1. Diabetic Ketoacidosis
Dr Mohamed Shaheed
ED Registrar
Werribee Mercy Hospital

2. Case presentation
● Received an AV call at 00.30 Hrs regarding an unconscious patient
with GCS 3/15, Spo2 84, and spontaneously breathing
● Patient arrived in 5 minutes
● History from the ambulance crew ( limited hx)
● 51 year old lady found in wash room, unconscious ,She had been
in the wash room following a party. She has been there for 2
hours. AV received the call from her flatmate

3. Background
● Type 1 DM - with multiple previous DKA presentation due to non
compliance
● Hypertension

4. Primary assessment
● A- Airway patent , no vomitus, or obstruction,
● B- breathing spontaneously, mild stridor, RR-25/m, B/L Air entry equal,
no rhonchi or crepitation
● C- Pale, dehydrated with dry mouth and skin, poor skin turgor, HR-
75/m, peripheral pulse not palpable, BP- unrecordable, heartbeat
s1s2 present
● D- GCS- 3/15, M1V1E1, no response at all, Body very cold, temperature
cannot be recorded, ,B/L pupil dilated and non reactive
● VBG- PH- 6.86, PCO2 33.3, HCO3 5.5 ,Na+- 123, K+- 4.9, lactate- 7.3,
glucose 57 mmol/l,

5. Initial management
● Started with 15 LPM via non rebreathing mask/ BVM
● 0.40 AM - SPO2- 98%
● IV access Obtained in Right arm and right leg,
● VBG- PH- 6.86, pco2-33.3, HCO3 5.5 ,Na+- 123, K+- 4.9, lactate- 7.3, glucose 57
mmol/l,
● Iv bolus 2 L of 0.9 % normal saline started and continued fluid management
● 1.06 AM IV bolus insulin actrapid 10 u given + insulin drip started
● 1.20 Am - Arterial line was inserted on left arm- initial MAP left hand 70/40
● ABG- PH-6.854, PCO2- 25, HCO3 5.5, Na- 124, K+- 4.5, Lactate- 6.4, Glucose- 53

6. Progress at ED
Continue IV fluids according to DKA protocol
1.40 AM Inotropes was started - noradrenaline drip 5 to 10 microgram/min
1.50 AM- kcl 10 mmol/h infusion drip was started
1.50 Am - IDC inserted and Core temperature via IDC 28 C, warming with fluid warmer
and bear hugger, warm high flow O2 commenced, pre oxygenation via BVM/NRM 15 L,
2.AM- GCS - 7/15 M4,V2, E1- Aggressive - given sedation IV ketamine
2.08 AM - Intubation done
NG tube inserted
2.40 Am - Sodium bicarbonate 8.4 gram vial was given
Management done according to DKA protocol, informed ICU and transferred.

7. Diabetic Ketoacidosis (DKA)
● What is DKA?
● Understand the Pathophysiology of DKA
● Criteria of diagnosis
● Clinical and laboratory features
● Discuss the management and approach to a patient
with DKA
● Appreciate the complications that occur during
treatment

8. What is DKA?
DKA is a medical emergency
A state of absolute or relative insulin deficiency aggravated by ensuing
hyperglycemia, Dehydration and acidosis producing derangements in
intermediary metabolism including production of serum Acetone.
Can occur in both type 1 and type 2 Diabetes, in type 2 diabetes with
insulin deficiency/ dependency

9. Pathophysiology
● Hyperglycemia results from impaired glucose uptake because of insulin
deficiency and excess glucagon with resultant gluconeogenesis and
glycogenolysis.
● Glucagon excess also increases lipolysis with the formation of ketoacids.
● Ketone bodies provide alternative usable energy sources in the absence
of intracellular glucose.
● The keto acids (acetoacetate, β-hydroxybutyrate, acetone) are products of
proteolysis and lipolysis
● Hyperglycemia causes an osmotic diuresis that leads to excessive loss of
free water and electrolytes.
● Resultant hypovolemia leads to tissue hypoperfusion and lactic acidosis

