Diabetic Ketoacidosis (DKA)

Quick Answer

One-liner: DKA is a life-threatening metabolic emergency characterised by hyperglycaemia (greater than 11 mmol/L), ketosis (ketones greater than 3.0 mmol/L), and acidosis (pH less than 7.3), requiring immediate fluid resuscitation, potassium replacement, and fixed-rate insulin infusion.

Diabetic Ketoacidosis represents absolute or relative insulin deficiency combined with counter-regulatory hormone excess, causing uncontrolled lipolysis, ketogenesis, and metabolic acidosis. Despite improved outcomes with protocolised management, DKA remains a significant cause of morbidity with mortality ranging from less than 1% in expert centres to 5-10% in elderly patients or those with severe comorbidities. [1,2]

Key ACEM Exam Points:

• Fluids FIRST, insulin SECOND (after initial 1L resuscitation)
• Potassium less than 3.5 mmol/L = HOLD INSULIN until replaced
• Fixed-rate insulin 0.1 units/kg/hr (NOT variable-rate sliding scale)
• Add 10% dextrose when glucose falls below 14 mmol/L
• Continue insulin until ketones less than 0.6 mmol/L (not just glucose normalisation)
• Euglycaemic DKA (SGLT2 inhibitors) - low glucose does NOT exclude DKA

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ACEM Exam Focus

Fellowship Written Relevance

• High-yield topics: Diagnostic criteria, fluid resuscitation protocols, potassium replacement, insulin dosing, cerebral oedema prevention, euglycaemic DKA recognition
• SAQ themes: Management of severe DKA (pH less than 7.0), SGLT2-associated EDKA, paediatric DKA differences, transition to subcutaneous insulin
• Calculations: Anion gap, corrected sodium, osmolality, fluid replacement calculations

Fellowship OSCE Relevance

• Resuscitation station: Managing critically unwell DKA patient in resus bay
• Communication station: Explaining DKA to patient/family, sick-day rules education
• Examination station: Assessing dehydration, neurological status, precipitant identification
• Key domains tested: Medical Expert, Collaborator, Communicator

Primary Exam Relevance

• Physiology: Insulin action, counter-regulatory hormones, ketogenesis, acid-base physiology
• Pathology: Metabolic acidosis, electrolyte shifts, osmotic diuresis
• Pharmacology: Insulin pharmacokinetics, SGLT2 inhibitor mechanism, potassium replacement

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Key Points

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Epidemiology

Australian/New Zealand Context

• Aboriginal and Torres Strait Islander: 3-4 times higher diabetes prevalence, earlier onset, higher rates of DKA presentation [6,7]
• Maori and Pacific Islander: 2-3 times higher diabetes prevalence, increased DKA hospitalisations [8]
• Rural/remote: Delayed presentation, limited access to specialist care, higher complication rates [9]
• RFDS retrievals: DKA represents significant proportion of aeromedical diabetes retrievals from remote Australia [10]

Risk Factors for DKA

The "5 I's" Mnemonic: [1]

1. Infection (30-40%)
2. Insulin omission/error (20-40%)
3. Infarction (MI, stroke)
4. Intercurrent illness (pancreatitis, surgery)
5. Initial presentation of T1DM (10-25%)

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Pathophysiology

The Core Defect

DKA results from absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, growth hormone). [2,11]

Three parallel metabolic derangements occur:

Insulin Deficiency + Counter-Regulatory Excess
                    ↓
    ┌───────────────┼───────────────┐
    ↓               ↓               ↓
Hyperglycaemia  Ketogenesis    Electrolyte
(Glucose greater than 11)   (β-OHB greater than 3.0)   Disturbance
    ↓               ↓               ↓
Osmotic        Metabolic      Hypokalaemia
Diuresis       Acidosis       (Total Body)
    ↓               ↓               ↓
Dehydration     pH below 7.3       Arrhythmia Risk
(5-8L deficit)

