DKA in Pregnancy

INTRODUCTION
 Definition
 Epidemiology
 Pathophysiology
 Diagnosis
 Investigation
 Treatment
TRIAD OF DIABETIC
KETOACIDOSIS

Hyperglycaemia

DKA
Ketosis Acidosis
EPIDEMIOLOGY
 DKA is a medical emergency associated with:
 Fetalloss rates 9 to 36%
 Maternal mortality rates less than 1%
 DKA in pregnancy most commonly occurs in
women with:
 Poorly controlled:
 T1DM
 T2DM or GDM
 First presentation of T1DM in pregnancy
 DKA IS COMMON DURING PREGNANCY.
WHY?
 Pregnancy is a state of Relative Insulin
resistance especially in 2nd & 3rd Trimesters.
 Increased levels of HPL, Progesterone &
Cortisol act as insulin antagonist & impair
maternal insulin sensitivity.
 State of respiratory alkalosis associated with
a compensatory drop in bicarbonate levels;
this impairs the renal buffering capacity.
PRECIPITATING FACTORS OF
DKA
 Protracted vomiting
 Starvation
 Hyperemesis gravidarum
 Infections
 Insulin non-compliance
 Medications precipitating diabetic
ketoacidosis in pregnancy
 Insulin pump failure
 Conditions such as gastroparesis
SIGNS & SYMPTOMS
 Nausea or vomiting
 Abdominal pain
 Polyuria or polydipsia
 Blurred vision
 Muscle weakness
 Drowsiness
 Lethargy
 Change in mental status
 Hyperventilation (Kussmaul breathing)/pear drop odour
 Tachypnoea
 Hypotension
 Tachycardia
 Coma
 Shock
 Abnormal fetal heart tracing
INVESTIGATIONS

Glucose >11.0mmol/l or known Diabetic Mellitus

PITFALLS IN DKA
 Potassium level may be falsely
normal/elevated
 High
 WBC count without infection
 Blood urea with pre-renal 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

 DKA can develop more rapidly than in non-

pregnancy women

 Nausea and vomiting are common

MANAGEMENT
 MDT APPROACH
Patient monitoring in ICU admission:
HDU  pH<7.0
Consider:  Altered consciousness
 IV line  Poor response to
 Arterial line resuscitation
 Urinary catheter (if no  More intensive
UO after 3 hours) monitoring anticipated
 Nasogastric tube (if ( e.g. K+, intercurrent
drowsy/vomting) illness)
MANAGEMENT OF DKA
Goals:
 Re-hydration (IV fluid)
 Normalisation of serum glucose ( IV Insulin)
 Electrolyte correction
 Correction of acidemia (?bicarbonate
administration)
 Elimination of underlying cause
 Monitoring of maternal and fetal responses
 Goal is to correct total fluid deficit over 12-24
hours.
 ACIDOSIS- CORRECTION?
The use of bicarbonate is not Consider bicarbonate:
recommended. Why?
1. pH <6.9
1. Bicarbonate inhibits the
compensatory hyperventilation 2. pH<7.0 with
Co2 partial pressure haemodynamic
fetal oxygen delivery. instability
2. Paradoxical fall in CSF pH 3. HyperK+ with ECG
changes
3. Delays the wash out of ketones
4. Worsens HyperK+
DKA RESOLUTION CRITERIA
 Blood ketone level <0.6mmol/l
(>3.0)
 pH >7.3 (<7.3)
 Bicarbonate >15mmol/l (<15)
 Anion gap ≤ 12 (>12)
FETAL CONSIDERATIONS
FETAL CONSIDERATIONS
 Fetuses exposed to maternal acidosis,
dehydration and electrolyte disturbances
(K+) may have:
 Decreased variability
 Late decelerations
 Fetal death
 Maternal O2 therapy is always useful in non-
reassurring FHR
 Fetal biophysical profile and doppler studies
may also reflect the fetal acidotic status.
DELIVERY
 Delivery decision should be individualised
depending on:
 Maternal clinical status
 Gestational age
 Results of fetal investIgations e.g. CTG
 Delivery of a compromised fetus should be
undertaken ONLY after the mother is
metabolically stable.
 MOD- guided by fetal, maternal and
obstetrics indications
BEST PRACTICE
 Aimed at educating the patient to avoid
further recurrence and an increased
surveillance to ensure adequate diabetic
control and compliance with treatment.
TAKE HOME MESSAGE
 DKA during pregnancy is a life threatening
condition.
 DKA may be the first presentation of DM
during pregnancy.
 Rapid dignosis with rapid initiation of a MDT
management could help to reduce maternal
and fetal mortality and morbidity.
 Patient education will form the main
framework to reduce the risks associated
with DKA during pregnancy.