Neobook — clinical reference

Diabetic Ketoacidosis represents a hyperglycaemic and obstetric emergency posing significant risk for maternal and fetal morbidity and mortality.

Although typically encountered in Type 1 Diabetes mellitus (T1DM), pregnant women with any form of hyperglycaemia (including Type 2 Diabetes mellitus (T2DM), Gestational diabetes (GDM) and newly diagnosed diabetes) may be affected. DKA may develop at any time during pregnancy but is most common in the second and third trimesters.

For the following reasons, a high index of suspicion of DKA in any pregnant woman who is unwell, is judicious:

Symptoms can be misleading, non-specific and resemble normal pregnancy
DKA can happen with mild hyperglycaemia (euglycaemic DKA)
DKA can occur without prior diagnosis of diabetes

Common presenting symptoms

Nausea, vomiting, abdominal pain,
generalised fatigue, blurred vision,
polyuria, polydipsia,
evidence of volume depletion (dry mucous membranes, decreased skin turgor),
tachycardia, hypotension
Severe symptoms: Rapid, shallow breathing (Kussmaul’s respiration), ketotic breath, altered mental state

Diagnostic Criteria for DKA in Pregnancy

Diagnostic Criteria for DKA in Pregnancy

Hyperglycaemia: BG ≥ 11mmol/L
(Some guidelines omit hyperglycaemia in the definition. DKA in Pregnancy can frequently occur at lower or normal BG levels - euglycemic DKA. Therefore, if other criteria are met, DKA can be diagnosed in the presence of normal/near- normoglycaemia and is still an emergency).
Metabolic acidosis: pH ≤ 7.3 / HCO₃ ≤ 18mmol/L (High anion gap - >12)
Ketonaemia: Blood ketones ≥ 3mmol/L / Urine ketones 2+
- Note: Blood beta-hydroxybutyrate is the preferred test for the diagnosis and monitoring of diabetic ketoacidosis (this is currently best done on a validated point of care (Freestyle®) glucometer using ketone strips)
- Anion gap >12mmol/L indicates increased anion gap metabolic acidosis

Aspects of Treatment

Confirm diagnosis (clinical suspicion and blood gas confirmation)
Secure airway and oxygenation
Admit to highest level of care available (if Obstetric Critical Care Unit is full, initial management will need to be in labour ward until OCCU bed available)
Obtain IV access and insert indwelling urinary catheter
Volume Repletion: Fluid rehydration
Electrolyte Repletion: Potassium replacement (hypokalaemia can be life-threatening – mom and baby)
Address Hypoinsulinaemia and ketogenesis with IV Insulin: weight-based fixed-rate insulin infusion to reverse ketosis (avoid hypoglycaemia by adjusting IV fluid type)
Identify and address precipitating cause
Ongoing close surveillance with monitoring of blood glucose, electrolytes and fluid status and adjusting treatment as indicated
Delay fetal monitoring (even in viable babies) until the acute phase is over and then only start fetal monitoring once the mother is stable enough for potential surgery
Patient education and prevention of recurrence of DKA

Fluids

FLUIDS
Type of Fluid	Examples	Indications
Isotonic	0.9% NaCl (also Ringer’s lactate, Balsol, Plasmalyte B)	For rehydration (in absence of hypernatremia)
Isotonic with 5% Dextrose	0.9% NaCl with 5% Dextrose	BG <14 and No hypernatremia
Isotonic with 10% Dextrose	0.9% NaCl with 10% Dextrose (see ‘Calculation’ section for method of mixing to 10% concentration)	BG <10 and No hypernatremia
Hypotonic	0.45% NaCl	Na >150 (add 5% dextrose) or Hyperchloremic (normal anion gap) acidosis

Interpretation of Blood Ketones

Interpretation of Blood Ketones (use Freestyle® glucometer with KETOstrips – available in OCCU)
Value	Interpretation	Follow-up
0.0 – 0.5mmol/L	Normal	Nil unless clinical picture changes
0.6 – 1.5mmol/L	Ketones present	Check 4-hourly
1.6 – 2.9mmol/L	High risk for DKA	Treat if clinical suspicion of DKA. Otherwise recheck 2-hrly
≥3.0mmol/L	DKA confirmed	Initiate treatment