10. DKA Criteria of diagnosis
Hyperglycemia > 250 mg/dl or BGL >11 mmol/l
• Dehydration
• Ketonemia > 1 mmol/l & Ketonuria
• Metabolic Acidosis
– pH < 7.30
– Bicarbonate < 15 mEq/L

11. Precipitants of DKA
● Treatment error with insulin omission- misdoing,
underdosing
• Insulin pump line failure
• Infection- UTI, pneumonia
• Acute Myocardial infarction
• Pancreatitis
• New medication- corticosteroids
• Drugs and Alcohol
• Miscellaneous including pregnancy

12. Degree of severity in DKA

13. Symptoms of DKA
● Polyuria
● Polydipsia
● Blurred vision
● Nausea/Vomiting
● Abdominal Pain
● Fatigue
● Confusion
● Coma

14. Signs of DKA
● •
● Tachycardia
● Dehydration
● Dry mucous membrane
● Delayed capillary refill
● Poor skin turgor
● Hypotension
● Kussmaul breathing
● Decreased sensorial mental status, varies from sleepiness, drowsiness,
confusion, semi coma & coma

15. Laboratory
• Blood glucose
• Urinary/plasma ketones
• Serum electrolytes
• BUN/Cr
• Osmolarity
• CBC, blood culture (if infection is suspected)
• Venous blood gas/ ABG

16. Management
Correction of the following:
● Dehydration
● Hyperglycemia
● Electrolytes deficits
● Metabolic acidosis
● Underlying precipitating factors
Infection, omission of insulin, stress, …

17. Fluid management ( WMH ED guideline)
● Insert a large bore peripheral intravenous line (minimum of 18 gauge
needle)
● Commence Normal Saline infusion 1 to 2 litres stat,
● Then 1 litre over 1- 2 hours,
● Then 1 litre over 2 – 4 hours
● Most patients need several litres of fluid in the first 4 hours

18. Insulin
● Give intravenous insulin bolus of : *6 – 10 units of Insulin Neutral
(Actrapid®)
6 u insulin if BGL< 25 mmol/L , 10 units Insulin if BGL >25 mmol/L
● Commence Insulin infusion - IV insulin infusions must be delivered via 50
units insulin in 49.5 ml Normal Saline .( Concentration is 1.0 unit/ml
infusion at 0.1 unit/kg/hr (5-10units/hr) Use a higher infusion rate in
severely ketoacidotic patients or for those patients whose daily insulin
use is at the higher end of the normal range 0.5units/kg/day )
(Note: An insulin infusion should not be started until a patient’s
potassium level is known and is > 4.0mmol/L )

19. Potassium Replacement

20. Bicarbonate
●
Should be used with caution for severely acidotic patients (pH< 7.05) or with
ECG changes associated with severe hyperkalaemia and only after discussion
with a Consultant. There is not evidence that bicarbonate replacement
improves outcomes for patients with DKA

21. Other Management Considerations

22. Complication
Cerebral Edema- main complication
• Thrombosis
• Cardiac arrhythmias
• Pulmonary edema
• Renal failure
• Rhabdomyolysis
• Infection –Aspiration pneumonia –Sepsis

23. Hyperosmolar hyperglycaemic states (HHS)
● Hyperosmolar hyperglycaemic states (HHS) refer to severe persistent
hyperglycemia, in the absence of ketosis, and accompanied by profound
dehydration.
● HHS is more common in type 2 diabetes in the presence of acute sepsis
(eg urinary tract infection, pneumonia), after a cardiovascular event
(myocardial ischaemia or stroke) or in people with renal dysfunction.
● HHS usually affects older people. Coma may develop in some patients
and neurological impairment is common.
● HHS may sometimes occur with DKA in a mixed clinical picture of
ketoacidosis and a hyperosmolar state.

24. References
● DKA- WMH ED guideline
● DKA- NSW guideline
● DKA- Anzcor guideline
● DKA- Therapeutic guideline
● DKA- uptodate
● DKA - RACGP