RESEARCH DESIGN AND METHODS â We describe 2.5 yr of close fol- low-up of a Bedouin woman who was hospitalized for DKA while pregnant with her.
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RESEARCH DESIGN AND
Diabetic Ketoacidosis A rare complication of gestational diabetes MAXIMO MAISLOS, MD ILANA HARMAN-BOHEM, MD SIMON WEITZMAN, MD
OBJECTIVE — To describe a case of severe DKA in an otherwise healthy pregnant woman. RESEARCH DESIGN AND METHODS — We describe 2.5 yr of close follow-up of a Bedouin woman who was hospitalized for DKA while pregnant with her 11th child. Plasma glucose returned to normal levels immediately after delivery of a dead conceptus. Four months later, while normoglycemic, the patient became pregnant again. During the subsequent pregnancy, GDM was diagnosed at week 20 of gestation. Tight plasma glucose control was achieved with an insulin regimen, and the patient delivered a healthy girl at term. Plasma glucose again returned to normal and remained so to date, 18 mo postpartum. An OGTT and a euglycemic hyperinsulinemic clamp were performed between pregnancies; another OGTT was performed at week 14 of the last pregnancy. Plasma glucose, insulin, and C-peptide were measured in blood samples during these procedures. RESULTS— We established beyond doubt that the patient developed GDM and returned to essentially normal glucose tolerance after her last (12th) delivery. During the 11th pregnancy, gestational diabetes was complicated by severe DKA. CONCLUSIONS — GDM is a common abnormality of glucose metabolism during pregnancy, which affects fetal development and leads to peripartum complications. Our report stresses that under certain circumstances, gestational diabetes can be complicated by DKA and become life-threatening to the mother and fetus.
G
DM, a self-limited disorder of glucose metabolism that ends after delivery, is present in —2-3% of all pregnancies (1). Many women who have had GDM will develop overt diabetes in
the future, most likely N1DDM (2). Appearance of ketosis-prone IDDM after GDM is rare (3). In this study, we describe a woman with GDM who developed DKA during pregnancy.
FROM THE FRAIDA FOUNDATION DIABETES-METABOLISM
SERVICE, SOROKA MEDICAL CENTER OF KUPAT
HOLIM, BEN-GURION UNIVERSITY FACULTY OF HEALTH SCIENCES, BEER-SHEVA, ISRAEL. ADDRESS CORRESPONDENCE AND REPRINT REQUESTS TO MAXIMO MAISLOS, MD, FRAIDA FOUNDATION DIABETES-METABOLISM SERVICE, SOROKA MEDICAL CENTER OF KUPAT HOLIM, BEN-GURION FACULTY OF HEALTH SCIENCES, PO BOX 151, RECEIVED FOR PUBLICATION 3 JUNE 1991 DKA,
DIABETIC KETOACIDOSIS;
GDM,
TOLERANCE TEST; B M I , BODY MASS INDEX.
968
UNIVERSITY
BEER-SHEVA, ISRAEL.
AND ACCEPTED IN REVISED FORM 4 DECEMBER
1991.
