Diabetic ketoacidosis (DKA) is an acute medical emergency. It increases the morbidity and mortality for both mother and fetus. This is increased by delay in recognition and errors in management .
It is more commonly seen in patients with type 1 diabetes but can occur in the presence of type 2 and gestational diabetes . It might also be the first presentation with diabetes in pregnancy.
Most presentations occur in the second and third trimester.
The risk of maternal mortality is low (0.17%) if DKA is recognised and treated promptly . There were no deaths in the most recent UK confidential enquiry report due to DKA . A review from 2014 reported fetal demise in 15.6%, preterm births in 46.3% and neonatal intensive care unit (NICU) admissions in 59% of pregnancies . In another slightly older review fetal death occurs in 60% at the time or within a week of the DKA and 40% within 1–11 weeks after the event. The exact reason is not understood . Information on the long-term effect of DKA on the surviving fetus is lacking (pmjbmj.com/content/79/934/454). Diabetic ketoacidosis sin pregnancy).
Prompt recognition and management of this medical emergency complicating pregnancy is essential in order to optimize perinatal outcome for both mother and fetus. Incidence and mortality are likely higher in developing countries .
a. Accelerated starvation (especially in the second and third trimester)
b. Dehydration and decreased caloric intake (e.g. nausea or hyperemesis gravidarum)
c. Decreased buffering capacity (compensated respiratory alkalosis of pregnancy with bicarbonates usually reduced to 18–20 mmol/L)
d. Increased production of insulin antagonists (human placental lactogen, prolactin and cortisol) 
e. Increased prevalence of obesity which increases insulin resistance
2. Precipitating risk factors for the development of DKA (as in non-pregnant patients) are
a. Infection-related acute illness (viral/bacterial)
b. Failure to take insulin as prescribed (usually due to patient non-compliance)
c. Less common
i. Insulin pump failure (rare with modern pumps equipped with alarms to alert the patient when there is a lack of insulin delivery, but as pumps run fast acting insulin only if they are blocked the patient is entirely deprived of insulin and at risk to develop DKA quickly)
ii. Concurrent use of medications (e.g. steroids, β-adrenergic medications)
iii. Diabetic gastroenteropathy
iv. Physician management errors
Pathophysiology of DKA
Insulin enables glucose to enter muscle, liver and adipose tissues to cover energy demands and lowers the serum glucose concentration. If there is a reduction in effective circulating insulin and/or an increase in counter-regulatory hormones such as glucagon, catecholamines, cortisol, growth hormone, prolactin or human placental lactogen, then this results in insulin-sensitive tissues not being able to utilise glucose and more remains in the circulation. The liver increases glucose production, gluconeogenesis and glycogenolysis. These mechanisms cause hyperglycaemia, glucosuria and osmotic diuresis and dehydration.
The liver further starts the pathway to gain energy from ketogenesis. The accumulation of ketone bodies results in metabolic acidosis. The ketone bodies in DKA are predominantly 3-β-hydroxybutyrate. These can be measured in urine or serum.
The adipose tissue undergoes lipolysis, which is exquisitely sensitive to inhibition by insulin. Its activity is increased by the counter-regulatory hormones (especially catecholamines and cortisol). This further increase acidosis.
Fluid depletion occurs in DKA via the following mechanisms:
a. Osmotic diuresis due to hyperglycaemia
b. Vomiting – commonly associated with DKA
c. Reduced level of consciousness leading to inability of adequate fluid intake
Key Symptoms and Signs
i. Polyuria (at the initial stage)
ii. Abdominal pain (can be mistaken for threatened preterm labour)
iii. Generalised malaise
iv. Distinct smell on the breath (‘pear drops’)
c. Dehydration (consequence of hyperosmolarity and polyuria)
i. Dry skin/mouth
ii. Blurred eyesight
v. Drop of blood pressure, shock
vi. Lethargy, confusion, coma (cerebral dehydration and possible hypoxia, late sign)
d. +/− Infection/ sepsis
i. Cough, shortness of breath, fever if chest infection
ii. Dysuria and/or loin pain if urinary tract infection/pyelonephritis
2. Fetal signs
a. Acidosis (diabetic ketoacidosis, lactacidosis, hyperuraemia and hypoxaemia) are all toxic to the fetus.
Cardiotocograph (CTG) monitoring is advisable if fetus is of a viable gestation >28 weeks. Below this gestation the use of CTG is controversial. CTG is likely to show abnormal features with reduced variability +/− shallow decelerations. The treatment is resuscitation of the mother, which will lead to potential reversal of CTG changes. Delivery is associated with greater maternal complications and high fetal mortality and not a priority unless considered for maternal treatment, that is chorioamnionitis. Discussion with the fetal medicine team were available should occur if the CTG remains abnormal >4–8 hours  after her improvement, to exclude other causes of fetal compromise.
Diagnosis of DKA in Pregnancy
1. Presence of diabetes of any kind
Women with diabetes may have only very modest elevation of blood glucose with DKA and do not need to reach >11 mmol/L.
a. Urinary ketones >2+ on dipstick or
b. Blood ketones >3.0 mmol/L (the risk of developing ketosis increases when the level rises above 1.5 mmol/L)
a. Venous blood gas (VBG) pH <7.3 mmol/L and /or
b. Bicarbonates (HCO3−) <15 mmol/L
Often an anion gap of >12 and elevated base deficit >4 mEq/L are mentioned in the literature as other helpful findings .
Oxygen saturation and pulse rate in the maternity early obstetric warning score (MEOWS) levels should be adapted for pregnancy.
Call for help early and escalate faster if one of more of the following are present :
1. Blood ketones >6 mmol/L
2. Bicarbonate level <5 mmol/L
3. pH <7.0 (from venous or arterial sample)
4. Anion gap >16 [calculation of anion gap = (Na+ + K+) − (Cl− + HCO3−)]
5. Hypokalaemia on presentation <3.5 mmol/L
6. Systolic blood pressure <90 mm Hg
7. Pulse >110 beats/minute or <60 beats/minute
8. GCS <12 or abnormal AVPU (alert, verbal, pain, unresponsive) scale
9. Oxygen saturation below 94% on air
These patients may require intensive therapy unit (ITU) admission and require urgent senior physician and anaesthetic input or further multidisciplinary team input based on the underlying cause (i.e. if underlying cause is appendicitis with vomiting, intervention will be needed, requiring multidisciplinary team input, including obstetric and surgical, to reduce morbidity and mortality).
Involve a senior obstetrician and the diabetes or medical team and an anaesthetist, urgently. Care should be in a level 2/high dependency unit setting. ITU is indicated in haemodynamic instability or coma or severe DKA in pregnancy.
There are four main aspects of management which will happen simultaneously. They should be initiated as soon as possible.
a. Typical deficits in a DKA in adults
i. Water 100 mL/kg
ii. Sodium 7–10 mmol/kg
iii. Chloride 3–5 mmol/kg
iv. Potassium 3–5 mmol/kg
b. Two randomised controlled trials compared the use of 0.9% sodium chloride to Hartmann’s solution, with neither showing superiority [14, 15]. The rationale for using 0.9% sodium chloride here is its availability, ability to add potassium as required and long time of use. However, one must be aware of the risk of hyperchloremic metabolic acidosis, which may lead to renal arteriolar vasoconstriction, oliguria and slowing resolution. In this case compound sodium would be the better fluid, but potassium management is more challenging.
c. If the systolic BP is <90 mm Hg