Hyperglycaemia Mechanisms

1. Hepatic glucose overproduction: Glycogenolysis (depleted within 24h) + gluconeogenesis (from amino acids, lactate, glycerol) [11]
2. Peripheral underutilisation: GLUT4 transporter remains intracellular without insulin - glucose cannot enter cells [11]
3. Result: Blood glucose typically 20-30 mmol/L (range 11-50+ mmol/L)

Ketogenesis Cascade

1. Lipolysis: Hormone-sensitive lipase (HSL) unopposed → massive triglyceride breakdown [11]
2. Free fatty acid (FFA) flux: FFAs flood liver at 10-20x normal rates [11]
3. β-oxidation: FFAs converted to acetyl-CoA in hepatic mitochondria [11]
4. Ketone synthesis: Acetyl-CoA → acetoacetate → β-hydroxybutyrate (predominant) + acetone [11]

Ketone Bodies:

• β-hydroxybutyrate (β-OHB): Measured in blood, predominant in DKA (ratio 3:1)
• Acetoacetate: Detected by urine dipstick
• Acetone: Volatile, causes "fruity" breath odour

Metabolic Acidosis

Ketone bodies are strong organic acids (pKa ~3.5-4.5) → dissociate → release H+ → consume HCO3- → high anion gap metabolic acidosis (HAGMA). [11]

Anion Gap = [Na+] - ([Cl-] + [HCO3-])

• Normal: 8-12 mmol/L
• DKA: typically greater than 16 mmol/L (often 20-30 mmol/L)

The Potassium Paradox

Critical concept for ACEM exams: [1,2]

Result: Hypokalaemia is the leading iatrogenic cause of death in DKA management. [2]

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Clinical Approach

Recognition

Suspect DKA in any unwell patient with:

• Known diabetes (T1DM or T2DM)
• Polyuria, polydipsia, weight loss, vomiting
• Kussmaul breathing (deep, sighing respirations)
• Fruity/acetone breath odour
• Altered mental status
• Abdominal pain (present in 30-40%)

Initial Assessment

Primary Survey

• A: Usually maintained unless GCS significantly reduced
• B: Kussmaul breathing, tachypnoea (respiratory compensation), SpO2 usually normal
• C: Tachycardia, hypotension (severe dehydration), prolonged CRT, dry mucous membranes
• D: GCS (correlates with severity), pupils, focal neurology (precipitant vs cerebral oedema)
• E: Temperature (infection?), injection sites, diabetic foot

Rapid Bedside Diagnosis (5 minutes)

History

Key Questions

Red Flag Symptoms

Examination

Dehydration Assessment

Average deficit in DKA: 5-8 litres (100 mL/kg) [1]

Cardiovascular

• Tachycardia (compensatory)
• Postural hypotension → frank hypotension (severe)
• Prolonged capillary refill time (greater than 2 seconds)

Respiratory

• Kussmaul breathing: Deep, labored, regular breaths (blowing off CO2)
• Tachypnoea (greater than 20 breaths/min)
• Fruity/acetone breath odour (~50% of patients)

Neurological

• GCS correlates inversely with severity of acidosis and osmolality [2]
• Confusion/drowsiness (20-30%)
• Coma (rare, below 10%) - suggests severe DKA or alternative diagnosis

Abdominal

• Tenderness (especially epigastric) in 30-40%
• May mimic acute surgical abdomen
• Reduced bowel sounds (ileus from hypokalaemia)
• Re-assess after initial resuscitation before considering surgery

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Investigations

Immediate Bedside Tests

Severity Classification

Additional high-risk features requiring ICU: [1]

• Ketones greater than 6 mmol/L
• K+ below 3.5 mmol/L on presentation
• GCS below 12
• SpO2 below 92% on air
• SBP below 90 mmHg
• Pregnancy

Laboratory Investigations

Venous Blood Gas

Expected respiratory compensation: PaCO2 = (1.5 x [HCO3-]) + 8 (±2) [11]

Biochemistry

Anion Gap Calculation

Anion Gap = [Na+] - ([Cl-] + [HCO3-])

• Normal: 8-12 mmol/L
• DKA: greater than 16 mmol/L (typically 20-30 mmol/L)
• Represents unmeasured anions (ketones, lactate)

HAGMA Differential (GOLDMARK): [12]

