Introduction

Diabetic ketoacidosis (DKA) is a life-threatening metabolic emergency that occurs in approximately 1–3% of diabetic pregnancies. It is associated with significant maternal and perinatal morbidity and mortality, with reported fetal loss rates of up to 35%.^3,4,7 

Fetal compromise during maternal DKA is common and is frequently reflected in pathological cardiotocography (CTG) patterns. These changes are often reversible following correction of the maternal metabolic state.⁸ However, distinguishing potentially reversible fetal compromise from irreversible deterioration remains a major clinical challenge, particularly at preterm gestations. This case report describes a critically unwell pregnant woman with type 1 diabetes mellitus (T1DM) presenting with severe DKA and persistent pathological CTG, highlighting the complexity of multidisciplinary decision-making regarding timing of delivery. 

Case Presentation

A 31-year-old woman, gravida 2 para 0, with a booking body mass index (BMI) of 37 and T1DM presented with severe DKA at 29 + 2 weeks gestation to a major metropolitan level 5 maternity service. She had been vomiting since the previous day and had missed her regular antihyperglycaemic medications, Levemir, and fast-acting insulin Aspart. 

She had multiple prior admissions for hyperemesis gravidarum, which led to episodes of starvation ketosis and diabetic ketoacidosis secondary to suboptimal adherence to insulin therapy. Her pregnancy was further complicated by gestational hypertension, recurrent urinary tract infections, anaemia, and superficial thrombophlebitis of the upper limb. 

On admission, the patient appeared unwell and tachypnoeic. She reported mild, intermittent abdominal pain, uterine tightening, and decreased fetal movements. She denied vaginal bleeding, fever, cough, altered urinary or bowel habits, or symptoms suggestive of pre-eclampsia. 

On examination, the patient appeared dehydrated, with a blood pressure of 138/82 mmHg and a respiratory rate of 30 breaths per minute. The abdomen was soft, with mild palpable uterine activity. Bedside ultrasound did not demonstrate evidence of placental abruption. Gross fetal movements were absent during the scan; however, umbilical artery Doppler studies were within normal limits. 

Initial biochemical investigations revealed severe metabolic acidosis (arterial pH < 7.0), marked hyperglycaemia (> 38 mmol/L), hyperkalaemia (K+ 5.8 mmol/L), and elevated ketone levels (5.9 mmol/L). Intravenous fluids and an Actrapid insulin infusion were commenced. Subsequently, her blood pressure rose to 159/92 mmHg, for which 20mg of intravenous labetalol was administered (Table 1).  

Initial cardiotocography (CTG) demonstrated a normal baseline and variability. However, following labetalol administration, the CTG evolved to show absent variability, late decelerations, and absence of accelerations, raising concern for fetal compromise (Figure 1). 

Figure 1. Cardiotocograph (CTG) trace before and after intravenous labetalol administration.

Table 1 – Laboratory data on presentation and after starting treatment.

Case Management and Outcome 

Despite gradual biochemical improvement in maternal acidosis and hypovolaemia with treatment, the CTG remained pathological with absent variability, recurrent decelerations, and a rising baseline for more than four hours. Full correction of maternal biochemistry was anticipated to take several more hours, during which there was a significant risk of further fetal deterioration. This raised consideration of an early delivery due to ongoing fetal distress while awaiting CTG improvement (Figure 2).  

The multidisciplinary team discussed the risks of immediate delivery versus continued in utero resuscitation. Given the persistent pathological antepartum CTG, despite maternal stabilisation efforts, and the high perceived risk of intrauterine fetal demise, a decision was made to proceed with urgent delivery following discussion with the patient and her partner. In utero transfer options were explored; however, the nearest tertiary hospital neonatal intensive care unit reported no bed availability. Magnesium sulphate was commenced for fetal neuroprotection. An emergency caesarean section was performed. 

Figure 2. Cardiotocograph (CTG) recorded five hours post-admission, demonstrating absent baseline variability and recurrent decelerations.

