Diabetic Ketoacidosis In Pregnancy

Both the mother and the fetus are put at risk when diabetic ketoacidosis occurs during pregnancy. In addition to newly emerging type 1 diabetes patients, it typically happens in the latter stages of pregnancy.

Although its incidence rates and prognosis have improved over time, gestational diabetes still poses a significant therapeutic challenge.

And it is because it frequently occurs at lower blood glucose levels and more swiftly than in non-pregnant people, delaying evaluation.

What is Diabetic Ketoacidosis?

A dangerous and potentially fatal diabetes condition is diabetic ketoacidosis (DKA). The majority of persons with type 1 diabetes have diabetic ketoacidosis. Diabetic ketoacidosis can occur in people who have type 2 diabetes as well.

When your body doesn’t produce enough insulin, blood sugar can’t enter your cells to be used as energy, which leads to diabetic ketoacidosis.

Instead, your liver converts fat into ketone-producing acids through a process called lipolysis. When ketones are created excessively and quickly, they might accumulate in your body in fatal quantities.

Use a meter to check your blood for ketones every four to six hours or an over-the-counter ketone test kit to examine your urine whenever you’re ill or your blood glucose is 240 mg/dL or higher.

If you exhibit any of the diabetic ketoacidosis symptoms, you should also be tested for ketones. If your ketones are medium to high, call your doctor.

Elevated ketones are an indication of diabetic ketoacidosis, a medical emergency that requires rapid treatment.

How does Diabetic Ketoacidosis Occur in Pregnancy?

There are a few physiological changes that can be the triggering factor for diabetic ketoacidosis in pregnancy.

The following list includes some specific physiological causes of DKA in pregnancy:

1. Due to the respiratory alkalosis that takes place during pregnancy and the compensatory decrease in bicarbonate levels, the pregnant woman is more likely to experience diabetic ketoacidosis.
2. The basis for diabetic ketoacidosis in pregnancy is relative insulin resistance during pregnancy, accelerated lipolysis, and increased free fatty acids.
3. Maternal insulin sensitivity is compromised by hormonal changes, including elevated levels of progesterone, cortisol, and human placental lactogen.

Diabetic ketoacidosis is much more frequently observed during pregnancy in women with type 1 diabetes.

However, it can also occur during gestational diabetes mellitus and type 2 diabetes. The triggering factors can be vomiting, starvation, non-compliance with insulin, various medications, and insulin pump failure.

Typical signs and symptoms of diabetic ketoacidosis during pregnancy

• Hyperventilation
• Polyuria
• Vomiting
• Hypotension
• Polydipsia
• Nausea
• Weakness
• Abdominal pain
• Ketotic breath
• Disorientation
• Tachycardia
• Coma
• Dry mucus membranes

What may cause Diabetic Ketoacidosis during Pregnancy?

There are a bunch of factors that can cause a sudden incidence of diabetic ketoacidosis during pregnancy.

• β-Sympathetomimetic drugs.
• Poor management
• Corticosteroids
• Infection (particularly in the urinary tract)
• Non-compliance
• Emesis
• Insulin pump failure

On another note, the onset of labor prematurely in pregnant women who already suffer from diabetes can cause a sudden increase in the chances of diabetic ketoacidosis during pregnancy since there is a requirement for systemic steroids for fetal lungs and tocolysis.

In a study conducted to analyze the causes of diabetic ketoacidosis during pregnancy, it was concluded that in 17% of the cases, non-compliance was the cause and in 25% of the cases, it was a contributory factor. [ref]

How does Diabetic Ketoacidosis in Pregnancy cause Fetal Loss?

It is unclear exactly how maternal diabetic ketoacidosis harms the fetus. Both glucose and ketones may pass through the placenta with ease.

It is uncertain which condition worsens the fetus more: maternal acidosis, hyperglycemia, severe volume loss, or electrolyte imbalance.

Cardiotocography performed on patients with diabetic ketoacidosis during pregnancy has revealed:

• the absence of baseline heart rate variability,
• prolonged late deceleration, and
• unsettling biophysical profile, all of which are signs of fetal distress.

There is no doubt that the unfavorable intrauterine environment demonstrated by the significant death rate is linked with diabetic ketoacidosis.