• Glycol (ethylene glycol)
• Oxoproline
• Lactate
• D-lactate
• Methanol
• Aspirin
• Renal failure
• Ketones (DKA, alcoholic, starvation)

Osmolality

Calculated osmolality = 2 x [Na+] + [Glucose] + [Urea]

• Normal: 275-295 mOsm/kg
• DKA: Usually below 320 mOsm/kg
• HHS: greater than 320 mOsm/kg (key differentiator)

Other Investigations

ECG Monitoring

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Management

Principles: The "Three Rs" [1]

1. Restore Volume - IV fluids to reverse dehydration
2. Replace Electrolytes - Potassium to prevent arrhythmias
3. Reverse Ketosis - Fixed-rate insulin to suppress ketogenesis

Key Concepts:

• Fluids FIRST, insulin SECOND
• Fixed-rate insulin (NOT variable-rate sliding scale)
• Potassium is the killer - K+ below 3.5 mmol/L = HOLD INSULIN
• Never stop basal (long-acting) insulin during DKA treatment

Step 1: Fluid Resuscitation

If Hypotensive (SBP below 90 mmHg)

• 500-1000 mL 0.9% saline IV bolus over 15 minutes
• Reassess haemodynamics
• Repeat if still hypotensive (max 30 mL/kg)
• Consider septic shock (antibiotics, vasopressors/ICU)

Standard Fluid Protocol (normotensive)

Fluid Choice

Australian Practice: Either 0.9% saline OR balanced crystalloid is acceptable. [1,13]

• Hartmann's/Plasma-Lyte: May resolve DKA 2-3 hours faster, less hyperchloraemic acidosis [13]
• Avoid Hartmann's: If severe lactic acidosis coexists

Special Populations

• Elderly/Heart Failure: Reduce rates (1L over 2h, then slower), monitor for overload
• Pregnancy: More aggressive resuscitation (fetal perfusion depends on maternal BP)
• Renal Failure: Reduce volumes, may need RRT

Step 2: Potassium Replacement

Delivery: 40 mmol KCl per litre of 0.9% saline (use pre-mixed bags)

Monitoring: K+ levels hourly for first 4 hours, then 2-hourly

Step 3: Fixed-Rate Insulin Infusion (FRIII)

Why Fixed-Rate (NOT Sliding Scale)?

• Fixed-rate: 0.1 units/kg/hr - constant, predictable ketogenesis suppression [1,14]
• Sliding scale: Variable based on glucose - ineffective at suppressing ketogenesis
• Goal: Suppress ketogenesis (NOT just lower glucose)

Protocol

Preparation: 50 units Human Actrapid in 50 mL 0.9% saline (= 1 unit/mL)

Dose: 0.1 units/kg/hour

• Example: 70 kg patient = 7 units/hour

Timing: Start AFTER initial 1L fluid resuscitation (not immediately on arrival) [1]

DO NOT reduce insulin based on glucose alone - continue until ketones cleared

Continue Basal Insulin

If patient on long-acting insulin (Lantus, Levemir, Tresiba) - DO NOT STOP IT [1]

Rationale: Prevents rebound ketosis when IV insulin stopped

Step 4: Add Dextrose When Glucose Falls

When glucose drops below 14 mmol/L: [1]

• Start 10% Dextrose at 125 mL/hr (via separate line)
• Continue fixed-rate insulin at 0.1 units/kg/hr
• Continue 0.9% saline (reduce to 125-250 mL/hr)

Rationale:

• Goal is to clear KETONES (not just normalise glucose)
• Ketone clearance requires continuing insulin
• Dextrose prevents hypoglycaemia while maintaining insulin

At glucose below 14 mmol/L, patient has 3 concurrent infusions:

1. 0.9% saline (+ KCl) at 125-250 mL/hr
2. 10% Dextrose at 125 mL/hr
3. Fixed-rate insulin at 0.1 units/kg/hr

Step 5: Bicarbonate - DON'T (Usually)

JBDS-IP Recommendation: DO NOT give bicarbonate routinely [1]

Rationale: [2]

