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Despite recent advances in the evaluation and medical treatment of diabetes in pregnancy, diabetic ketoacidosis (DKA) remains a matter of significant concern. The fetal loss rate in most contemporary series has been estimated to range from 10% to 25%. Fortunately, since the advent and implementation of insulin therapy, the maternal mortality rate has declined to 1% or less. In order to favorably influence the outcome in these high-risk patients, it is imperative that the obstetrician/provider be familiar with the basics of the pathophysiology, diagnosis, and treatment of DKA in pregnancy.
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DKA is characterized by hyperglycemia and accelerated ketogenesis. Both a lack of insulin and an excess of glucagon and other counter-regulatory hormones significantly contribute to these problems and their resultant clinical manifestations. Glucose normally enters the cell secondary to the effects of insulin. The cell then may use glucose for nutrition and energy production. When insulin is lacking, glucose fails to enter the cell. The cell responds to this starvation by facilitating the release of counter-regulatory hormones, including glucagon, catecholamines, and cortisol. These counter-regulatory hormones are responsible for providing the cell with an alternative substrate for nutrition and energy production. By the process of gluconeogenesis, fatty acids from adipose tissue are broken down by hepatocytes to ketones (acetone, acetoacetate, and β-hydroxybutyrate [BHB] = ketone bodies), which are then used by the body cells for nutrition and energy production (Fig. 11-1). The lack of insulin also contributes to increased lipolysis and decreased reutilization of free fatty acids, thereby providing more substrate for hepatic ketogenesis. A basic review of the biochemistry involving DKA is presented in Fig. 11-1.
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Now that we have an understanding of how and why ketone bodies are produced during DKA, what are the maternal consequences resulting from excessive ketogenesis? In general, ketone bodies are considered to be moderately strong acids. In response to the fall in pH in most body fluids created by an accumulation of these acids, the body reacts physiologically to correct the resultant metabolic acidosis. The respiratory rate and depth increase (Kussmaul respirations) in an attempt to blow off carbon dioxide, initiating a corrective trend toward compensatory respiratory alkalosis. Serum bicarbonate levels decline, and as a result, the anion gap becomes abnormally elevated. In addition to increasing fatty acid production, poor glucose utilization results in severe hyperglycemia. Untreated hyperglycemia leads to marked glycosuria, initiating a significant osmotic diuresis. As a result, dehydration, electrolyte depletion, and, if left untreated, cardiac failure and death may follow.
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A vicious cycle is created by an increase in dehydration-mediated serum hyperosmolarity and catabolism, propagated by Kussmaul respiration, leading ...