Treatment Pillars

1. Fluid:

Principle:	Total volume loss (approximates 6-10 L) should be replaced within the first 24-36 hours)
Rapid rehydration (1^st 8 hrs):	Fluid: Isotonic fluid (e.g. 0.9% NaCl) Rate: - 1 litre stat, then - 1 litre over an hour, then - 1 litre over 2 hrs (500ml/h), then - 1 litre over 4 hrs (250ml/h)
Rehydration (rest of 24 - 48 hrs):	To avoid Hypoglycaemia, check blood glucose (BG) when prescribing fluid
BG ≥ 14mml/L:	0.9% NaCl at 150ml/hr
BG 10.0 -13.9mmol/L:	5% dextrose @ 150ml/hr
BG <10mmol/L:	Assess acidosis: - If still acidotic, aim to maintain insulin infusion but increase dextrose concentration to 10% - If acidosis resolving, halve insulin infusion rate (e.g. 0.1u/kg to 0.05u/kg) and continue 5% dextrose infusion
Maintenance Fluid:	Fluid: 0.9% NaCl (if no hypernatremia) Rate: 125 - 150ml/h (min 3L/24hr)

2. Potassium:

Principle:	Hypoinsulinaemia, and acidosis result in total body potassium deficit despite normal serum potassium concentration. Rapid DKA correction increases risk of hypokalaemia and life-threatening cardiac arrythmias or respiratory muscle weakness. AFTER the first litre of stat fluid, KCl supplementation should be added to the Rehydration fluid (1L) and run at appropriate rehydration rate. NB: MARK the fluid clearly as containing (x) mmol/L KCl.
Rehydration phase:	If K⁺ < 3.5mmol/L: Continue fluid rehydration but withhold IV insulin until potassium >3.5mmol/L Add 40 mmol KCl/l in the rapid rehydration fluid vaculiter. Check K⁺ after an hour If K⁺ ≥3.5mmol/L: start insulin infusion 1hr after rehydration fluid started
Maintenance phase:	K⁺ <3.5mmol/L: 40mmol KCl/l in 1L maintenance fluid K⁺ 3.5 – 4.9mmol/L: 20mmol KCl/l in 1L maintenance fluid K⁺ ≥5.0mmol/L: No added KCl Repeat K⁺ in an hour *Monitor K+ 4hrly once stable.

3. Insulin:

Principle:	IV Insulin therapy is needed to correct the underlying metabolic derangement – addresses both hyperglycaemia and ongoing ketogenesis. Delay insulin initiation until K⁺is ≥3.5mmol/L.
Insulin infusion preparation:	(2 healthcare professionals should be present / check concentration) Need concentration of 1 unit/mL of short-acting insulin E.g., Mix 200 units Actrapid® with 200ml 0.9% NaCl Prime IV-line with insulin solution before connecting to avoid delay in patient receiving insulin-containing fluid.
Fixed rate:	weight-based Insulin infusion: 0.1 units/kg/h (e.g., 6ml/hr if 60 kg) Titrate insulin hourly according to targets. Increase by 1 U/h if targets below are not reached.
Hourly targets:	- 10% to 20% drop in BG - 0.5mmol/L drop in blood ketones - 3mmol/L increase in HCO₃
Maintenance phase:	Addressing acidaemia requires insulin but takes longer to correct than hyperglycaemia does. therefore... DO NOT STOP INSULIN while in DKA (unless BG < 4mmol/L) Keep BG between 8 - 12mmol/L until DKA resolved.

