Successful Management of Diabetic Ketoacidosis in Pregnancy

Author Information
Sarita Channawar*, Madhva Prasad**, Neha Jain***, Anahita R. Chauhan****
(* Assistant Professor, **Registrar, *** Second Year Resident, **** Additional Professor Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


Diabetic ketoacidosis (DKA) is a complication seen in type 1 diabetes mellitus (DM) but can also occur in pregnancies complicated by type 2 DM or gestational diabetes mellitus (GDM). DKA is a medical emergency with high maternal and fetal mortality, and requires treatment in an intensive care setting. Prompt recognition and resuscitative therapy improves medical and obstetric outcomes. This report of DKA in a case of GDM provides insight into pathophysiology and successful management.


Normal pregnancy is characterized by a state of decreased insulin sensitivity, accelerated lipolysis and ketogenesis.[1, 2, 3, 4] The concentration of serum ketones is estimated to be two to four times greater than in nonpregnant state.[1, 5] Despite these changes, the incidence of DKA in pregnant diabetics is only 1 to 3%.[2, 3] Fetal mortality rates of 30 to 90% in the past have now decreased to 9% due to improvements in neonatal and diabetic management.[2, 3]

Case History

A 22 year old primigravida with 34+6 weeks of gestation was referred to our tertiary care center with giddiness, polyuria, polydipsia, candidial vagina discharge and deranged blood sugars (fasting blood glucose 280 mg/dl and post-meal value 410 mg/dl a few days back). She had stable vital signs, 34 weeks’ sized relaxed gravid uterus with cephalic presentation and normal fetal heart sounds. She had been diagnosed by her primary care obstetrician as GDM one month earlier and referred to us; however she did not report nor was she on any treatment. Recent sonography revealed oligohydramnios (amniotic fluid index 7 cm) but no fetal malformations.
A diagnosis of DKA was made. She was urgently hospitalized. Her hemoglucotest (HGT) on admission was 590 mg%, urinary sugars were 3+, urinary ketones 2+, venous blood gas (VBG) analysis showed pH of 7.32, bicarbonate of 17.3 meq/L, sodium of 125 meq/L and potassium of 3.9 meq/L. She was initially hydrated with normal saline (NS) 1liter over 1 hour, followed by 500 ml NS with 20 ml potassium chloride (KCl) over the next hour, and continued on 500 ml NS with 10 ml KCl over next 4 hours. Insulin therapy was initiated with bolus dose of 16 units human insulin subcutaneously followed by insulin drip (50 units in 500 ml NS at 70 ml/h). Monitoring was performed with hourly HGT, 4 hourly urinary sugars/ketones, and 6 hourly serum electrolytes and VBG. The patient stabilized on insulin drip: blood sugar value was 314 mg% after 3 hours, which reduced over 10 hours to 115mg%. Urine ketones also disappeared. Hence insulin drip was discontinued. Fetal heart rate monitoring was done while on insulin drip and was normal. She was converted to high doses of subcutaneous regular and isophane human insulin (20 + 30 units respectively), and maintained on thrice daily doses which were tapered gradually, along with diabetic diet, so as to maintain her blood glucose levels within normal range. The patient was managed jointly with the endocrinologist. She remained hospitalized, blood sugars were monitored six times a day and insulin was continued with good glycemic control. Fetal assessment was done clinically with daily fetal movement count, nonstress test on alternate days and weekly Doppler studies, all of which were normal. Labor was induced electively at 37 weeks’ gestation; however emergency LSCS was done for failed induction and she delivered a healthy female weighing 2.6 kg. Postoperatively her blood sugars were normal; and insulin was not required. She was managed on diabetic diet and oral hypoglycemic agent Metformin 250 mg twice daily for 10 days, after which it was omitted and she was discharged.


Diabetic ketoacidosis is a life-threatening, acute metabolic state due to insulin deficiency. Hence all patients with diabetes in pregnancy including GDM patients should be monitored for DKA. Low levels of insulin cause increased gluconeogenesis while decreasing glucose uptake and utilization. Increased levels of counter-regulatory hormones (glucagon, cortisol, catecholamines and growth hormone) accelerate the development of ketoacidosis by increasing gluconeogenesis, glycogenolysis, ketogenesis and insulin resistance. Insulin deficiency also leads to high anion gap metabolic acidosis. Hyperglycemia and hyperosmolality in patients with DKA produce the characteristic osmotic diuresis causing intravascular volume depletion; if not corrected by intravenous fluids and insulin, DKA can rapidly progress to a state of poor tissue perfusion, diminished cardiac and renal function, multisystem failure and death. A number of physiological changes during pregnancy influence carbohydrate and fat metabolism.[2, 3, 4] 
  1. Placental lactogen and increased cortisol contribute to increased insulin resistance, particularly later in pregnancy.
  2. Pregnant women have respiratory alkalosis with decreased serum bicarbonate concentrations and reduced capacity to buffer organic acids.
  3. Pregnancy being an accelerated state of starvation, overnight fast can increase lipolysis and ketone body concentrations 2-4 times greater than in nonpregnant state.[1, 5]
  4. Predisposing factors for DKA include stress of labor, cessation of insulin therapy, use of β-sympathomimetic agents and emesis with accompanying dehydration.
  5. Both fetus and placenta utilize large quantities of glucose resulting in lower maternal fasting glucose levels.[2, 3, 4 ]

Hence DKA in pregnancy can develop more rapidly and at lower serum glucose concentrations often causing delay in the diagnosis.[2, 3, 4] Several cases of “normoglycemic” DKA have been reported, although in almost every case glucose has exceeded 130 mg/dl. Our patient had levels of 590 mg%, low bicarbonate concentration, positive anion gap and VBG pH of 7.3 suggestive of acidosis; possibly starvation ketosis contributed to development of high anion gap metabolic acidosis. Management principles in DKA include aggressive volume replacement, intravenous insulin therapy, correction of acidosis and electrolyte abnormalities, and management of precipitating factors, as well as monitoring of maternal-fetal response to treatment. Nonreassuring fetal heart rate pattern may be seen due to associated fetal hypoxemia and acidosis, but correction of maternal metabolic abnormalities should be a priority and delivery considered only after maternal stabilization if indicated. Prevention strategies include education of diabetic pregnant women about the risks of DKA, precipitating factors, and the importance of timely reporting of signs and symptoms. A multidisciplinary approach including obstetrician, endocrinologist, intensivist and neonatologist is necessary for good outcome.


1.      Carroll MA, Yeomans ER. Diabetic ketoacidosis in pregnancy. Crit Care Med 2005;33: S347–S353.
2.      Kamalakannan D, Baskar V, Barton DM, Abdu TAM. Diabetic ketoacidosis in pregnancy. Postgrad Med J 2003;79: 454–457.
3.      American College of Obstetricians and Gynecologists. ACOG practice bulletin No. 60: pregestational diabetes. Obstet Gynecol 2005;105:675–685.
4.      Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001;24:131–153
5.      Sibai BM, Viteri OA. Diabetic ketoacidosis in pregnancy. Obstet Gynecol 2014;123(1): 167-78.


Channawar S, Madhva Prasad M, Jain N, Chauhan AR. An Unusual Case of Hyperemesis Gravidarum. JPGO 2014 Volume 1 Number 5 Available from: