Diabetic ketoacidosis in pregnancy.
ABSTRACT Episodes of diabetic ketoacidosis (DKA) can represent a life-threatening emergency for mother and fetus. The cornerstones of treatment of DKA are aggressive fluid replacement and insulin administration while ascertaining which precipitating factors brought about the current episode of DKA, and then treating accordingly to mitigate those factors. The incidence of DKA and factors unique to pregnancy are discussed in this article, along with the effects of the disease process on pregnancy. Clinical presentation, diagnosis, and treatment modalities are covered in detail to offer ideas to improve maternal and fetal outcome.
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ABSTRACT: Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as "accelerated starvation." Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids.01/2014; 2014:906283. DOI:10.1155/2014/906283
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ABSTRACT: Diabetic ketoacidosis (DKA) during pregnancy is a serious complication in both mother and fetus. Most incidences occur during late pregnancy in women with type 1 diabetes mellitus. We report the rare case of a woman with type 1 diabetes mellitus who had normal glucose tolerance during the first trimester but developed DKA during late pregnancy. Although she had initially tested positive for screening of gestational diabetes mellitus during the first trimester, subsequent diagnostic 75-g oral glucose tolerance tests showed normal glucose tolerance. She developed DKA with severe general fatigue in late pregnancy. The patient's general condition improved after treatment for ketoacidosis, and she vaginally delivered a healthy infant at term. The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester. The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester.Symptoms including severe general fatigue, nausea, and weight loss are important signs to suspect DKA. Findings such as Kussmaul breathing with ketotic odor are also typical.Urinary test, atrial gas analysis, and anion gap are important. If pH shows normal value, calculation of anion gap is important. If the value of anion gap is more than 12, a practitioner should consider the presence of metabolic acidosis.01/2014; 2014:130085. DOI:10.1530/EDM-13-0085
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ABSTRACT: Three cases of ketosis decompensation occurring immediately in type I diabetic after corticotherapy for lung foetal maturation (LFM) are reported. Few of observations have been published. Increasing doses of insulin is mandatory under close monitoring of blood glucose levels, in particular according to the protocol proposed by Kaushal et al.: infusion of insulin adapted to the results of glucose levels, as a supplementation to the usual doses in each patient. Diabetes does not lead to hesitate prescribing a corticotherapy for LFM, but requires a strict control of needs in insulin to avoid a ketosis decompensation.Journal de Gynécologie Obstétrique et Biologie de la Reproduction 01/2013; DOI:10.1016/j.jgyn.2013.08.012 · 0.62 Impact Factor