Cautionary notes: Insulin Therapy

Insulin type:

Only short (and ultra-short)- acting insulin is used in the management of DKA

Dangers of Hypoglycaemia:

While insulin therapy is essential to address acidaemia in DKA, hypoglycaemia, is life-threatening too
Guard against allowing the blood glucose to drop to hypoglycaemic levels (<4.0 mmol/L). Counter-regulatory hormones will be activated resulting in rebound ketosis, necessitating a longer duration of treatment
Rapid correction of hyperglycemia and hyperosmolarity may also shift water rapidly to the hyperosmolar intracellular space and so induce cerebral oedema

Management of Hypoglycaemia during a DKA:

Confirm BG <4mmol/L with a second point-of-care glucose test
Stop insulin infusion
Give 50ml 50% dextrose IV stat
Repeat blood glucose 15min later
If still <4mmol/L – repeat 50ml 50% dextrose IV stat
If >4mmol/L – restart insulin infusion at half the rate. Use 10% Dextrose fluid
If there is a second hypoglycaemic episode, discard the insulin solution and mix a new bag (1 unit Actrapid/ml 0.9% NaCl) and ensure that two health professionals are present to check the concentration is accurate
If hypoglycaemia is an ongoing concern, please escalate to the Department of Internal Medicine/Endocrinology for review

Thromboprophylaxis

The cumulative risk of diabetes, ketosis and pregnancy places the patient at high risk for thromboembolic events.
Routine thromboprophylaxis is indicated. Use Enoxaparin 40mg SC daily or unfractionated heparin 7500iU SC twice daily as thromboprophylactic agents.

Nil per Os vs Early Oral Feeding

At initial treatment of the DKA, it is safest and simplest to keep the patient nil by mouth.
If, however, the patient is stabilising and requests food, early oral feeding should not be discouraged even if acidosis is not fully resolved.

Prerequisites: Patient awake, orientated and maintaining airway

Test tolerance of clear fluids prior to allowing solids. IV insulin infusion should be adequate to cover the requirements of small meals. No subcutaneous insulin boluses should be used at this time.

Monitoring

Acute Phase
Measure	Frequency	Treatment Aim
Blood Glucose	Hourly	10-20% drop in BG per hour
Potassium (K⁺) (On calibrated blood gas machine)	Hourly	3.5-5.5
Blood gas	2-4 hourly	Increase of 3mmol/l/hr in bicarbonate
Input / Output	Hourly	0.5ml/kg/hr
Blood Ketones (point-of-care Freestyle machine; ketone strips)	2-hourly	0.5mmol drop in ketones/hr
Plasma Na⁺, K⁺, Cl^-	12-hourly	Aim for normal range, adjusting fluids to compensate.

Stable Phase
Measure	Frequency	Treatment Aim
Blood Glucose	Hourly (until 4hrs on SCI)	BG range 8-12mmol/L
Potassium (K⁺) (On calibrated blood gas machine)	4-hourly	3.5-5.5
Blood gas	4-6hourly	Normalising of all parameters
Input / Output	4-hourly	0.5ml/kg/hr
Blood Ketones (point-of-care Freestyle machine; ketone strips)	12-hourly	Negative ketones
Plasma Na⁺, K⁺, Cl^-	12-hourly (daily once normal)	Aim for normal range, adjusting fluids to compensate.

DKA Precipitant – Identify, Record, and Treat

Actively look for infection/inflammation by history and clinical examination (e.g., pyelonephritis, respiratory, chorioamnionitis, ear infection, sinusitis, cellulitis, tooth abscess, cholecystitis, deep vein thrombosis)
Do empiric screening (e.g., urine-, sputum (for MCS / GXP) & blood cultures)
Check for other causes of DKA (e.g., lipohypertrophy on injection sites, insulin dosing errors, skipping of insulin due to food insecurity or ignorance, using expired insulin, beta-sympathomimetic drugs or administered glucocorticoids (e.g., for fetal lung maturity)

Fetal Monitoring during DKA

Electronic fetal monitoring prior to the mother being metabolically stable enough for an emergency anaesthetic, is NOT recommended
Typically, DKA is not an indication for delivery and CTG abnormalities seen in the acute phase of DKA, are usually reversible
Confirm (and document) the fetal heart once the mother is stable, and daily until maternal metabolic abnormalities are corrected

Fetal Outcomes:

Fetal mortality is quoted up to 36%. Surviving fetuses have a risk of long-term neurodevelopmental abnormalities due to a direct toxicity of ketone bodies on the fetal brain. For this reason, please book all women admitted with DKA for a fetal neuro ultrasound at TBH 3-4 weeks after DKA

Transition to Subcutaneous Insulin

Prerequisites:

Patient stable, awake & able to tolerate oral intake
DKA is biochemically resolved – strict criteria in pregnancy not established, but these can be used:
- pH > 7.3
- HCO₃ ≥ 18mmol/
- blood ketones < 0.6mmol/L
- anion gap ≤ 12.0mmol/L

NB! INSULIN OVERLAP
To prevent reoccurrence of DKA, IVI and SC insulin need to overlap by at least 4hours. Do not stop IVI insulin earlier than 4hrs after first basal SC insulin (Protaphane^® or Glargine) is given.

