Management of diabetic ketoacidosis in pregnancy
Dr/ Ahmed Walid Anwar MoradAssistant professor of OB/GYN
Benha University2017
This talk spotlights on• Definition • Epidemiology• Pathophysiology • Diagnosis • Differential diagnosis• Prevention • Treatment • Pitfalls in DKS
Epidemiology
• DKA is an acute medical emergency associated with:
- Fetal loss rates more than 50%.
- Maternal mortality rates less than 1%.
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
PATHOPHYSIOLOGY
Glucose Homeostasis
DKA is common during pregnancyWHY?
• 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.
Precipitating factors of DKA in pregnancy
• Insufficient or no insulin• Protracted vomiting• Hyperemesis gravidarum• Starvation• Infections• Medications precipitating DKP• Conditions such as diabetic gastroparesis
Diagnosis of DKA in pregnancy
• DKP may be
the first
presentati
on of
diabetes in
pregnancy
Laboratory confirmation of DKA in pregnancy
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.
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.
Differential diagnosis of DKA
Complications
Fetal• Distress• Perinatal death• Brain injury• Long term
developmental impacts.
Management of DKA in pregnancy
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)
Management of DKA in pregnancy
Goals1. Re-hydration (IV fluid therapy)2. Normalization of serum glucose (IV insulin
therapy)3. Electrolyte correction4. Correction of acidemia (need for bicarbonate
administration)5. Elimination of the underlying cause 6. Monitoring of maternal and fetal responses
-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
Insulin & K+ therapy are complementary
Phosphate
• Not usually indicated.
• Considered if severe hypophosphataemia
(<0.35mmol/L) +/- cardiorespiratory
depression
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
ketones4. Worsen hypokalaemia
• Consider Bicarbonate:
1. PH < 6.9
2. PH < 7 with homodynamic instability
3. Hyperkalemia with EG changes
• Limited studies
DKA resolution criteria
• Blood ketone level < 6mmol/ l
• pH > 7.3
• Bicarbonate > 15mmol/l
• Anion gap ≤ 12
Broad spectrum antibiotics
Fetal considerations
The frequency of fetal monitoring is unknown and nodefinite recommendations are currently available.
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.
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.
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.
Fetal considerationsAvoid 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.
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.
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.
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.
Thank You
Any Questions or Comments?