• Does NOT improve outcomes
• May worsen intracellular/CSF acidosis
• Increases cerebral oedema risk (especially children)
• Can cause hypokalaemia, alkalosis overshoot

Rare Indication: pH below 6.9 WITH life-threatening hyperkalaemia or cardiac arrest

• Dose: 1.26% sodium bicarbonate (NOT 8.4%)
• Seek senior/ICU input

Step 6: Treat Precipitants

Monitoring During Treatment

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Resolution Criteria and Transition

DKA Resolution Criteria [1]

ALL of the following must be met:

Important Note: Glucose normalises BEFORE ketones clear. Do NOT stop DKA protocol based on glucose alone.

Transition to Subcutaneous Insulin

1. Calculate Total Daily Dose (TDD): 0.5-0.8 units/kg/day
2. Split 50:50: 50% basal (long-acting once daily), 50% bolus (short-acting before meals)
3. Timing is CRITICAL: Give SC insulin 30-60 minutes BEFORE stopping IV insulin
4. Monitor: Capillary glucose 4-hourly, ketones daily

Failed DKA Resolution

If ketones NOT falling greater than 0.5 mmol/L per hour: [1]

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Complications

Hypokalaemia and Arrhythmias

Leading iatrogenic cause of death in DKA [2]

• Mechanism: Insulin drives K+ into cells + ongoing urinary losses
• ECG: Flattened T waves, U waves, prolonged QT, ventricular ectopics
• Prevention: Hourly K+ monitoring, HOLD insulin if K+ below 3.5 mmol/L

Cerebral Oedema

Incidence: 0.5-1% paediatric DKA; rare in adults (age greater than 25) [5] Mortality: 20-25% [5]

Risk Factors:

• Age below 5 years, new-onset T1DM
• Severe acidosis (pH below 7.1) or hyperglycaemia (greater than 40 mmol/L)
• High urea at presentation
• Failure of sodium to rise as glucose falls
• Excessive IV fluids or rapid glucose correction

Clinical Features (typically 4-12 hours after treatment): [5]

• Headache (new or worsening)
• Vomiting
• Irritability, confusion
• Cushing's triad: Bradycardia, hypertension, irregular breathing
• Reduced GCS, seizures, cranial nerve palsies

Management: [5]

1. Immediate (do NOT wait for CT):
   • 3% Hypertonic saline 2-3 mL/kg IV over 10-15 min (first-line)
   • OR Mannitol 0.5-1 g/kg IV over 15-20 min
2. Reduce IV fluid rate by one-third
3. Head elevation to 30 degrees
4. Urgent CT head (once stabilised)
5. ICU transfer, neurosurgery consult if herniation

Prevention:

• Avoid excessive fluid resuscitation (especially children)
• Gradual glucose correction (3-5 mmol/L per hour)
• Avoid hypotonic fluids
• Hourly GCS monitoring

Hypoglycaemia

Incidence: 5-10% [2]

Causes: Continuing FRIII without dextrose when glucose below 14 mmol/L

Prevention: Add 10% dextrose when glucose below 14 mmol/L; do NOT reduce insulin rate

Thromboembolism

Incidence: 1-2% [2]

Prevention: Prophylactic LMWH (enoxaparin 40 mg SC daily) for ALL adults

Hyperchloraemic Metabolic Acidosis

Incidence: 30-50% with 0.9% saline resuscitation [13]

• Anion gap normalises (ketones cleared) but pH remains below 7.35
• Generally benign, self-limiting (resolves 24-48 hours)
• Prevention: Use balanced crystalloids (Hartmann's/Plasma-Lyte)

Aspiration Pneumonia

Risk factors: Reduced GCS, vomiting

Prevention: NBM until GCS greater than 12, consider NG tube if persistent vomiting

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Euglycaemic DKA (EDKA)

Definition

DKA with glucose below 14 mmol/L (sometimes below 11 mmol/L) but with ketosis (greater than 3.0 mmol/L) and acidosis (pH below 7.3). [15,16]

Causes

SGLT2 Inhibitor-Associated EDKA

Drugs: Dapagliflozin, empagliflozin, canagliflozin [15,16]

