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 cardioâpulmonary
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