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| Year : 2007 | Volume
: 18
| Issue : 4 | Page : 590-593 |
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| Euglycemic Diabetic Ketoacidosis in Pregnancy |
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Nauman Tarif1, Wisam Al Badr2
1 Department of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia
2 Department of Medicine, King Faisal Specialist Hospital, Riyadh, Saudi Arabia
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 Abstract | | |
Diabetic ketoacidosis (DKA) can be a catastrophic event during pregnancy, complicating almost nine percent of diabetics in pregnancy. It induces both maternal and fetal mortality. Ketosis has been implicated in fetal distress and causes adverse neurological outcome. DKA with a relatively low blood sugar levels is called euglycemic DKA, which is a rare entity and reported usually in type I diabetic patients. A 37-year-old Saudi female patient known to have type II diabetes developed euglycemic [blood glucose level 4.3 mmol/L (78 mg/dl)] DKA while in her fifth pregnancy. She responded to intravenous dextrose and insulin with gradual improvement. Euglycemic DKA should be considered in type II diabetics during pregnancy and treated promptly. Keywords: Euglycemia, Diabetes mellitus, Ketoacidosis
How to cite this article:
Tarif N, Al Badr W. Euglycemic Diabetic Ketoacidosis in Pregnancy. Saudi J Kidney Dis Transpl 2007;18:590-3 |
| Introduction | |  |
Diabetic ketoacidosis (DKA) is a state characterized by hyperglycemia (glucose >250 mg/dl), acidosis (pH <7.35), low serum bicarbonate, high anion gap and positive serum and urinary ketones. [1],[2],[3],[4] DKA is the result of an absolute or relative deficiency of insulin and increase in the level of counter regulatory hormones. The pathophysiology of DKA is based on the inability of cells to take up and utilize glucose and an increased degree of lipolysis and proteolysis, the end-result being volume depletion and a high anion metabolic acidosis. Burge et al, in their study noted that a fast of short duration (32 hours) predisposes type I diabetic subjects to an accelerated development of ketoacidosis during insulin deficiency with normal serum glucose levels. [5] They proposed that suppressed glucose production was due to the depletion of hepatic glycogen reserves after a 32-hour fast.
Gestational Diabetes Mellitus (GDM) is a common abnormality of glucose metabolism during pregnancy, which affects fetal development and leads to peripartum complications. [3] The prevalence of DKA in pregnant type I and type II diabetics was reported to be 9.3% by Cousins in a review of all pregnant diabetic women presenting from 1965 till 1985 at their institution. [6] The development of diabetic ketoacidosis in pregnancy is a medical emergency, requiring treatment in an intensive care setting. Both the mother and the fetus are at risk for significant morbidity and mortality. [4] Normal glucose level, euglycemia, with DKA is a rare occurrence and commonly associated with type I diabetic patients. Euglycemic DKA needs consideration in the correct scenario and treated promptly. We present here a case of Type II diabetic pregnant female with euglycemic DKA.