Incidence: 0.1-0.2% per year in SGLT2 users [16]

Precipitants (SIPS): [16]

• Surgery (fasting)
• Infection/Illness
• Pregnancy
• Starvation/low-carb diet

Management

Same as standard DKA with modifications: [1,15]

1. STOP SGLT2 inhibitor immediately
2. Fluid resuscitation as per protocol
3. Fixed-rate insulin 0.1 units/kg/hr
4. Start dextrose EARLIER (when glucose below 12 mmol/L)
5. Close glucose monitoring (rapid hypoglycaemia risk)

Discharge: Do NOT restart SGLT2 inhibitor; reinforce sick-day rules

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DKA vs HHS Comparison

Management Differences

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Special Populations

Paediatric DKA

Key difference: Higher risk of cerebral oedema (0.5-1%) [5]

Pregnancy

• Lower threshold for diagnosis (glucose may be below 11 mmol/L)
• Develops faster (accelerated starvation ketosis)
• More aggressive fluid resuscitation
• Continuous fetal heart rate monitoring
• Severe DKA = ICU admission regardless of pH

Elderly

• Higher mortality (5-10%)
• Cautious fluid resuscitation (cardiac/renal comorbidities)
• May have atypical presentation (less polyuria/polydipsia)
• Higher threshold for ICU admission

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Maori Considerations:

Diabetes Burden: [6,7,8]

• Aboriginal and Torres Strait Islander: 3-4x higher diabetes prevalence, earlier onset (often below 40 years)
• Maori and Pacific Islander: 2-3x higher diabetes prevalence
• Higher rates of DKA presentation, often with more severe acidosis

Barriers to Care:

• Geographic isolation (remote communities)
• Limited access to endocrinology/specialist diabetes services
• Cultural and linguistic barriers
• Socioeconomic factors affecting medication access/compliance
• Higher rates of chronic kidney disease affecting management

Cultural Safety Considerations:

• Engage Aboriginal and Torres Strait Islander Health Workers/Practitioners
• Involve Maori Health Workers where available
• Whanau (family) involvement in care planning and education
• Use of interpreter services for language barriers
• Culturally appropriate sick-day rules education
• Consider extended family/community support networks

Specific Management Considerations:

• May present later with more severe DKA due to access barriers
• Higher comorbidity burden (CKD, cardiovascular disease)
• Post-discharge: Link with Aboriginal Community Controlled Health Services
• Ensure follow-up with Diabetes Educator familiar with cultural context
• Consider social determinants of health in discharge planning

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Remote/Rural Considerations

Pre-Hospital

• Early recognition and initiation of fluid resuscitation by paramedics
• Communicate with receiving hospital for advance preparation
• RFDS retrieval criteria: Severe DKA (pH below 7.1), reduced GCS, haemodynamic instability

Resource-Limited Setting

Modifications when limited access to hourly blood ketones: [9,10]

• VBG pH/bicarbonate more frequently (1-2 hourly)
• Anion gap trending
• Clinical assessment (Kussmaul breathing resolution, mental status)
• Urine ketones (less accurate but available)

Limited potassium monitoring:

• Frequent ECG monitoring for hypokalaemia signs
• More cautious potassium replacement strategy
• Lower threshold for retrieval to tertiary centre

RFDS/Retrieval Considerations

Indications for aeromedical retrieval: [10]

• Severe DKA (pH below 7.0)
• Cerebral oedema or altered GCS
• Haemodynamic instability despite fluid resuscitation
• Paediatric DKA (higher cerebral oedema risk)
• Pregnancy with DKA
• Failed improvement after 6 hours of management

Pre-retrieval optimisation:

• Commence DKA protocol immediately (do not wait for retrieval)
• Secure IV access (two large-bore cannulae)
• Catheterise for accurate urine output monitoring
• Prepare for clinical deterioration during transport

Telemedicine

• Video/phone consultation with endocrinology/ICU
• Real-time guidance on insulin dosing adjustments
• Support for complex cases (cerebral oedema, pregnancy, EDKA)
• NSW Health Emergency Care Institute: 1800 626 900

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: DKA Resuscitation

Format: Resuscitation Time: 11 minutes Setting: ED Resuscitation Bay

Candidate Instructions:

You are the senior doctor in the emergency department. A 22-year-old female with Type 1 diabetes has been brought in by ambulance with decreased level of consciousness. Lead the resuscitation of this patient.

