Intensive Care Medicine

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State

Comprehensive evidence-based guide to DKA and HHS management in the intensive care unit, covering pathophysiology, fluid resuscitation, insulin therapy, electrolyte replacement, and complications

Updated 24 Jan 2026
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Clinical board

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • Altered consciousness or coma (GCS below 8)
  • Severe hypokalaemia (K+ below 3.3 mmol/L) - DO NOT give insulin
  • Cerebral oedema signs (headache, bradycardia, hypertension)
  • Severe acidosis (pH below 6.9)

Linked comparisons

Differentials and adjacent topics worth opening next.

  • Type 1 Diabetes Mellitus
  • Type 2 Diabetes Mellitus
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Clinical reference article

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State

Quick Answer: Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS) are life-threatening hyperglycemic emergencies requiring prompt ICU-level management. DKA is characterised by hyperglycaemia (greater than 11 mmol/L), ketosis (β-hydroxybutyrate greater than 3 mmol/L), and metabolic acidosis (pH below 7.3, HCO3 below 18 mmol/L). HHS presents with severe hyperglycaemia (greater than 33.3 mmol/L), marked hyperosmolality (greater than 320 mOsm/kg), and minimal or absent ketosis. Both conditions result from insulin deficiency with excess counter-regulatory hormones. Management priorities are: (1) aggressive fluid resuscitation with 0.9% NaCl initially, switching to 0.45% NaCl when euvolaemic; (2) IV insulin infusion at 0.1 U/kg/hr (check K+ greater than 3.3 mmol/L first); (3) potassium replacement targeting 4-5 mmol/L; and (4) identification and treatment of precipitating factors. Add dextrose when glucose falls below 14 mmol/L (DKA) or 16.7 mmol/L (HHS) to allow continued insulin to clear ketones. DKA mortality is 1-5% but rises to 10-20% in HHS due to the typically older population with comorbidities.

CICM Second Part Exam Focus

Exam Focus: High-Yield Topics for CICM Second Part:

  1. Diagnostic Criteria - Know exact cut-offs for DKA vs HHS vs mixed states
  2. Pathophysiology - Insulin deficiency + counter-regulatory hormone excess cascade
  3. Fluid Management - Initial 0.9% NS, when to switch to 0.45%, corrected sodium calculation
  4. Insulin Therapy - 0.1 U/kg/hr, the "glucose-ketone gap", when to add dextrose
  5. Potassium Dynamics - Why K+ falls despite total body depletion, target 4-5 mmol/L
  6. Bicarbonate Controversy - Evidence against routine use (PMID: 3004246, 21411511)
  7. Cerebral Oedema - Risk factors, recognition, osmotic therapy
  8. Euglycemic DKA - SGLT2 inhibitor-associated, early dextrose requirement
  9. Complications - Hypokalaemia, hypoglycaemia, cerebral oedema, VTE, ARDS
  10. Transition to SC Insulin - 1-2 hour overlap rule, basal-bolus regimens

Common Viva Scenarios:

  • Young Type 1 diabetic with DKA and severe hypokalaemia
  • Elderly patient with mixed DKA/HHS and sepsis
  • SGLT2 inhibitor-associated euglycemic DKA
  • Paediatric DKA with suspected cerebral oedema
  • Refractory DKA despite adequate insulin

Key Points

Key Points: - DKA Triad: Hyperglycaemia (greater than 11 mmol/L), ketosis (β-OHB greater than 3 mmol/L), acidosis (pH below 7.3)

  • HHS Criteria: Glucose greater than 33.3 mmol/L, osmolality greater than 320 mOsm/kg, pH greater than 7.3, minimal ketones
  • DO NOT start insulin if K+ below 3.3 mmol/L - life-threatening arrhythmia risk
  • Fluid first: 15-20 mL/kg 0.9% NS in first hour (typically 1-1.5 L)
  • Insulin rate: 0.1 U/kg/hr (or 0.14 U/kg/hr without bolus)
  • Target glucose drop: 3-4 mmol/L per hour (50-70 mg/dL/hr)
  • Add dextrose when glucose below 14 mmol/L (DKA) or below 16.7 mmol/L (HHS)
  • Potassium target: 4-5 mmol/L throughout resuscitation
  • Bicarbonate: Only consider if pH below 6.9 (not routine - no mortality benefit)
  • Osmolality correction: No faster than 3 mOsm/kg/hr to prevent cerebral oedema
  • Resolution criteria: pH greater than 7.3, HCO3 ≥15 mmol/L, anion gap ≤12 mmol/L, glucose below 11 mmol/L
  • Overlap rule: Continue IV insulin for 1-2 hours after first SC insulin dose