GESTATIONAL DIABETES MELLITUS; OGTT, ORAL GLUCOSE
METHODS— A 40-yr-old Bedouin woman, gravida 11, para 10, 30-32 wk pregnant, was admitted to the obstetrics ward of the Soroka Medical Center because of fever, dysuria, and dyspnea of 6-day duration. The patient had been previously healthy and felt well until the onset of the illness. She had not had prenatal care during her previous pregnancies, and the only available obstetric data was that from four of her deliveries attended to at our hospital. They were unremarkable but for the large weight of her babies—each >4,000 g (8.82 lb). The patient started taking oral amoxycillin 4 days before hospitalization. On admission, the patient was pale, diaphoretic, and tachypneic at 36 respirations/min; her pulse was weak, at 106 beats/min; her blood pressure was 93/62 mmHg; her lungs were clear, and examination of the heart was normal except for tachycardia; her abdomen was soft, with no peritoneal signs elicited; her flanks were not tender. An ultrasound performed on admission revealed marked polyhydramnios, gestational age of —30-32 wk but no apparent fetal pulse. The chest X-ray and electrocardiogram were normal. The urinalysis revealed ketones 4+, glucose 4+; the sediment revealed numerous leukocytes but no bacteria. Blood chemistries revealed glucose 25.8 Mm, Na + 136 mM, K+ 3,6 mM, creatinine 88.4 jxM, urea 6.42 mM, and plasma ketones 4 + . The blood count revealed HbA 9.2 g/dl, hematocrit 27.7%, leukocytes 12,2 X 109/L with a shift to the left. Blood gases revealed pH 7.01, pO 2 132 mmHg, pCO 2 13.3 mmHg, and bicarbonate 9.1 mM. The diagnosis of DKA, partially treated ascending urinary tract infection, and antepartum fetal death, were established. After initiation of an infusion of intravenous saline solution (and K + ), human crystalline insulin, and antibiotics (ampicillin and gentamicin), the patient was transferred to the medical ward. Within 8 h, her condition im-
DIABETES CARE, VOLUME 15,
NUMBER 8, AUGUST
1992
Maislos, Harman-Bohem, and
Weitzman
Table 1—OGTTs (100 g) performed before (OGTT1) and at week 14 of pregnancy (OGTT2)
the fasting level by infusion of variable amounts of 50% dextrose; plasma insulin was measured every 20 min. The M value (amount of infused glucose measured INSULIN (PM) C-PEPTIDE ( N M ) GLUCOSE (MM) during the last 20 min of each period) OGTT2 OGTT1 OGTT2 OGTT1 OGTT2 was 4.2 and 8.8 mg • kg~x • min" 1 , reMIN OGTT1 spectively (Fig. 1). These results were 102 .27 .27 5.7 5.0 66 0 within the normal expected values for 114 174 7.9 .53 .61 3 7.8 the achieved steady-state plasma insulin 10.0 162 354 .83 1.00 60 9.6 8.6 234 264 .94 levels (312 and 1212 pM, respectively). 9.4 .95 90 8.2 204 276 1.11 1.16 120 7.7 To our amazement, 1 mo later, 4 312 384 1.11 8.1 1.20 180 7.8 mo postpartum, the patient became pregnant again. This time, the patient was closely monitored. During the first 16 wk of pregnancy, fasting and postproved markedly (pH went to 7.21, bi- mum 324 pM. Plasma C-pep tide (dou- prandial plasma glucose remained norcarbonate to 12.8 mM, blood glucose to ble-antibody RIA kit, DPC) rose from mal, between 5 and 5.8 mM and 6.7 and 8 mM, respectively. Another OGTT per11.9 mM, plasma ketones to 24-, Na + to 0.26 to 1.1 nM. + 139 mM, and K to 3.8 mM). FortyTo measure insulin sensitivity, a formed at week 14 revealed results simeight hours after diagnosis, the patient two-step euglycemic hyperinsulinemic ilar to those found in the previous test was afebrile, well hydrated, free of clamp (4) was performed (Fig. 1). Insu- (Table 1). HbAlc measurements were 6.3 plasma ketones, and her blood glucose lin was infused during two 80-min peri- and 6.6% at weeks 8 and 16, respecwas —11 mM. Delivery of the dead fetus ods, at a rate of 1 and 2 |iU • kg" 1 • tively. was induced. Soon thereafter, oral intake min" 1 , respectively. Plasma glucose was From week 20, fasting plasma was started, and intravenous insulin was measured every 5 min and sustained at glucose became abnormal; the diagnosis replaced by a combination of subcuof GDM was established, and treatment taneous isophane insulin and crystalline with human insulin (NPH 12 U, crystalinsulin. Subsequently, the patient develline 6 U at 0800) was initiated. The paplasma insulin, pM plasma glucose, mM oped signs and symptoms of hypoglycetient was taught to self-monitor blood mia (blood glucose 2.72, 3.11 mM); the glucose and was asked to perform at least insulin dose was rapidly tapered and four measurements daily (fasting, and completely withdrawn before discharge before lunch, supper, and bed). She was from hospital 10 days after admission. followed on a biweekly basis. Fasting and postprandial capillary glucose levels At follow-up visits in the diabetes were maintained