Examiner Instructions: Initial observations: GCS 12 (E3V4M5), HR 125, BP 85/55, RR 32 (Kussmaul), SpO2 96% RA, Temp 37.8C Capillary glucose: 32 mmol/L Blood ketones: 6.4 mmol/L (if requested) VBG: pH 7.02, HCO3 6, K+ 3.3 mmol/L, lactate 2.5 (if requested)

Progression:

• After fluid bolus: BP improves to 100/65
• If insulin started before K+ replacement: K+ drops to 2.8 (ECG shows U waves)
• If K+ replaced first then insulin: gradual improvement

Actor/Patient Brief: Simulated patient. Moans, confused, responds to verbal commands. Parents available for collateral history - she hasn't been taking insulin for 2 days.

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Recognition that K+ below 3.5 = hold insulin; appropriate escalation to ICU

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Station 2: Breaking Bad News - New T1DM Diagnosis

Format: Communication Time: 11 minutes Setting: ED relatives room

Candidate Instructions:

A 16-year-old boy was brought in unconscious and found to have diabetic ketoacidosis. He has been stabilised in ICU. His parents are waiting in the relatives room. They have been told he has a "sugar problem." Please speak with them about the diagnosis and what this means.

Examiner Instructions: Parents are anxious, tearful. Father is asking "will he die?" Mother is asking "is it our fault - did we give him too much sugar?"

Expected discussion points:

• Type 1 diabetes diagnosis (autoimmune, not caused by diet)
• Lifelong insulin requirement
• DKA explanation (what happened, why, treatment)
• Current status (stable in ICU)
• Prognosis (can live normal life with good management)
• Support available (diabetes team, education)

Actor Brief (Parents):

• Father: Anxious, protective, wants facts
• Mother: Tearful, guilty, worried about lifestyle implications
• Neither has medical background
• Ask about: cause, treatment, long-term outlook, sport/school

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Addresses parental guilt; explains lifelong insulin clearly

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Station 3: DKA Clinical Examination

Format: Examination Time: 11 minutes Setting: Clinical examination area

Candidate Instructions:

This 45-year-old woman has been brought in by ambulance feeling unwell for 2 days. She has a history of Type 2 diabetes. Please examine her and present your findings to the examiner.

Examiner Instructions: Findings:

• General: Unwell, drowsy, Kussmaul breathing, fruity breath odour
• Vital signs: HR 110, BP 100/70, RR 28, Temp 38.2
• Dehydration: Dry mucous membranes, reduced skin turgor, prolonged CRT
• Respiratory: Air entry normal, no added sounds
• Abdominal: Generalised tenderness, no guarding
• Neurological: GCS 14, no focal signs
• Other: Cellulitis on right lower leg

Provide information if specifically examined (e.g., "capillary glucose 26 mmol/L" if BGL requested).

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Recognition of Kussmaul breathing; identification of cellulitis as precipitant

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SAQ Practice

Question 1 (6 marks)

Stem: A 28-year-old woman with Type 1 diabetes presents to the emergency department with DKA. Her initial blood tests show: pH 7.18, ketones 5.8 mmol/L, glucose 24 mmol/L, K+ 4.8 mmol/L.

Question: List the 6 key components of the initial management of this patient over the first hour.