| Case Report | | |
A 37-year-old Saudi female patient developed GDM in her third pregnancy nine years ago. The patient continued to be diabetic postpartum and was treated with oral hypoglycemic medications. The fourth pregnancy was uneventful with use of insulin during pregnancy. During her current pregnancy (fifth), insulin was started with regular follow-up in the antenatal clinic. Three weeks prior to presentation (32-weeks gestation), she had presented to the emergency room with hyperglycemia and her dose of insulin was adjusted. At 35-weeks of gestation she presented to the emergency room again with nausea and diffuse abdominal pain of 48-hours duration, which prevented her from taking any food orally. She therefore omitted her insulin doses during the 48-hours prior to hospitalization. She did not have fever, urinary tract or respiratory tract symptoms. She had two episodes of self limiting diarrhea a day before. Physical examination revealed euvolemia. She was afebrile, blood pressure was 120/63 mm Hg without a postural fall, mild diffuse abdominal tenderness with normal bowel sounds. There was no other abnormality detected on physical examination. Fetal monitoring was normal. The laboratory data, on presentation to the emergency room, revealed a blood glucose level of 4.3 mmol/L (77.4 mg/dl) with normal urea and creatinine levels. Her total leukocyte count was normal with no shift to the left. The arterial blood gases revealed a pH of 7.32, carbon dioxide 21.9 and serum bicarbonate of 10.4 mmol/L and an anion gap of 17 indicating high anion gap metabolic acidosis. The liver function tests and coagulation profile were within normal limits. The urine analysis was significant for +4 ketones with no hematuria or leukocyturia. The patient in the meantime was hydrated with normal saline. A repeat blood gas revealed worsening of metabolic acidosis with a pH of 7.23 and serum bicarbonate 7.5 mmol/L. Conditions causing high anion gap metabolic acidosis were considered. Serum lactate and renal profile were normal. The osmolal gap was only 3 mosml/L, which ruled out ingestion of any acidic substances. Serum salicylate level also was low. Serum amylase and abdominal ultrasound were normal which excluded any intra-abdominal pathology such as bowel ischemia. The patient's blood glucose levels were repeatedly below 11.0 mmol/L (200 mg/dl). A diagnosis of euglycemic DKA was therefore entertained and she was started on insulin and dextrose simultaneously. Improvement in plasma pH, serum bicarbonate and gradual clearing of ketoneuria as well as her abdominal pain was noted [Table - 1]. She was asymptomatic by the fourth day and infusions were stopped. She was discharged in stable condition five days later.
| Discussion | | |
In general, DKA presents with blood glucose levels of >13.9 mmol/L (250 mg/dl).[2],[7] Our patient had normal, or indeed low blood glucose levels, 4.8 mmol/L (86 mg/dl] and moderate degree of DKA, anion gap of >12, serum bicarbonate < 15 mmol/L and pH reaching 7.27. All the possible causes of high anion gap metabolic acidosis were excluded and therefore euglycemic DKA was considered. 15% of DKA patients present with blood glucose levels below 300 mg/dL. [8] Various reasons noted for this discrepancy include insulin pump use, administration of insulin on the way to the hospital, pregnancy, prolonged fasting and alcohol consumption. In our patient, pregnancy and fasting due to nausea were the only factors, however a self-limiting viral infection causing gastroenteritis could be the precipitating reason. DKA is commonly seen in type I diabetics with pregnancy, although gestational diabetics have also been frequently reported to present with DKA.[9],[10],[11],[12]
Euglycemia does not rule out DKA and a high index of suspicion is required in the appropriate clinical setting as in our case.[5],[6],[8],[13] Most of the euglycemic DKA patients are young, well hydrated, on insulin and facing an intercurrent illness. [6] The exact cause of euglycemic ketoacidosis is unknown, but it is important to recognize the condition early. Delay in diagnosis will preclude early insulin infusion in the absence of hyperglycemia as in our case. Fasting occurs frequently in conjunction with DKA, either as a result of the underlying condition such as infection, myocardial infarction, pancreatitis, etc. or as a result of the worsening ketoacidosis itself. Fasting could result in decreased glucose production or increased glucose utilization. [5] Burge et al, in type I diabetic pregnant patients, noted that decreased rate of glucose production was the primary mechanism and a likely explanation for supperssed glucose production in cases of euglycemic DKA. [5] They also noted progressive development of ketosis in both DKA and euglycemic DKA conditions, but the rate of rise of plasma ketones increased in the fasting state. They suggested that accelerated development of ketosis might be attributable to the effects of elevated levels of glucagon and/or catecholamines on lipolysis. [5] Insulin therefore, must still be administered to correct the ketoacidotic state and intravenous glucose must be given concurrently to prevent resultant hypoglycemia.[9],[11] Our patient, firstly being pregnant, had the appropriate setting for developping euglycemic DKA; a mild viral illness that led to nausea, decreased appetite and fasting for almost 48 hours could have been contributory factors.
