Discussion

Our case had many similarities to cases reported in the literature. Our patient presented with a recent acute starvation with nausea and vomiting and was tachypnoeic and tachycardic with a significant acid-base disturbance. The signals of the respiratory distress were present at a gestation of 34 weeks with complaints of dyspnoea and a respiratory rate of 24 breaths per minute. The laboratory results revealed a severe metabolic acidosis with a high anion gap (22.6 mmol/L). Anion gap is used to distinct the aetiology of the metabolic acidosis. Causes of a high anion gap are the presence of high lactate, ketones or exogenous acids. Our patient did not have an elevated lactate (1.9 mmol/L) or signs of been exposed to any exogenous acids during pregnancy. In our patient, there were elevated amounts of ketones present in her urine sample. Causes of ketoacidosis within pregnancy are alcohol induced, uncontrolled diabetes or starvation induced.5 Alcoholic-induced acidosis typically occurs in the setting of excessive alcohol consumption followed by prolonged vomiting. In our patient, there were no signs of alcohol abuse. Diabetic ketoacidosis is characterized by hyperglycaemia (glucose >13.9 mmol/L)9, therefore this diagnosis was excluded. The acute starvation that our patient endured, prior to the worsening of her symptoms made the diagnosis of starvation ketoacidosis more likely. Furthermore, the aspect that in our case the metabolic disturbance rapidly could be corrected with glucose intravenous fluids, helped to confirm our diagnosis. This diagnosis became more likely because the electrolytes disturbance could be rapidly corrected with a glucose containing intravenous fluids.
In healthy non-pregnant women, it takes up to 14 days to reach the maximum of severity of starvation ketoacidosis, which would manifest with mildly elevated ketoacid levels and minimal acid-base disturbances.5 Early research has shown that starvation ketoacidosis can be present in such an accelerate state, that it might manifest, even within 12-14 hours.5 This accelerated development is due to many factors including insulin resistance, increased lipolysis and ketogenesis that occur during pregnancy.5-6 In the third trimester, in normal pregnancy, plasma bicarbonate concentration decreases, which reduces buffering capacity.8 Hepatic glycogen stores are depleted after prolonged fasting, leading to fatty acid metabolism and ketone body formation and acidosis. Women with comorbidities such as preeclampsia and gestational diabetes may be more at risk for starvation. Preeclampsia can cause severe vomiting, which may worsen the process of starvation due to less nutritional intake. In our case, the diagnosis of gestational diabetes lead to fasting.
Maternal metabolic acidosis may have serious consequences for both mother and the fetus. Maternal metabolic acidosis causes an increased maternal respiratory rate to decrease levels of pCO2 to return the pH level to a normal rate.10-12 The elevated respiratory rate is in turn associated with an increased risk for cardio‐pulmonary arrests and ICU admission.13-15 Furthermore, the reduced blood flow caused by vasoconstriction due to decreased levels of pCO2 in the maternal circulation can possibly cause fetal acidosis. This may result in impaired fetal neuronal function.4Furthermore, the acidity within pregnancy is associated with intrauterine death. It is thought to be caused by the transfer of ketones through the placenta, the maternal electrolyte imbalance and maternal volume depletion.6