Epidemiology

Incidence and Prevalence

Diabetic ketoacidosis remains the leading cause of mortality in children and young adults with Type 1 diabetes mellitus. The annual incidence of DKA in the United States ranges from 4.6 to 8 episodes per 1,000 patients with diabetes. [1,2] Among children with established Type 1 diabetes, DKA occurs at a rate of approximately 1-10% per patient-year. [3]

Hyperosmolar hyperglycemic state is less common than DKA but carries significantly higher mortality. HHS accounts for less than 1% of all diabetes-related hospital admissions but is increasing in incidence, particularly among elderly patients with Type 2 diabetes. [4] The typical HHS patient is aged 55-70 years with undiagnosed or poorly controlled Type 2 diabetes.

Mortality

DKA mortality has declined substantially over the past three decades with improved recognition and standardised management protocols:

ConditionOverall MortalityICU MortalityKey Risk Factors
DKA (Adults)1-5%2-5%Age, sepsis, hypokalaemia, cerebral oedema
DKA (Paediatric)0.15-0.3%0.5-1%Cerebral oedema (21-24% of deaths)
HHS10-20%15-25%Age greater than 65, osmolality greater than 350, comorbidities
Mixed DKA/HHS5-15%10-20%Combined metabolic stress

The higher mortality in HHS compared to DKA reflects the older patient population with multiple comorbidities, delayed presentation due to insidious onset, and the severe degree of dehydration (fluid deficits often 8-12 litres). [5,6]

Australian Context

In Australia, diabetic emergencies account for approximately 2-3% of ICU admissions across ANZICS-registered units. Aboriginal and Torres Strait Islander peoples experience disproportionately higher rates of hyperglycemic crises, with hospitalisation rates 4-6 times higher than non-Indigenous Australians. [7] This disparity reflects barriers to healthcare access, higher rates of undiagnosed diabetes, and socioeconomic factors affecting medication adherence.

Precipitating Factors

Identification of the precipitating cause is essential for management and prevention of recurrence:

DKA Precipitants:

  • Infection (30-40%): Pneumonia, UTI, skin/soft tissue infections
  • Insulin omission/non-adherence (25-35%): Most common in young patients
  • New diagnosis of diabetes (15-25%): Especially in children
  • Medications: SGLT2 inhibitors (euglycemic DKA), corticosteroids, antipsychotics
  • Acute illness: Myocardial infarction, stroke, pancreatitis, trauma
  • Substance use: Cocaine, alcohol (starvation ketosis contribution)
  • Insulin pump failure: Technical malfunction, site problems

HHS Precipitants:

  • Infection (40-60%): Pneumonia, UTI, sepsis
  • Cardiovascular events: MI, stroke, PE
  • Medications: Thiazides, glucocorticoids, phenytoin, β-blockers
  • Non-adherence or undiagnosed diabetes (20-30%)
  • Dehydration: Reduced access to fluids, vomiting, diarrhoea
  • Renal impairment: Reduced glucose excretion capacity

Pathophysiology

Fundamental Mechanism: Insulin Deficiency + Counter-Regulatory Hormone Excess

The pathophysiology of hyperglycemic crises is driven by a critical imbalance: severe deficiency of insulin combined with excess counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). [1,8] This hormonal environment shifts metabolism from an anabolic state to a catabolic state, leading to hyperglycaemia, dehydration, and ketogenesis.

Counter-Regulatory Hormone Actions

HormonePrimary ActionMetabolic Consequence
GlucagonStimulates glycogenolysis and gluconeogenesis; activates CPT-1Hyperglycaemia; hepatic ketogenesis
CortisolIncreases proteolysis; promotes insulin resistanceAmino acid substrate for gluconeogenesis
CatecholaminesActivates hormone-sensitive lipase; inhibits insulin releaseLipolysis with increased FFA delivery
Growth HormoneAntagonises insulin action; enhances lipolysisHyperglycaemia and increased ketone production

DKA Pathophysiology

In DKA, absolute or relative insulin deficiency prevents glucose uptake by peripheral tissues and removes the normal inhibition of hepatic glucose production and adipose tissue lipolysis:

