A.R. is a 33-year-old caucasian woman initially diagnosed with diabetes during a recent pregnancy. The routine glucose challenge test performed between 28 and 29 weeks gestation was elevated at 662 mg/dl. A random glucose completed 1–2 days later was also elevated at 500 mg/dl. A follow-up HbA1c was elevated at 11.6%. Additional symptoms included a 23-lb weight loss over the past 3–4 weeks with ongoing “flu-like” symptoms, including fatigue, nausea, polyuria, and polydypsia.
A.R. had contacted her obstetrician’s office when her symptoms first appeared and was told to contact her primary care provider for the “flu” symptoms. She had called a nurse triage line several times over the previous 2–3 weeks with ongoing symptoms and was told to rest and take fluids.
She presented to her primary care provider 3 days after the HbA1c was drawn for ongoing evaluation of hyperglycemia. At that time, she was symptomatic for diabetic ketoacidosis. She was hospitalized and started on an insulin drip.
A.R.’s hospitalization was further complicated with gram-negative sepsis, adult respiratory distress syndrome, and Crohn’s disease with a new rectovaginal fistula. She was intubated as her respiratory status continued to decline and was transferred to a tertiary medical center for ongoing management. She required an emergency Caesarian section at 30 1/7 weeks gestation due to increased fetal distress.
A.R. had no family history of diabetes with the exception of one sister who had been diagnosed with gestational diabetes. Her medical history was significant for Crohn’s disease diagnosed in 1998 with no reoccurrence until this hospitalization. Her pre-pregnancy weight was 114–120 lb. She had gained 25 lb during her pregnancy and lost 23 lb just before diagnosis.
A.R.’s blood glucose levels improved postpartum, and the insulin drip was gradually discontinued. She was discharged on no medications.
At her 2-week postpartum visit, home blood glucose monitoring indicated that values were ranging from 72 to 328 mg/dl, with the majority of values in the 200–300 mg/dl range. A repeat HbA1c was 8.7%. She was restarted on insulin.
1. What is the differential diagnosis of gestational diabetes versus type 1 diabetes?
2. At what point during pregnancy should insulin therapy be instituted for blood glucose control?
3. How can communication systems be changed to provide for integration of information between multiple providers?
Gestational diabetes is defined as “any degree of carbohydrate intolerance with onset first recognized during pregnancy. This definition applies whether insulin ... is used for treatment and whether or not the condition persists after pregnancy.”1 Risk assessment is done early in the pregnancy, with average-risk women being tested at 24–28 weeks’ gestation and low-risk women requiring no additional testing.1,2 A.R. met the criteria for average risk based on age and a first-degree family member with a history of gestational diabetes.
Screening criteria for diagnosing diabetes include 1) symptoms of diabetes plus casual plasma glucose >200 mg/dl (11.1 mmol/l), or 2) fasting plasma glucose >126 mg/dl (7.0 mmol/l), or 3) 2-h plasma glucose >200 mg/dl (11.1 mmol/l) during an oral glucose tolerance test (OGTT).3 For women who do not meet the first two criteria, a glucose challenge test (GCT) measuring a 1-h plasma glucose following a 50-g oral glucose load is acceptable. For those women who fail the initial screen, practitioners can then proceed with the OGTT.1
In A.R.’s case, she most likely would have met the first criterion if a casual blood glucose had been measured. She had classic symptoms with weight loss, fatigue, polyuria, and polydypsia. Her 1-h plasma glucose following the glucose challenge was >600 mg/dl, which suggests that her casual glucose would also have been quite high.
Medical nutrition therapy (MNT) is certainly a major part of diabetes management. However, with this degree of hyperglycemia, MNT would not be adequate as monotherapy. Treatment for gestational diabetes includes the use of insulin if fasting blood glucose levels are >95 mg/dl (5.3 mmol/l) or 2-h postprandial values are >120 mg/dl (6.7 mmol/l).1
Several days passed from the time of A.R.’s initial elevated blood glucose value and the initiation of insulin therapy. While HbA1c values cannot be used for diagnostic purposes, in this case they further confirmed the significant degree of hyperglycemia.
Plasma blood glucose values initially improved in the immediate postpartum period. A.R. was sent home without medications but instructed to continue home glucose monitoring.
At her 2-week postpartum visit, whole blood glucose values were again indicating progressive hyperglycemia, and insulin was restarted. A.R.’s postpartum weight was 104 lb—well below her usual pre-pregnancy weight of 114–120 lb. Based on her ethnic background, weight loss, abrupt presentation with classic diabetes symptoms, and limited family history, she was reclassified as having type 1 diabetes.
In immune-mediated, or type 1, diabetes, b-cell destruction can be variable, with a slower destruction sometimes seen in adults.3 Presentation of type 1 diabetes can also vary with modest fasting hyperglycemia that can quickly change to severe hyperglycemia and/or ketoacidosis in the presence of infection or other stress.3 A.R. may have had mild hyperglycemia pre-pregnancy that increased in severity as the pregnancy progressed.
The final issue is communication among multiple health care providers. A.R. was part of a system that uses primary care providers, specialists, and triage nurses. She accessed all of these providers as instructed. However, the information did not seem to be clearly communicated among these different types of providers. A.R. called triage nurses several times with her concerns of increased fatigue, nausea, and weight loss. The specialist performed her glucose challenge with follow-up through the primary care office. It seems that if all of these providers had the full information about this case, the diagnosis could have been made more easily, and insulin could have been initiated more quickly.
1. Hyperglycemia diagnosed during pregnancy is considered to be gestational diabetes until it is reclassified in the postpartum period. Immune-mediated diabetes can cause mild hyperglycemia that is intensified with the increased counterregulatory hormone response during pregnancy.
2. Insulin therapy needs to be instituted quickly for cases in which MNT alone is inadequate.
3. The GCT is an appropriate screening test for an average-risk woman with no symptoms of diabetes. In the face of classic symptoms of diabetes, a casual plasma glucose test can eliminate the need for the glucose challenge.
4. As part of the health care industry, we need to continue to work on information systems to track patient data and share data among multiple providers. Patients can become lost in an ever-expanding system that relies on “protocols” and does not always allow for individual differences or for cases with unusual presentation.
Ginny Lewis, ARNP, FNP, CDE, is a nurse practitioner at the Diabetes Care Center of the University of Washington School of Medicine in Seattle.