Glucose monitoring during transition:

Continue hourly BG for 6 hours after IVI is stopped
Thereafter BG is checked before and after meals (pre & post prandial BG-monitoring)

Preventing Recurrent DKA

If new diagnosis of diabetes or not previously done:
- Do Anti-GAD / Anti-Islet Antibodies
- Prescribe glucometer and testing strips
ALL patients with DKA
- Early referral to Diabetes Educator for education on survival skills, insulin technique
- Confirm patient is provided with written information about the correct use of insulin

Multi-disciplinary Approach is Essential

Acute management should be the responsibility of the on-call team in the area where the patient is admitted (e.g., OCCU or labour ward). However, please involve an MDT early.

After-hours:

Involve internal medicine registrar on call if there are concerns
Involve on-call Obstetrics consultant

Office-hours:

Refer patient to Special Care Team early to help streamline take-over of management when patient is stable
Notify Dr on call for Endocrinology. Request consult if needed
Refer patient early to Diabetes Educator (currently Mrs Lourentia van Wyk)

Useful Calculations

1. How to mix 5% or 10% Dextrose solution:

For 5% solution:

Start with 1L 0.9% NaCl
remove 100ml volume
add 100ml 50% dextrose to 1L 0.9% NaCl bag = 5% solution

For 10% solution:

Start with 1L 0.9% NaCl
remove 200ml volume
add 200ml 50% dextrose to 1L 0.9% NaCl bag = 10% solution

2. Calculating the Anion Gap

[Na] – ([Cl] – [HCO₃]) = anion gap (or use MDCalc^® or equivalent application) A difference of ≥12mEq/L along with a bicarbonate level (<18mEq/L) demonstrates an anion gap metabolic acidosis - a defining feature of DKA.

Pitfalls & Pearls

Avoid using only urinary ketones to diagnose DKA
- As these may be present during fasting, exercise or pregnancy even without any metabolic abnormality. In DKA, the two main ketones produced are acetoacetate and betahydroxybutyrate. Urinary dipsticks measure only acetoacetate and is associated with both false positive and false negative results.
Practicalities – Serum ketone testing:
- Use dedicated ketone testing strips on Freestyle^® point-of-care glucometers
- Freestyle^® glucometers and ketone sticks should be available in both C2A west and east (OCCU)
- The strips can be ordered from the pharmacy
Venous blood gas vs Arterial Blood gas:

*VENOUS blood samples are adequate to assess and monitor acidosis in the context of DKA.

Practical tips:

Still use HEPARIN PRIMED SYRINGES whether ABG or VBG
Do not take VBG from the IV cannula where IV Fluid was attached. Use different vein distal to cannula site

VBG vs ABG - Interpreting aspects of blood gas:

pH: VBG pH is on average 0.03-0.04 less than the ABG pH values (even in DKA)
Bicarbonate: HCO3 correlates well between VBG and ABG. (it’s a calculated, not measured value. If absolute value needed – send serum to laboratory)
Lactate: good correlation. Difference <1. VBG useful to trend patient
Base deficit (BE) correlates well between ABG, VBG
pO₂ and pCO₂: least correlation between VBG and ABG. If these values are imperative, an ABG should be done