The following are the possible mechanisms behind this:

1. Fetal acidity and an electrolyte imbalance may result from maternal acidosis.
2. If severe, maternal hypokalemia and fetal hyperinsulinemia might result in fetal hypokalemia, which would decrease the fetus’s heartbeat and result in deadly arrhythmia.
3. With reduced oxygen supply to the fetus, maternal hypophosphatemia linked to diabetic ketoacidosis can reduce 2,3-diphosphoglycerate levels.
4. Osmotic diuresis causes a decrease in uteroplacental blood flow, which decreases the volume and causes maternal acidosis, which might induce fetal hypoxic injury.

Risk factors for diabetic ketoacidosis during pregnancy:

Certain factors that predispose a pregnant woman to diabetic ketoacidosis are listed below.

Insulin antagonistic state

Insulin resistance occurs throughout pregnancy. It has been shown that insulin sensitivity decreases by as much as 56% after 36 weeks of pregnancy. [ref]

This is mostly due to the development of insulin-antagonistic hormones such as cortisol, prolactin, and human placental lactogen.

Because of this, the amount of insulin needed increases during the course of pregnancy, which accounts for the increased prevalence of diabetic ketoacidosis in the second and third trimesters.

Additionally, the natural increase in progesterone during pregnancy causes a reduction in gastrointestinal motility, which increases carbohydrate absorption and promotes hyperglycemia.

Effect of emesis

Due to elevated levels of human chorionic gonadotrophin in the first trimester and elevated oesophageal reflux in the second, nausea and vomiting are frequently experienced.

Insulin antagonistic hormones are increased as a result of the stress and fasting condition that follows. Ketoacidosis is brought on by this, combined with the subsequent dehydration.

Increased hunger

During pregnancy, especially in the second and third trimesters, there is a relative condition of increased hunger.

Maternal fasting glucose decreases as a result of the fetus and placenta using a significant quantity of maternal glucose as a key source of energy.

This results in an increase in free fatty acids. These are then metabolized to ketones in the liver due to relative insulin insufficiency.

Reduced buffering capacity

Pregnancy-related increases in minute alveolar ventilation cause respiratory alkalosis, which is countered by an increase in bicarbonate excretion from the kidneys.

As a result, when subjected to an acid load like ketones, the buffering capacity is reduced.

The clinical consequence of these metabolic changes is that pregnant diabetics are not only more likely to develop ketoacidosis than non-pregnant diabetics, but that it can also happen much more quickly and at much lower glucose levels.

This is demonstrated in the case study we used to illustrate the point.

How do you manage diabetic ketoacidosis during pregnancy?

To lower the risk of maternal and fetal death, diabetic ketoacidosis during pregnancy must be treated quickly and aggressively in a high-dependency unit, This too under integrated medical and obstetric care.

Aggressive volume replacement, insulin infusion, close monitoring of electrolytes, and a search for and adjustment of aggravating causes are all part of the treatment.

Compared to diabetic ketoacidosis in women who are not pregnant, the initial fluid loss is greater in pregnant women.

Dextrose infusion may be required in addition to insulin therapy if acidosis is seen at lower beginning glucose levels than in non-pregnant individuals.

Although cerebral edema, particularly in children, is a potential risk factor for diabetic ketoacidosis, its correlation with vigorous fluid replacement has not always been shown.

• For fetus:

To evaluate the wellness of the fetus, continuous fetal monitoring is required. Although these may be signs of fetal impairment in the ketoacidosis patient, non-reactive fetal cardiac tracings, frequent late decelerations, or unsettling biophysical profiles may not always point to the need for early delivery.

Inducing labor in a patient might worsen the condition of the mother while providing little to no benefit to the unborn child.

• Positive note:

It’s interesting to note that fetal impairment may no longer be noticeable if hyperglycemia and acidosis are corrected and maternal stabilization is reached.

Magnesium sulfate is the preferred tocolytic in cases of premature labor, while 2-agonists are often contraindicated.

• Best step:

The foundation of care for this illness is, in essence, a technique that combines in-utero resuscitation with maternal stabilization, hydration, and reversal of hyperglycemia and metabolic acidosis under combined medical and obstetric monitoring.