Model Answer:

1. IV access and monitoring - Two large-bore cannulae, continuous cardiac monitoring, urinary catheter (1 mark)
2. Fluid resuscitation - 1 litre 0.9% saline over first hour (or balanced crystalloid) (1 mark)
3. Potassium assessment and replacement - Add 40 mmol KCl per litre once K+ confirmed greater than 3.5 but below 5.5 mmol/L (1 mark)
4. Fixed-rate insulin infusion - 0.1 units/kg/hour (NOT sliding scale) after initial fluid resuscitation (1 mark)
5. Continue basal insulin - If on long-acting insulin, do NOT stop it (1 mark)
6. Search for precipitant - Blood/urine cultures, CXR, ECG; history for insulin omission, infection, MI (1 mark)

Examiner Notes:

• Accept: Mention of VTE prophylaxis (LMWH)
• Do not accept: Bicarbonate (not indicated at pH 7.18)

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Question 2 (8 marks)

Stem: A 55-year-old man with Type 2 diabetes is on empagliflozin (an SGLT2 inhibitor) for heart failure. He presents with fatigue and vomiting. His glucose is 10.2 mmol/L, but blood ketones are 4.6 mmol/L and pH is 7.25.

Question: a) What is the diagnosis? (1 mark) b) Explain why the glucose is relatively low despite the diagnosis. (2 marks) c) List 5 key differences in management compared to standard DKA. (5 marks)

Model Answer:

a) Euglycaemic diabetic ketoacidosis (EDKA) secondary to SGLT2 inhibitor use (1 mark)

b) SGLT2 inhibitors block the sodium-glucose co-transporter 2 in the proximal tubule, causing glycosuria and lowering blood glucose. (1 mark) However, they increase the glucagon:insulin ratio, promoting lipolysis and ketogenesis despite the lower glucose level. (1 mark)

c) Key differences in management: (5 marks, 1 each)

1. Stop SGLT2 inhibitor immediately and do not restart
2. Start dextrose earlier (when glucose below 12 mmol/L rather than below 14 mmol/L)
3. Close glucose monitoring - higher risk of hypoglycaemia
4. Educate about sick-day rules - specifically to stop SGLT2i during illness
5. Consider alternative cardiorenal protection - discuss with cardiology/nephrology for alternative agents

Examiner Notes:

• Accept: Mention of SIPS precipitants (Surgery, Infection, Pregnancy, Starvation)
• Accept: Warning about restarting SGLT2i

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Question 3 (6 marks)

Stem: An 8-year-old Aboriginal boy from a remote community is retrieved by RFDS with severe DKA (pH 6.95). At 6 hours into treatment, he develops headache and becomes irritable. His heart rate drops from 120 to 65 bpm.

Question: a) What complication has developed? (1 mark) b) Describe your immediate management (3 actions). (3 marks) c) List 2 risk factors for this complication that are present in this case. (2 marks)

Model Answer:

a) Cerebral oedema (1 mark)

b) Immediate management (3 marks):

1. 3% Hypertonic saline 2-3 mL/kg IV over 10-15 minutes (first-line osmotic therapy) (1 mark)
2. Reduce IV fluid rate by one-third (1 mark)
3. Elevate head of bed to 30 degrees (1 mark)

Alternative acceptable answers: Mannitol 0.5-1 g/kg IV; intubation if GCS below 8; urgent CT head; neurosurgery consult

c) Risk factors present (2 marks):

1. Young age (8 years - highest risk in below 5 years but still elevated risk) (1 mark)
2. Severe acidosis (pH 6.95, below 7.1) at presentation (1 mark)

Alternative acceptable: New-onset diabetes (if stated in expanded scenario); possible late presentation (remote community)

Examiner Notes:

• Do NOT accept: Dexamethasone (not indicated)
• Accept: Discussion of RFDS retrieval to tertiary centre with neurosurgery

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Question 4 (6 marks)

Stem: You are working in a regional emergency department. A 40-year-old Maori woman presents with DKA. She lives 2 hours away and has limited access to healthcare services.

Question: List 6 considerations for culturally safe care and discharge planning for this patient.