*ABG most relevant with hypoxaemic patients

If, for some reason, IV insulin with infusion pump is not available (e.g., at referral hospital, while awaiting transport), an alternative regimen of 0.1u/kg insulin lispro (e.g., Humalog^®) can be used subcutaneously as a temporising measure until patient is transferred to unit where insulin driver available. This dose of insulin can be repeated every 2 hours. Hourly BG monitoring needs to continue. If Insulin lispro is not available, short-acting human insulin (Actrapid^®) can be used with due cognisance that it’s effect can last 6 hours, thus sequential dosages will likely have an additive effect, increasing the risk for hypoglycaemia
A raised white cell count should not be over-interpreted as this may be due to both the pregnancy and the DKA itself
If hyperchloremic (normal anion gap) acidosis occurs in the recovery phase of DKA (possibly due to use of 0.9% NaCl), minimise hyperchloraemia by using 0.45% saline or 5% dextrose water
IV Bicarbonate: This is generally not recommended (can worsen hypoxaemia, hypokalaemia, intracellular acidosis, and cerebral oedema) unless the ABG/VBG shows pH<6.9 (and then under expert supervision)
Individualised fluid management needs to be made (in conjunction with OCCU consultant) in women with kidney disease, heart failure or pre-eclampsia

*Summary of this guideline for quick reference available as Addendum 1.

Abbreviations used:
ABG -arterial blood gas	IVI (intravenous insulin)
BG (blood glucose) in mmol/L	MDT – multi-disciplinary team
D (dextrose)	SCI (subcutaneous insulin)
DKA – diabetic ketoacidosis	T1DM – Type 1 Diabetes mellitus
GDM – Gestational Diabetes	T2DM – Type 2 Diabetes mellitus
JDBS – Joint British Diabetes Society	VBG – venous blood gas

References

SEMDSA. (2017). SEMDSA 2017 Guidelines for the Management of Type 2 diabetes mellitus SEMDSA Type 2 Diabetes Guidelines Expert Committee. JEMDSA 2017; 22(1)(Supplement 1): S1-S196. Journal of Endocrinology, Metabolism and Diabetes of South Africa. www.jemdsa.co.za

Dhanasekaran, M., Mohan, S., & Egan, A. (2022). Diabetic Ketoacidosis in Pregnancy: An Overview of Pathophysiology, Management, and Pregnancy Outcomes. EMJ Diabetes, August. https://doi.org/10.33590/emjdiabet/10194487

Eshkoli, T., Barski, L., Faingelernt, Y., Jotkowitz, A., Finkel-Oron, A., & Schwarzfuchs, D. (2022). Diabetic ketoacidosis in pregnancy – Case series, pathophysiology, and review of the literature. European Journal of Obstetrics and Gynecology and Reproductive Biology, 269, 41–46. https://doi.org/10.1016/j.ejogrb.2021.12.011

Mohan, M., Baagar, K. A. M., & Lindow, S. (2017). Management of diabetic ketoacidosis in pregnancy. The Obstetrician & Gynaecologist, 19(1), 55–62. https://doi.org/10.1111/tog.12344

Bonner, S., & Schofield, J. (2019). Diabetic Ketoacidosis in Pregnancy. In Obstetric Decision-Making and Simulation (pp. 277–285). https://doi.org/10.1017/9781108296793.035

Sibai, B. M., & Viteri, O. A. (2014). Diabetic ketoacidosis in pregnancy. Obstetrics and Gynecology, 123(1), 167–178. https://doi.org/10.1097/AOG.0000000000000060

Addendum 1: Diabetic Ketoacidosis (DKA) in pregnancy

DKA Basics:

Is caused by an extreme lack of insulin that forces the body to produce ketones for energy
Is synonymous with at least 10% dehydration
Rehydration and insulin are used for treatment
Hypokalaemia (life threatening) should be pre-empted & prevented
Hypoglycaemia (due to the aggressive & fixed rate insulin infusion needed to reverse ketosis) is a real risk that should be prevented in advance by adjusting IV fluid type

DKA defined:

Ketonaemia: Blood ketones ≥3mmol/L /
Urine ketones ≥2⁺
**Hyperglycaemia: BG ≥ 11mmol/L
Metabolic Acidosis: pH ≤ 7.3 / HCO₃ ≤ 18mmol/L

Interpretation of Blood Ketones:
- 0.0 - 0.5mmol/l: normal
- 0.6 – 1.5mmol/l: ketosis (check 4 hourly)
- 1.6 – 2.9mmol/l: high risk for DKA (check 2hrly)