Despite contemporary methods of diabetes care, near-normal plasma glucose levels are not enough to preclude diabetic ketoacidosis especially in a pregnant diabetic. Cullen et al reported 11 cases of DKA in pregnancy, four of whom had near normal blood glucose of <11.0 mmol/L (200mg/dl). [8]
Montoro MN et al studied 20 consecutive cases of ketoacidosis during pregnancy in type I diabetic women. [9] Two of their patients had euglycemic DKA with blood glucose <11.0 mmol/L (200 mg/dl) despite profound ketoacidosis. As noted, all these mentioned cases were diagnosed in type I diabetic patients. In the study by Cousins et al, DKA was noted in 9.3% of pregnant diabetic patients. [6] Although their review included both type I and gestational diabetics, they however did not specify the type.
Euglycemic DKA occurring in a pregnant type II diabetic patient is not common. [5],[6],[8],[11],[12],[13] Our patient was on oral hypoglycemic agents prior to pregnancy and insulin was given only during pregnancy. We retrospectively reviewed 4466 visits to the obstetrics emergency room over a period of nine months for a diagnosis of DKA in the presence of gestational diabetes or diabetics prior to pregnancy. We could clearly identify only one case of DKA with hyperglycemia. This however needs further confirmation as DKA might be diagnosed after admission to the hospital or, documentation in the emergency room might have been incomeplete.
In conclusion, DKA is a possibility in type II pregnant diabetic women with vague presentation and normal blood glucose. Prompt diagnosis and management with intravenous insulin along with dextrose will prevent significant morbidity for both the mother and the fetus.
| References | | |
| 1. | Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24(1):131-53.  |
| 2. | Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic Crises in diabetes. Diabetes Care 2004;27:S94-102. [PUBMED] [FULLTEXT] |
| 3. | Maislos M, Harman-Bohem I, Weitzman S. Diabetic ketoacidosis. A rare compli-cation of gestational diabetes. Diabetes Care 1992;15(8):968-70. |
| 4. | Carroll MA, Yeomans ER. Diabetic ketoacidosis in pregnancy. Crit Care Med 2005;33:S347-53. [PUBMED] [FULLTEXT] |
| 5. | Burge MR, Hardy KJ, Schade DS. Shortterm fasting is a mechanism for the development of euglycemic keto-acidosis during periods of insulin defi-ciency. J Clin Endocrinol Metab 1993; 76(5):1192-8. |
| 6. | Cousins L. Pregnancy Complications among diabetic women: Review 1965-1985. Obstet Gynecol Surv 1987;42:140-9. [PUBMED] |
| 7. | Omrani GR, Shams MA, Afkhamizadeh, MA, Kitabchi AE. Hyperglycemic Crises in Diabetic Patients, Int J Endocrinol Metab 2005;1:52-61. |
| 8. | Cullen MT, Reece EA, Homko CJ, Sivan E. The changing presentations of diabetic ketoacidosis during pregnancy. Am J Perinatol 1996;13(7):449-51. |
| 9. | Montoro MN, Myers VP, Mestman JH, Xu Y, Anderson BG, Golde SH. Outcome of pregnancy in diabetic ketoacidosis. Am J Perinatol 1993;10:17-20. [PUBMED] |
| 10. | Mahoney C. Extreme gestational starvation ketoacidosis. Case report and review of pathophysiology. Am J Kidney Dis 1992;20:276-80. |
| 11. | Franke B, Carr D, Hatem MH. A case of Euglycemic diabetic ketoacidosis in pregnancy. Diabetes Med 2001;18:858-9. |
| 12. | Kilvert JA, Nicholson HO, Wright AD. Ketosis in diabetic pregnancy. Diabetes Med 1993;10:278-81. |
| 13. | Foster DW, McGarry JD. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 1983;309:159-69. [PUBMED] |
Correspondence Address:
Nauman Tarif
Department of Medicine, King Khalid University Hospital, PO Box 2925, Riyadh 11461
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 17951948 
[Table - 1] |
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