Step 1: Hyperglycaemia

  • Reduced insulin leads to decreased glucose uptake by skeletal muscle and adipose tissue
  • Glucagon stimulates hepatic glycogenolysis and gluconeogenesis
  • Blood glucose rises progressively, typically reaching 20-40 mmol/L

Step 2: Osmotic Diuresis and Dehydration

  • Hyperglycaemia exceeds renal threshold (approximately 10 mmol/L)
  • Glycosuria causes osmotic diuresis with loss of water and electrolytes
  • Typical fluid deficit: 5-10% body weight (3-6 litres in adults)
  • Electrolyte losses: Na+ 7-10 mmol/kg, K+ 3-5 mmol/kg, Cl- 3-5 mmol/kg

Step 3: Ketogenesis

  • Lipolysis releases free fatty acids (FFAs) from adipose tissue
  • FFAs undergo β-oxidation in hepatic mitochondria
  • Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate)
  • Glucagon activation of carnitine palmitoyltransferase I (CPT-1) is essential for this process
  • Ratio of β-hydroxybutyrate to acetoacetate is typically 3:1 but can reach 10:1 in severe DKA

Step 4: Metabolic Acidosis

  • Accumulation of ketoacids (pKa approximately 4) exceeds buffering capacity
  • Anion gap metabolic acidosis develops: AG = Na - (Cl + HCO3) greater than 12 mmol/L
  • Respiratory compensation (Kussmaul breathing) with low PaCO2
  • Severe cases: pH below 7.0, bicarbonate below 5 mmol/L

HHS Pathophysiology

HHS differs from DKA in that sufficient insulin remains to prevent lipolysis and ketogenesis, but is inadequate to prevent hyperglycaemia:

  • Residual insulin (even small amounts) inhibits hormone-sensitive lipase
  • Ketone production is minimal or absent
  • Hyperglycaemia is more pronounced due to prolonged osmotic diuresis before presentation
  • Hyperosmolality causes intracellular dehydration and neurological dysfunction
  • Mortality is higher due to extreme dehydration (10-15% body weight), older age, and comorbidities

Mixed DKA/HHS

Approximately 20-30% of patients present with features of both conditions. [6] This is increasingly recognised and typically presents with:

  • Significant hyperglycaemia (greater than 30 mmol/L)
  • Moderate ketosis
  • Variable acidosis
  • Elevated osmolality (greater than 300 mOsm/kg)

Management follows DKA protocols but with attention to the slower osmolality correction required in HHS.

Corrected Sodium and Effective Osmolality

Understanding sodium dynamics in hyperglycemic crises is essential:

Corrected Sodium Formula:

Corrected Na = Measured Na + [1.6 × (Glucose - 5.6) / 5.6] mmol/L

or approximately:

Corrected Na = Measured Na + [0.3 × (Glucose - 5.6)] mmol/L

Effective (Calculated) Osmolality:

Effective Osmolality = 2 × Na + Glucose (mmol/L)

Note: Urea is not included as it freely crosses cell membranes and does not contribute to effective osmolality.

Potassium Dynamics

Despite total body potassium depletion (typically 3-5 mmol/kg), serum potassium is often normal or elevated at presentation due to: [1,9]

  1. Insulin deficiency - reduced cellular K+ uptake
  2. Acidosis - H+/K+ exchange (each 0.1 pH drop raises K+ by approximately 0.6 mmol/L)
  3. Hyperosmolality - osmotic water movement drags K+ out of cells
  4. Proteolysis - releases intracellular K+ stores

With treatment (insulin and fluid resuscitation), K+ rapidly shifts intracellularly, and hypokalaemia develops if not anticipated and replaced. This is the most dangerous electrolyte abnormality in DKA management.

Clinical Presentation

DKA Presentation

Symptoms (typically develop over below 24 hours):

  • Polyuria, polydipsia, nocturia
  • Nausea, vomiting (up to 80% of patients)
  • Abdominal pain (particularly in children)
  • Weakness, lethargy, fatigue
  • Weight loss
  • Altered mental status (in severe cases)

Signs:

  • Dehydration: Dry mucous membranes, reduced skin turgor, tachycardia, hypotension
  • Kussmaul breathing: Deep, rapid respirations (respiratory compensation)
  • Fruity breath odour: Acetone (present in 10-20% of patients)
  • Abdominal tenderness (can mimic acute abdomen)
  • Hypothermia (due to peripheral vasodilation from acidosis)
  • Altered level of consciousness (correlates with osmolality)

HHS Presentation

Symptoms (insidious onset over days to weeks):