**Normoglycaemia does not exclude DKA in Pregnancy. Euglycemic DKA is a life-threatening emergency.

Summary of Management Guideline

Initiate Rehydration. Keep pt NPO. Do a Venous Blood Gas (Arterial BG if A-line in situ)
Before starting insulin, take the necessary precautions to prevent hypokalaemia
An hour after fluid initiation, start with a fixed rate of 0.1 U Insulin/kg/h ALONGSIDE potassium as indicated
Continue to monitor & prevent hypokalaemia
Monitor blood glucose (BG) hourly and take precautions to prevent hypoglycaemia

1. Fluid:

Rapid Rehydration (1^st 8 hrs):	using 0.9% NaCl: - 1 litre stat then - 1 litre over an hour then - 1 litre over 2 hrs (500ml/h) then - 1 litre over 4 hrs (250ml/h)
Rehydration (rest of 24 – 48 hrs):	using 0.9% NaCl: 150ml/h
Maintenance Fluid (0.9% Saline):	125 - 150ml/h (min 3L/24hr)
Avoid Hypoglycaemia:	Aim to keep BG between 8 and 12
BG < 14:	5%D @ 150ml/h (replace 100ml IV-fluid with 100ml 50% dextrose)
BG < 10:	If still acidotic, use 10%D with same rate IVI (replace 200ml IV-fluid with 200ml 50% dextrose)
BG < 10:	If acidosis is improving, continue 5%D & halve IVI dose (e.g., 0.1 to 0.05 U/kg)
BG< 4:	- Stop insulin infusion. Give 50ml 50% dextrose IV stat - Repeat blood glucose 15min later - If >4mmol/L: restart insulin infusion at half the rate. Use 10% Dextrose fluid
Type of fluid, Examples & Indications:	Isotonic: 0.9% NaCl (Normal Saline), Balsol, Plasmalyte B, Ringer’s lactate) Indication: For rehydration & maintenance in the absence of hypernatremia Isotonic 5%D: replace 100ml of the isotonic fluid with 100ml 50% dextrose Indication: Use when BG < 14mmol/L in the absence of hypernatremia Hypotonic 5%D: 0.45% NaCl with 100ml fluid replaced by 100ml 50% dextrose Indication: Corrected Na > 150mmol/L/ Hyper-chloremic acidosis with normal anion gap

2. Potassium:

During rehydration phase:	Safe potassium level is required prior to initiating IV insulin
If K⁺ < 3.5mmol/L:	give 40mmol KCl in 1L rehydration fluid at appropriate rehydration rate Check K⁺ hourly
Rehydration and Maintenance:	Ongoing K⁺ monitoring and supplementation as needed in each vaculiter according to K⁺ level
Potassium replacement (mmol/L):	< 3.5mmol/L: 40mmol KCl/L in Rehydration/Maintenance fluid 3.5 – 4.9mmol/L: 20mmol KCl/L In Rehydration/Maintenance fluid ≥5.0mmol/L: Nil (repeat K⁺ in 1hour)

3. Insulin:

NB:	Do not start insulin if K⁺is unknown or < 3.5mmol/L
Prepare IV-insulin @ 1 unit/ml:	Mix 200 units Actrapid® with 200ml 0.9% NaCl. Prime IV-line with the insulin-solution before connecting (At least 2 HPs should be present when IVI is prepared) Give 0.1 units/kg/h (e.g. 6ml/h if 60 kg)
Hourly targets:	- A 10% to 20% drop in BG - 0.5mmol/L drop in blood ketones - 3mmol/L increase in HCO₃ INFORM a senior doctor if targets are not reached; increase IVI rate by (1 U/hr) until reaching targets Keep BG between 8 - 12mmol/L until DKA resolved: - Use 5% Dextrose when BG <14 - Use 10% Dextrose when BG <10 NB: Only if acidosis is improving, continue 5%D & halve the rate of insulin (e.g., from 0.1 to 0.05 U/kg) when BG falls below 10mmol/L
DO NOT STOP INSULIN while in DKA: (unless BG < 4mmol/L)	NB: To prevent DKA relapse, See STEP 7 (Transition to SC insulin) as a 4-6hr overlapping of IVI and SCI is required

