This document discusses the management of diabetic ketoacidosis (DKA) during pregnancy. DKA is a medical emergency associated with high rates of fetal loss and maternal mortality. It most commonly occurs in pregnant women with poorly controlled diabetes. The pathophysiology of DKA in pregnancy involves relative insulin resistance during pregnancy and other hormonal and metabolic changes. Diagnosis is based on clinical signs and laboratory confirmation of high blood glucose, ketones, and metabolic acidosis. Treatment involves fluid resuscitation, insulin therapy, electrolyte replacement, and monitoring of both mother and fetus until metabolic stabilization is achieved. Fetal well-being during treatment is assessed due to risks of acidosis, dehydration and electrolyte disturbances.

1. Management of diabetic
ketoacidosis in pregnancy
Dr/ Ahmed Walid Anwar Morad
Assistant professor of OB/GYN
Benha University
2017

2. This talk spotlights on
• Definition
• Epidemiology
• Pathophysiology
• Diagnosis
• Differential diagnosis
• Prevention
• Treatment
• Pitfalls in DKS

4. Epidemiology
• DKA is an acute medical
emergency associated with:
- Fetal loss rates more than 50%.
- Maternal mortality rates less
than 1%.

5. Epidemiology
• DKA in pregnancy most commonly occurs in
women with:
- Poorly controlled :
*T1DM
*T2DM or GDM under
- Glucocorticoids
- B-agonists / tocolytics
- First presentation of T1DM in pregnancy

6. PATHOPHYSIOLOGY

7. Glucose Homeostasis

9. DKA is common during pregnancy
WHY?
• Pregnancy is a stat of Relative insulin resistance
especially in 2nd
& 3rd
trimesters.
• Increased levels of HPL ,E, P & Cortisol act
as insulin antagonists& impair maternal
insulin sensitivity.
• Pregnancy is a state of respiratory alkalosis associated
with a compensatory drop in bicarbonate levels; this
impairs the renal buffering capacity.

10. Precipitating factors of DKA in
pregnancy
• Insufficient or no insulin
• Protracted vomiting
• Hyperemesis gravidarum
• Starvation
• Infections
• Medications precipitating DKP
• Conditions such as diabetic gastroparesis

11. Diagnosis of DKA in pregnancy
• DKP may be
the first
presentatio
n of diabetes
in pregnancy

12. Laboratory confirmation of DKA in
pregnancy

13. Pitfalls in DKA
• Potassium level may be falsely normal/elevated.
• High
– WBC count without infection.
– Blood urea with prerenal azotemia due to dehydration.
– Creatinine in absence of true impairment of renal function.
– Serum amylase even in absence of pancreatitis.

14. What is different in pregnancy?
• DKA occurs at lower blood
glucose level (Euglycaemic DKA)
• DKA can develop more rapidly
than in non-pregnant women
• Nausea and vomiting are common.

15. Differential diagnosis of DKA

16. Complications
Fetal
• Distress
• Perinatal death
• Brain injury
• Long term
developmental
impacts.

17. Management of DKA in pregnancy

18. Multidisciplinary approach
Patient monitoring in HDU
Consider
1. IV line
2. Arterial line
3. Urinary catheter (if not
producing urine after 3
hours).
4. 4. Nasogastric tube (if
drowsy / vomiting).
ICU admission
• pH < 7.0
• Altered consciousness
• Poor response to acute
resuscitation
• More intensive
monitoring anticipated
(e.g. K+, intercurrent
illness)

20. Management of DKA in pregnancy
Goals
1. Re-hydration (IV fluid therapy)
2. Normalization of serum glucose (IV insulin
therapy)
3. Electrolyte correction
4. Correction of acidemia (need for bicarbonate
administration)
5. Elimination of the underlying cause
6. Monitoring of maternal and fetal responses

21. -Hourly intake and output. Foley catheter ??
- Goal is correction of total fluid deficit over 12-24 hours.
- After BP and urine output stabilize may change fluids to 0.45 NS at
250-500 cc/hr and then may decrease infusion rate
- Avoid lactate-containing solution as this will aggravate acidosis.
-
Aim
Volume deficit
Time
Monitor
Type
Rate
Hypercholermic
acidosis

22. Insulin & K+ therapy are complementary

23. Phosphate
• Not usually indicated.
• Considered if severe hypophosphataemia
(<0.35mmol/L) +/- cardiorespiratory
depression

24. Correction of acidosis
• The use of bicarbonate is
not recommended why?
1. Bicarbonate inhibits the
compensatory
hyperventilation → ↑ CO2
partial pressure → ↓ fetal
oxygen delivery
2. Paradoxical fall in CSF PH.
3. Delays the wash out of
ketones
4. Worsen hypokalaemia
• Consider
Bicarbonate:
1. PH < 6.9
2. PH < 7 with
homodynamic
instability
3. Hyperkalemia
with EG changes
• Limited
studies

25. DKA resolution criteria
• Blood ketone level < 6mmol/ l
• pH > 7.3
• Bicarbonate > 15mmol/l
• Anion gap ≤ 12

26. Broad spectrum
antibiotics

27. Fetal considerations
The frequency of fetal monitoring is unknown and no
definite recommendations are currently available.

28. Fetal considerations
b. Fetuses exposed to maternal acidosis, dehydration and
electrolyte disturbance (K+) may have:
Decreased variability and late decelerations or even fetal death.
The ominous patterns will typically correctable with correction of maternal
metabolic disturbance (4–8 hours) .
Maternal oxygen therapy is always useful in nonreassuring
fetal heart rate.
Fetal biophysical profile and Doppler studies may also reflect
the fetal acidotic status.

29. Fetal considerations
c. Delivery decision should be individualized according to:
– Maternal clinical status
– Gestational age
– The results of fetal investigations such as fetal heart
tracing.
d. Delivery of a compromised fetus should be
undertaken ONLY after the mother is
metabolically stable.

30. Fetal considerations
• Continue the pregnancy with complete resolution
of DKP.
• After complete resolution of DKP, further fetal
monitoring especially in preterm fetus is not
recommended.
Mode of delivery is guided by fetal ,maternal
and obstetrical indications.

31. Fetal considerations
Avoid use of Betamimetics and corticosteroids while
DKA is being controlled.
The best practice, however, is aimed at educating the
patient to avoid further recurrence of DKP, and an
increased surveillance to ensure adequate diabetic
control and compliance with treatment.

32. Take home message
1. DKA during pregnancy is a life-threatening
condition.
2. DKA may be the first presentation of DM during
pregnancy.
3. Rapid diagnosis with rapid initiation of a
multidisciplinary team management could help to
reduce maternal and fetal mortality, and morbidity.
4. Decreased variability and late decelerations or even
fetal death are common findings.

33. Take home message
5.The ominous patterns will typically
correctable with correction of maternal
metabolic disturbance.
6.Avoid use of Betamimetics and corticosteroids
while DKA is being controlled.
7.Delivery decision should be individualized.
8.Delivery should be undertaken ONLY after the
mother is metabolically stable.

34. Take home message
9. Continue the pregnancy with complete
resolution of DKA.
10. Mode of delivery is guided by fetal, maternal
and obstetrical indications.
11. Patient education will form the main
framework to reduce the risks associated
with DKA.

35. Thank You
Any Questions or
Comments?