Case presentation

A 29 year old multipara woman, at 28 weeks of gestation, presented with dyspnoea, maternal tachycardia and tachypnea. Past medical history included an appendectomy and one uncomplicated previous pregnancy. At first presentation a CT-scan was performed, which showed no signs of lung embolism. At a gestation of 30 weeks, pregnancy induced hypertension was diagnosed with a blood pressure of 140/80 mmHg. Laboratory results did not show any abnormalities and the urinalysis was normal. Cardiotocograph was normal. After one week, at a gestation of 31 weeks and 2 days, blood pressure raised to 150/84 mmHg, after which methyldopa 500 mg 3 times a day was started. Fasting glucose was 7.7 mmol/L (normal range: <7.0 mmol/L) and the diagnosis gestational diabetes was concluded, although no anti-diabetic medication was started. At 34 weeks of gestation, the patient presented malaise and false contractions. Urinalysis showed 2+ protein with a protein-creatinine ratio of 92.1 mg/mmol (normal <30 mg/mmol). Dyspnoea and palpitations accompanied the complaints of malaise. Physical examination showed a maternal tachycardia of 124 bpm, a respiratory rate of 24 breaths per minute and a blood pressure of 130/75 mmHg. Due to the presence of hypertension and albuminuria, preeclampsia was diagnosed. Another CT-scan was performed, which again showed no signs of pulmonary embolism. Random glucose was 9.6 mmol/L without antidiabetic medication. Laboratory results showed a hypokalaemia of 3.3 mmol/L (normal 3.5-5.0 mmol/L) without other abnormalities. The patient was admitted at the obstetric unit for observation and further analysis, with preeclampsia.\sout The next day (34+1), the symptoms persisted and were accompanied by nausea. A physical examination showed a blood pressure of 135/69 mmHg, a heart rate of 110 bpm and a saturation of 99%. There was no registration of respiratory rate. There were no signs of oedema and the knee reflexes were normal. A systolic souffle was found during auscultation. Cardiologic exam concluded hyperdynamic circulation and anaemia (haemoglobin: 7.7 mmol/L). At a gestation of 34 weeks and 2 days, symptoms were unchanged. Due to high fasting glucose (7.2 mmol/L) treatment with insulin was started. Due to the gestational diabetes, an ultrasound examination was performed: head circumference (HC) p98, abdominal circumference (AC) >p100 and estimated fetal weight (EFW) >p100, from which macrosomia was concluded. Laboratory results still showed a hypokalaemia of 3.4 mmol/L, as well as an elevated uric acid of 0.57 mmol/L (0.12-0.34 mmol/L). 24-hour urine showed 0.66 grams of protein. At a gestation of 34 weeks and 4 days, symptoms worsened with vomiting (three times a day) and increase of malaise. Respiratory rate was 24 breaths per minute, saturation 99% without oxygen, blood pressure 140/90 mmHg and heart rate 120 bpm. During physical exam, no other abnormalities were found. Due to high blood pressure, methyldopa was changed to 1000mg three times day. Urinalysis showed 4+ ketones. Blood test showed an elevated uric acid of 0.77 and a random glucose of 6.8 mmol/L. Rehydration with sodium chloride 0.9% was started. The insulin dosage was increased. At 34 weeks and 5 days of gestation, the patient and her family expressed their concerns. Her blood pressure was 140/80 mmHg, maternal heart rate was 128 bpm and her respiratory rate was 20-25 per minute. Venous blood test showed a severe metabolic acidosis with an incomplete respiratory compensation (pH 7.15, pCO2 2.8 kPa, bicarbonate 7.4 mmol/L, base excess -19.5 mmol/L, Lactate 1.9) with an increased anion gap (22.6 mmol/L), for which the Intensive Care Unit (ICU) was consulted. With the probability diagnosis: starvation induced severe metabolic acidosis. Sodium bicarbonate (8.4%), glucose and thiamine were given intravenously.\sout Due to the severe acidosis, an emergency caesarean section was performed under general anaesthesia, with a total blood loss of 800cc. Peri-operative patient received 10% glucose IV to continue correcting the starvation. A male newborn (3850 grams) was delivered with an APGAR score of 2/5/7 and a pH level of 7.05, pCO2 7.3 kPa, base excess -14.9 mmol/L. Her child was transferred to an academic centre for continuous positive airway pressure (CPAP) treatment due to idiopathic respiratory distress syndrome (IRDS) and hypoglycaemia. On arrival at ICU, patient had a blood pressure of 151/94 mmHg, a pulse of 140/min and patient was still intubated. Admission arterial blood gas showed a persisting severe metabolic acidosis (pH 7.14, pCO2 4.1 kPa, base excess -17.2 mmol/L, bicarbonate 10.5 mmol/L). Further laboratory findings showed an anion gap 21 mmol/L, chloride 111.0 mmol/L, lactate 1.9 mmol/L and a glucose 22.5 mmol/L. The intravenous glucose (10%) fluid, alongside a sodium chloride fluid therapy was continued. Furthermore, intravenous insulin, potassium and thiamine were started, to compensate for the electrolyte shift induced by the therapy. The patient was extubated, quickly and successfully. The acid base balance returned to normal within 24 hours of the ICU admission. The ketonuria was completely gone within 48 hours of treatment. The patient was then discharged to the department of obstetrics.