Video Clips on DVD
- 12-1
PowerPoint Discussion of Appropriate Management of Diabetic Ketoacidosis
- 12-2
Discussion with Dr. Sibai on Acute Management of a Patient with Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is an infrequent complication of diabetes in pregnancy, but in the absence of prompt diagnosis and treatment it can be life threatening to mother and fetus. The reported incidence in pregnancies complicated by diabetes mellitus ranges from 1% to 5%. The incidence depends on the presence or absence of one or more of the risk factors listed in Table 12-1 .
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Case 1: Diabetic Ketoacidosis
A 37-year-old G5P3 presented at approximately 31 weeks of gestation complaining of nausea, vomiting, diarrhea for 2 days, and decreased fetal movement followed by no fetal movement for 24 hours. She gives a history of only one prenatal visit, and no previous prenatal blood work.
She was admitted with diagnosis of gastroenteritis with dehydration. On admission, the patient was dizzy and tachypneic with a respiratory rate of 26 beats per minute (bpm). Her temperature was 98.6° F, pulse was 127 bpm, and blood pressure of 124/80 mm Hg.
Laboratory blood tests revealed a glucose level of 983 mg/dL, K + of 5.3 mEq/L, anion gap of 34, and creatinine of 1.8 mg/dL. A complete blood count and platelet count were normal. Arterial blood gas revealed a pH of 7.26, a bicarbonate of 13 mEq/L, and base excess of −11.2. Serum and urine ketones were positive. Electrocardiogram (ECG) revealed sinus tachycardia. Fetal heart rate monitoring revealed absent accelerations, absent variability and presence of spontaneous decelerations ( Fig. 12-1A ). Ultrasound examination revealed normal fluid and a biophysical profile (BPP) of 2/10.
A diagnosis of DKA was made, and the patient received 15 µ of regular insulin as a loading dose followed by continuous IV infusion at a rate of 10 µ/hr. She also received large doses of fluids (4 L of normal saline during first 5 hours) and potassium replacement. After control of plasma glucose levels and correction of maternal acidosis and electrolytes, fetal heart rate tracing continued to be nonreassuring (see Fig 12-1B ) and repeat BPP was still 2/10. Despite that, delivery was not performed. Over the next several hours the fetal tracing continued to be nonreassuring and was followed by reduced base line and repetitive decelerations (see Fig. 12-1C ). Umbilical artery Doppler revealed absent diastolic flow, BPP was still 2/10. A decision for cesarean section was made, but the fetus died 20 minutes after the last testing and the patient underwent induction of labor with subsequent vaginal delivery of a stillborn fetus weighing 2000 g.
Discussion
Pregnancy is characterized by increased insulin resistance (higher insulin requirement), a relative state of accelerated starvation (increased free fatty acids), and a lowered buffering capacity (low serum bicarbonate levels). These changes are increased with advanced gestation as a result of increasing anti-insulin hormone production such as human placental lactogen, prolactin, cortisol, and progesterone. As a result, DKA usually develops after 20 weeks’ gestation, and predisposes diabetic pregnant women to develop DKA very rapidly (over hours) and at lower blood glucose levels (<300 mg/dL) than is seen in nonpregnant patients. In patients with pregestational or gestational diabetes, DKA results from inadequate circulating insulin and reduced glucose utilization in peripheral tissues ( Fig. 12-2 ).
This patient presented with classical signs and symptoms of hyperglycemia and ketoacidosis in a pregnant woman with poorly controlled diabetes. The clinical findings in patients with DKA are related to hyperglycemia, osmotic diuresis, severe volume depletion, acidosis, and electrolyte imbalance. The presenting signs and symptoms are listed in Table 12-2 .