A live female infant was delivered, weighing 1.4kg. The neonate was floppy, cyanosed, and apnoeic at birth, requiring immediate cord clamping and resuscitation by the paediatric team. Apgar scores were 5 at 1, 5, and 10 minutes. Venous cord gas showed a pH of 7.08 and lactate of 4.7 mmol/L; arterial cord gas could not be obtained. Capillary blood gas at 30 minutes of life revealed pH 6.97 and lactate 5.2 mmol/L. The neonate was admitted to the special care nursery and transferred the same day to a tertiary neonatal intensive care unit. 

Postoperatively, the mother required intensive care unit (ICU) admission and was subsequently transferred to the same tertiary centre as her infant. At follow-up, her blood pressure had normalised. However, medication adherence remained poor, including missed insulin doses, and she was not monitoring her blood pressure at home. Renal follow-up suggested resolving gestational hypertension. 

Discussion

This case illustrates the profound maternal and fetal consequences of DKA in pregnancy, and the complexity of decision-making when fetal compromise persists despite maternal resuscitation.  

Pregnancy confers a unique metabolic vulnerability to DKA due to increased insulin resistance, accelerated starvation, respiratory alkalosis with reduced buffering capacity, and the influence of counter-regulatory placental hormones.^1,5,6 Consequently, DKA can develop more rapidly and at lower blood glucose levels than in non-pregnant individuals, often leading to diagnostic delay. 

Fetal distress in maternal DKA is thought to result primarily from reduced uteroplacental perfusion secondary to maternal hypovolaemia, acidosis, and hypoxaemia.11 Additional contributing mechanisms include fetal hyperinsulinaemia, electrolyte disturbances such as hypokalaemia, and impaired oxygen delivery due to reduced 2,3-diphosphoglycerate levels in the setting of hypophosphataemia.⁶ 

When treating DKA, the emphasis is primarily on reducing ketoacidosis with supportive fluid management (Figure 3). Intravenous insulin infusions are resource intensive and are potentially dangerous because of the rapid drop in potassium and/or glucose that can occur. If insulin infusions are commenced in the emergency department, half-dose insulin infusion rates are used until the patient is transferred to the ICU or similar specialist area (Figures 4 and 5). Ketones are used as an indicator of disturbed normal biochemical function. Treatment is directed at reducing ketones because their presence indicates an ongoing disturbance of glucose metabolism.¹² 

Fig. 3. Fluid Replacement in DKA, Fig. 4. Insulin Therapy in DKA, Fig. 5. Potassium Replacement in DKA

 Numerous reports demonstrate that fetal heart rate abnormalities during DKA often resolve following correction of maternal metabolic derangements, supporting an initial strategy of aggressive maternal stabilisation rather than immediate delivery.9,10 

However, this case highlights a scenario in which fetal compromise persisted despite partial maternal improvement. While immediate caesarean delivery in DKA may exacerbate maternal instability and does not guarantee neonatal benefit, prolonged exposure of the fetus to a hostile intrauterine environment also carries significant risk. Compared with the previously reported cases by Yang Huang, Grace Ng et al., and M Á Gómez-Ríos et al., in which patients presented with moderate DKA and the CTG abnormalities resolved with medical management, our patient exhibited severe DKA at presentation, in association with preeclampsia. The concomitant use of antihypertensive agents and the severity of the metabolic disturbance may have contributed to the delayed resolution of fetal distress. A multidisciplinary team approach enabled a balanced assessment of maternal and fetal risks, supporting the decision for early delivery. 

Table 2 – Classification of DKA severity 

Conclusion

DKA in pregnancy remains a rare but devastating complication, associated with significant maternal and fetal risks. Prompt recognition, aggressive multidisciplinary management, and continuous fetal monitoring are essential. Although pathological CTG findings during maternal DKA are often reversible following correction of maternal metabolic abnormalities, persistent fetal compromise despite appropriate resuscitation may necessitate urgent delivery.