Endocrine Morning Report - Euglycemic DKA in pregnancy

A devastating complication of pregnancy in type I diabetics

A special thank you to Dr. Robert Silver for leading our discussion of the case.

           Today we discussed an interesting case of a 29 year old G1P0 female who presented at 32 weeks gestation with a chief complaint of shortness of breath.

On her third day of admission in hospital, she developed worsening of her symptoms and her respiratory rate increased to 40 breaths per minute, with a normal oxygen saturation (98%) on room air.

Her capillary blood glucose registered a blood sugar of 10 mmol/L, and it was only after examining her arterial blood gas that a diagnosis of diabetic ketoacidosis (DKA) could be established.

Her arterial blood gas (ABG) showed a pH of 7.29 / pCO2 of 14 / pO2 of 120 / HCO3 of 6.  Her serum electrolytes showed an anion gap of 31, and alarmingly a serum potassium of 4.7 (in the context of insulin deficiency, this is worrisome).

The appropriate intervention, being transfer to the intensive care unit, potassium replacement via a central line, and aggressive fluid resuscitation were all initiated. She was started on an insulin infusion as well as IV D10W to maintain her blood sugar, and within 24 hours she was completely stable and back to her normal state of health.  

Table 1: The American Diabetes Association diagnostic criteria for DKA: triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia.

Why do pregnant patient's decompensate into DKA at a lower glucose?

           There are a number of cases reported in the literature of euglycemic DKA in pregnant patients, and it is thought to be a rare but devastating complication of pregnancy in type 1 diabetics.  The frequency of occurrence is approximately 1% of all DKA's in pregnant patients (Guo, 2008).  It carries a high fetal mortality rate (30- 90%) and is often a missed diagnosis because of the falsely reassuring glucose readings (Guo, 2008).

Maternal Changes:
The pathophysiology of this process is  interesting.  The normal physiology of pregnancy results in a decrease in insulin sensitivity, and this is thought to be related to increased lipolysis and ketogenesis (Chico et. al, 2008).  Also, pregnant women have a baseline respiratory alkalosis due to pregnancy induced hyperventilation.  This results in a decreased serum bicarbonate and reduced buffering capacity (Chico et. al, 2008).

These normal physiologic changes reduce the body's ability to cope with acidosis, whether it be sepsis or DKA mediated.

Placental-Fetal Changes:
Furthermore, the growing placenta and fetus utilize large quantities of glucose and produce factors such as placental lactogen, progesterone and cortisol that further increase insulin resistance, especially towards the later stages of pregnancy.

The end product of both these maternal-fetal changes is that pregnant patients with T1DM are at an increased risk of developing DKA.  They also have a lower serum glucose threshold at which DKA will occur compared to non-pregnant women with T1DM (Guo, 2008).

The average glucose of pregnant patients with DKA was 16 mmol/L compared with 27 mmol/L in non-pregnant patients (Guo, 2008).

Take home message: In pregnant women with T1DM, a normal appearing glucose does not adequately rule out DKA and can have devastating consequences for both mother and the fetus.


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http://canadaam.ctvnews.ca/video?playlistId=1.1915992

References:

Guo, R.X., Yang, L.Z., Li, L.X., Zhao, X.P. Diabetic Ketoacidosis in pregnancy tends to occur at lower blood glucose levels: case-control study and a case report of euglycemic diabetic ketoacidosis in pregnancy. Journal of Obstetrical Gynaecology Research. 34(3):324-330. 2008.

Chico, M., Levine, S.N., Lewis, D.F. Normoglycemic diabetic ketoacidosis in pregnancy. Journal of Perinatology. 28(4): 310-2. 2008.