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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2007  |  Volume : 18  |  Issue : 4  |  Page : 590-593
Euglycemic Diabetic Ketoacidosis in Pregnancy

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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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

How to cite this URL:
Tarif N, Al Badr W. Euglycemic Diabetic Ketoacidosis in Pregnancy. Saudi J Kidney Dis Transpl [serial online] 2007 [cited 2023 Feb 4];18:590-3. Available from: https://www.sjkdt.org/text.asp?2007/18/4/590/36517

   Introduction Top

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 Top

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 Top

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 Top

1.Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24(1):131-53.  Back to cited text no. 1    
2.Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic Crises in diabetes. Diabetes Care 2004;27:S94-102.  Back to cited text no. 2  [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.  Back to cited text no. 3    
4.Carroll MA, Yeomans ER. Diabetic ketoacidosis in pregnancy. Crit Care Med 2005;33:S347-53.  Back to cited text no. 4  [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.  Back to cited text no. 5    
6.Cousins L. Pregnancy Complications among diabetic women: Review 1965-1985. Obstet Gynecol Surv 1987;42:140-9.  Back to cited text no. 6  [PUBMED]  
7.Omrani GR, Shams MA, Afkhamizadeh, MA, Kitabchi AE. Hyperglycemic Crises in Diabetic Patients, Int J Endocrinol Metab 2005;1:52-61.  Back to cited text no. 7    
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.  Back to cited text no. 8    
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.  Back to cited text no. 9  [PUBMED]  
10.Mahoney C. Extreme gestational starvation ketoacidosis. Case report and review of pathophysiology. Am J Kidney Dis 1992;20:276-80.  Back to cited text no. 10    
11.Franke B, Carr D, Hatem MH. A case of Euglycemic diabetic ketoacidosis in preg­nancy. Diabetes Med 2001;18:858-9.  Back to cited text no. 11    
12.Kilvert JA, Nicholson HO, Wright AD. Ketosis in diabetic pregnancy. Diabetes Med 1993;10:278-81.  Back to cited text no. 12    
13.Foster DW, McGarry JD. The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 1983;309:159­-69.  Back to cited text no. 13  [PUBMED]  

Correspondence Address:
Nauman Tarif
Department of Medicine, King Khalid University Hospital, PO Box 2925, Riyadh 11461
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 17951948

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