Monitoring:

Monitoring (part of step 1 to 3)

Hourly blood glucose (BG) aiming for a 10 to 20% drop in BG per hour
1 – 2 Hourly blood ketones aiming for a 0.5mmol/l drop per hour (6 hrly urine dipsticks only if blood ketone strips not in stock)
Hourly Potassium on calibrated blood gas machine during acute phase; 4 hourly during stable phase
Blood gas hourly during acute phase aiming for a 3mmol/l/h increase in bicarbonate; 4 – 6 hrly during stable phase
12 hourly formal plasma Na⁺,K⁺ & Cl (if previously abnormal; otherwise daily)
In & Output aiming for a urine output of 0.5ml/kg (acute phase – hourly; stable phase – 4hrly)

4. Other Investigations:

Other Investigations

Plasma BG (grey top)
Serum ketones only if blood ketone strips not in stock
CXR when indicated
Calculate anion gap if refractory acidosis*
(hyperchloremia can cause normal anion gap (< 12mmol/L)
Calcium, magnesium & phosphate
HbA1C (if not done in the previous 6 weeks)
Serum osmolality if Na+ abnormal on ABG/VBG
Amylase/ lipase if severe abdominal pain
Antibodies for T1D testing (Anti-GAD &/Anti-Islet) if not yet done (even if known with T2D)

*Insulin does not play a role in metabolic acidosis caused by hyperchloremia

5. Prescription checklist:

Prescription checklist

Fluids
Insulin
Potassium replacement
Blood ketone strips (if not in stock)
NPO in initial phase of DKA
Thromboprophylaxis
Order glucometer with strips soon after admission (if new diagnosis / patient does not have own meter)
Education on Survival Skills before discharge (causes & prevention of DKA, sick-day management, DSME, etc.)
Ensure patient is provided with written information re the correct use of insulin at home

6. Thromboprophylaxis:

Thromboprophylaxis

Routinely prescribe thromboprophylaxis: Enoxaparin 40mg SC daily or unfractionated heparin 7500iU SC twice daily

7. Transition to subcutaneous insulin:

Transition to subcutaneous insulin

Patient stable, awake & able to tolerate oral intake
DKA is resolved (pH > 7.3, HCO₃ ≥ 18mmol/l, blood ketones less than 0.6mmol/L & anion gap ≤12)
NB: Ensure an overlap of at least 4 hours after Basal (e.g., Protaphane or Glargine) SCI is given before stopping IVI (to prevent recurrence of DKA)
Continue hourly blood glucose (BG) for 6 hours after IVI is stopped; thereafter BG is checked before and after meals

RECORD CAUSE OF DKA CLEARLY IN NOTES:

Actively look for infection (e.g., urine-, sputum (for MCS/ GXP) & blood cultures) and treat accordingly
Check for other causes of DKA (e.g., lipohypertrophy on injection sites, skipping of insulin due to food insecurity or ignorance & using expired insulin) in those known with diabetes and educate accordingly

BEFORE TRANSFER OF THE PATIENT FROM THE UNIT TO A WARD:

Please ensure that the necessary education is done to avoid readmissions due to another DKA
A senior doctor and his/her consultant should approve discharge from the high care unit to a ward
Make sure that patient care, after discharge from critical care unit, is taken over by either Obstetric Special Care team or Endocrinology. Follow-up, patient education, and continuation of care is imperative

Abbreviations used BG (blood glucose) in mmol/L; D (dextrose); Na & K in mmol/L; IVI (intravenous insulin); SCI (subcutaneous insulin) SME (diabetes self-management education; TOD (Target Organ Damage), HPs (healthcare professionals)

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Tygerberg Hospital, Department of Obstetrics and Gynaecology;Diabetic Ketoacidosis (DKA) in Pregnancy: A Management Guideline for the Department of Obstetrics and Gynaecology Tygerberg Hospital; Version: July 2023; Last checked for updates by EMGuidance: Oct 2023

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