Article Type:Report
Date:Sep 1, 2011
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