  • Gradual polyuria and polydipsia
  • Progressive weakness and lethargy
  • Confusion, focal neurological deficits
  • Visual disturbances
  • Leg cramps

Signs:

  • Profound dehydration (more severe than DKA)
  • Altered mental status (stupor to coma in 25-50%)
  • Focal neurological signs (hemiparesis, seizures in 10-15%)
  • Hyperthermia or hypothermia
  • Minimal or absent Kussmaul breathing (pH usually greater than 7.3)

Severity Classification

ParameterMild DKAModerate DKASevere DKA
Arterial pH7.25-7.307.00-7.24below 7.00
Serum HCO3 (mmol/L)15-1810-14below 10
Anion Gapgreater than 10greater than 12greater than 12
Mental StatusAlertDrowsyStupor/Coma
β-OHB (mmol/L)greater than 3greater than 3greater than 3

Red Flags Requiring Immediate ICU Admission

⚠️ Warning: Indications for ICU Admission:

  • GCS below 12 or deteriorating conscious level
  • Severe acidosis: pH below 7.1 or HCO3 below 5 mmol/L
  • Severe hypokalaemia (below 3.0 mmol/L) or hyperkalaemia (greater than 6.5 mmol/L)
  • Oxygen saturation below 92% on room air
  • Systolic BP below 90 mmHg despite fluid resuscitation
  • Heart rate greater than 120 or below 60 bpm
  • Anion gap greater than 25 mmol/L
  • Acute coronary syndrome or arrhythmia
  • Pregnancy
  • Paediatric DKA (especially below 5 years)
  • Signs of cerebral oedema

Investigations

Initial Assessment

Immediate Bedside:

  • Blood glucose (point-of-care)
  • Capillary ketones (β-hydroxybutyrate preferred over urine ketones)
  • ECG (for hyperkalaemia signs, arrhythmia, ischaemia)
  • Urinalysis (ketones, glucose, infection screen)

Laboratory Studies:

  • Blood gas: Arterial or venous (pH, pCO2, HCO3, lactate, glucose)
  • Electrolytes: Na+, K+, Cl-, Mg2+, phosphate, calcium
  • Renal function: Urea, creatinine
  • Calculated osmolality and anion gap
  • Full blood count (leukocytosis common even without infection)
  • Lipase/amylase (pancreatitis as cause or consequence)
  • Cardiac troponin (if chest pain or greater than 50 years)
  • Blood cultures (if sepsis suspected)

Calculated Values:

Anion Gap = Na - (Cl + HCO3)    Normal: 8-12 mmol/L
Corrected AG = AG + 2.5 × (40 - Albumin g/L)
Delta Ratio = (AG - 12) / (24 - HCO3)   Helps identify mixed acid-base disorders
Effective Osmolality = 2 × Na + Glucose   Normal: 280-295 mOsm/kg

Anion Gap Interpretation

Delta RatioInterpretation
below 0.4Hyperchloraemic (non-AG) acidosis
0.4-0.8Mixed AG and non-AG acidosis
0.8-2.0Pure AG acidosis (typical DKA)
greater than 2.0AG acidosis + metabolic alkalosis OR pre-existing high HCO3

Venous vs Arterial Blood Gas

Venous blood gas is adequate for most purposes in DKA and HHS: [10]

  • pH: Venous pH is approximately 0.03 lower than arterial
  • pCO2: Venous pCO2 is approximately 6-8 mmHg higher than arterial
  • HCO3: Essentially equivalent
  • Arterial sampling indicated if: respiratory failure, need for precise PaO2, haemodynamic instability

Point-of-Care β-Hydroxybutyrate

Capillary blood ketone measurement (β-hydroxybutyrate) is preferred over urine ketone testing: [11]

  • More accurate reflection of ketosis severity
  • Urine ketones detect acetoacetate (may be falsely low early in DKA due to high β-OHB:AcAc ratio)
  • Can be used to monitor response to treatment
  • Target: below 0.6 mmol/L for resolution

Interpretation:

  • below 0.6 mmol/L: Normal
  • 0.6-1.5 mmol/L: Mild ketosis
  • 1.5-3.0 mmol/L: Moderate ketosis (risk of DKA)
  • greater than 3.0 mmol/L: Significant ketosis (likely DKA)

Imaging

  • Chest X-ray: If infection suspected, respiratory symptoms, or fluid overload risk
  • CT Head: If altered consciousness disproportionate to metabolic state, focal neurology, suspected cerebral oedema
  • CT Abdomen: If abdominal pain persists after metabolic correction (excludes surgical causes)

