The development of diabetic ketoacidosis (DKA) in pregnancy is a medical emergency. DKA results from inadequate insulin action resulting in perceived hypoglicemia at the level of target cells. Insulin counter-regulatory hormones are released into circulation in response to cellular hypoglycemia, causing ghiconeogenesis and glycogenosis in the liver and a decrease in glucose utilization in peripheral tissue. The incidence of DKA among pregestational type 1 or type 2 diabetic patients range from 5% to 10%. The true incidence of maternal mortality is unknown, though it is historically reported as 5% to 15%. The most common general factors associated with precipitating the onset of DKA during pregnancy are: emesis, infection, poor compliance/noncompliance, insulin pump failure, use of β-sympathomimethics, use of corticosteroids. DKA has classic clinical findings: patients generally present with hyperventilation, altered mental status, weakness, dehydratation, vomiting and polyuria. The laboratory findings seen in DKA can be used to help confirm a correct diagnosis of the disease. Findings of hyperglycemia, acidosis and ketonemia are generally seen in all cases of DKA. One of the most profound effects that DKA can have on a pregnancy outcome involves fetal loss. Current literature from the last decade supports a fetal loss rate from 5 to 15%. Treatment includes aggressive volume replacement, insulin infusion, correct electrolyte imbalances and treatment of the underlying causes of DKA. In conclusion, early recognition of clinical manifestations of DKA, followed by appropriate and timely treatment, remain the cornerstones to optimize maternal and fetal outcome.
|Translated title of the contribution||Diabetic ketoacidosis in pregnancy|
|Number of pages||5|
|Journal||Gazzetta Medica Italiana Archivio per le Scienze Mediche|
|Publication status||Published - Feb 2009|
ASJC Scopus subject areas