Model Answer: (6 marks, 1 each)

1. Engage Maori Health Worker if available - cultural liaison and communication support
2. Whanau (family) involvement - ask about family who should be contacted and involved in care planning
3. Use interpreter services if required - ensure full understanding of diagnosis and management
4. Explore barriers to care - medication access, transport, health literacy, competing priorities
5. Culturally appropriate sick-day rules education - using plain language and checking understanding
6. Link with community health services - Maori health providers, diabetes nurse educator, ensure follow-up appointment before discharge

Alternative acceptable answers:

• Address social determinants of health
• Ensure adequate medication supply before discharge
• Provide written information in appropriate language
• Consider extended family/community support networks
• Discuss telehealth options for follow-up

Examiner Notes:

• Accept any reasonable cultural safety consideration
• Key concept: Holistic approach beyond purely medical management

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Australian Guidelines

Therapeutic Guidelines Australia

• DKA Management: Follows JBDS-IP framework [1]
• Fluid choice: 0.9% saline or balanced crystalloid acceptable
• Insulin: Fixed-rate 0.1 units/kg/hr
• Potassium: Add 40 mmol/L when K+ below 5.5 mmol/L

State-Specific Protocols

NSW Health Clinical Guidelines:

• Emergency Care Institute DKA pathway
• Telemedicine consultation: 1800 626 900

Queensland Health:

• Statewide DKA Clinical Pathway
• Retrieval Services Queensland for paediatric DKA

Victoria:

• Royal Children's Hospital Clinical Practice Guidelines (paediatric DKA)
• PERT retrieval service for severe cases

ARC/ANZCOR

• ANZCOR Guideline 11.10: Management of Special Situations (includes metabolic emergencies)
• Emphasises early recognition and treatment initiation

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References

Guidelines

1. Joint British Diabetes Societies for Inpatient Care (JBDS-IP). The Management of Diabetic Ketoacidosis in Adults. 2023 Update. PMID: 37331331
2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343. PMID: 19564476
3. Australian Institute of Health and Welfare. Diabetes: Australian facts. AIHW Cat. no. CVD 82. 2023.

Key Evidence

4. Umpierrez GE, Kitabchi AE. Diabetic ketoacidosis: risk factors and management strategies. Treat Endocrinol. 2003;2(2):95-108. PMID: 15871546
5. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344(4):264-269. PMID: 11172153
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Additional References

39. Phelan H, Lange K, Engelen M, et al. Management of children and adolescents with diabetic ketoacidosis. Diabetes Res Clin Pract. 2022;191:110083. PMID: 36100008
40. Weinstock RS, Xing D, Maahs DM, et al. Severe hypoglycemia and diabetic ketoacidosis in adults with type 1 diabetes: results from the T1D Exchange clinic registry. J Clin Endocrinol Metab. 2013;98(8):3411-3419. PMID: 23760624
41. Menke A, Orchard TJ, Imperatore G, et al. The prevalence of type 1 diabetes in the United States. Epidemiology. 2013;24(5):773-774. PMID: 23903880
42. Fazeli Farsani S, Brodovicz K, Soleymanlou N, et al. Incidence and prevalence of diabetic ketoacidosis (DKA) among adults with type 1 diabetes mellitus (T1D): a systematic literature review. BMJ Open. 2017;7(7):e016587. PMID: 28765134

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Teaching Summary

The ACEM Exam Approach to DKA

Fellowship Written Questions: Expect SAQs on:

• Severe DKA management (pH below 7.0)
• Euglycaemic DKA recognition and management
• Paediatric DKA differences
• Complications (cerebral oedema, hypokalaemia)
• Transition to subcutaneous insulin

Fellowship OSCE Stations: Prepare for:

• Resuscitation station: Leading DKA management in resus bay
• Communication station: Breaking bad news (new T1DM diagnosis)
• Examination station: Assessing dehydration and precipitants

Core Exam Messages

1. Fluids first, insulin second - Never start insulin before initial fluid resuscitation
2. Potassium is the killer - K+ below 3.5 = HOLD insulin until replaced
3. Fixed-rate, not sliding scale - 0.1 units/kg/hr for consistent ketogenesis suppression
4. Ketones are the target - Continue insulin until ketones below 0.6 mmol/L
5. Euglycaemic DKA exists - Always check ketones in unwell diabetics regardless of glucose
6. Never stop basal insulin - Prevents rebound ketosis when IV insulin discontinued
7. Search for precipitants - Infection (30-40%), insulin omission (20-40%), MI, new diagnosis

ACEM Curriculum Mapping