Management

Overview: The Four Pillars

Management of hyperglycemic crises rests on four pillars, applied simultaneously:

  1. Fluid Resuscitation - Restore circulating volume and tissue perfusion
  2. Insulin Therapy - Suppress ketogenesis and reduce hyperglycaemia
  3. Electrolyte Replacement - Especially potassium, with monitoring of phosphate and magnesium
  4. Identify and Treat Precipitant - Infection, MI, medication, non-adherence

Fluid Resuscitation

Fluid therapy is the cornerstone of initial management and should commence before insulin in most cases. [1,12]

Initial Resuscitation (First Hour):

  • 0.9% Normal Saline: 15-20 mL/kg/hr (typically 1-1.5 L in first hour)
  • More rapid if haemodynamically unstable (up to 1 L boluses for shock)
  • Slower if elderly, cardiac disease, or renal impairment

Subsequent Fluid Replacement (Hours 2-24):

Corrected SodiumFluid ChoiceRate
Low or normal (below 135 mmol/L)0.9% NaCl250-500 mL/hr
High (greater than 135 mmol/L)0.45% NaCl250-500 mL/hr
Glucose below 14 mmol/L (DKA)Add 5% or 10% dextroseContinue at 100-200 mL/hr
Glucose below 16.7 mmol/L (HHS)Add 5% or 10% dextroseContinue at 100-200 mL/hr

Total Fluid Deficit Estimation:

  • DKA: 5-10% body weight (approximately 100 mL/kg)
  • HHS: 10-15% body weight (approximately 100-150 mL/kg)
  • Replace approximately 50% of deficit over first 12 hours, remainder over next 12-24 hours

Balanced Crystalloids vs Normal Saline:

Recent evidence from the SMART/SALT-ED trials suggests balanced crystalloids (Lactated Ringer's, Plasma-Lyte) may be superior to 0.9% NaCl in DKA: [13,14]

  • Faster time to DKA resolution (median 13.0 vs 16.9 hours)
  • Avoids hyperchloraemic acidosis
  • Shorter duration of insulin infusion
  • No difference in mortality or length of stay

However, most guidelines still recommend 0.9% NaCl as initial fluid, with consideration of balanced crystalloids for ongoing resuscitation.

Insulin Therapy

⚠️ Warning: CRITICAL: DO NOT start insulin if K+ below 3.3 mmol/L

Insulin will drive potassium intracellularly, potentially causing life-threatening hypokalaemia with cardiac arrhythmias. Replace potassium first until K+ greater than 3.3 mmol/L, then commence insulin.

Insulin Initiation:

Two equally acceptable regimens are recommended by the ADA: [1]

  1. Bolus + Infusion Protocol:

    • Bolus: 0.1 U/kg IV
    • Infusion: 0.1 U/kg/hr

  2. High-Dose Infusion (No Bolus):

    • Infusion: 0.14 U/kg/hr

For HHS alone (without significant ketosis), lower-dose insulin may be used:

  • JBDS recommends: 0.05 U/kg/hr for pure HHS [15]

Target Glucose Reduction:

  • Aim for glucose decrease of 3-4 mmol/L per hour (50-70 mg/dL/hr)
  • If glucose does not fall by at least 10% in first hour, give 0.1 U/kg bolus and reassess

The "Glucose-Ketone Gap":

A critical concept in DKA management is that glucose normalises faster than ketones clear. This leads to the common error of reducing insulin too early, resulting in prolonged ketosis and delayed resolution.

Adding Dextrose:

When blood glucose reaches the target threshold, ADD dextrose to allow continued insulin infusion:

  • DKA: Add 5% or 10% dextrose when glucose below 14 mmol/L (250 mg/dL)
  • HHS: Add 5% dextrose when glucose below 16.7 mmol/L (300 mg/dL)
  • Target glucose during resolution: 10-14 mmol/L (180-250 mg/dL)
  • Reduce insulin to 0.02-0.05 U/kg/hr when adding dextrose

Clinical Pearl: The Dextrose-Insulin Concept:

Think of dextrose as "fuel" that allows continued insulin administration to suppress ketogenesis. Reducing insulin too early to prevent hypoglycaemia will prolong the ketoacidosis. Instead, add dextrose and keep the insulin running until the anion gap closes.

Potassium Replacement

Potassium replacement is essential and should be guided by serum levels: [1,9]

Serum K+ (mmol/L)Action
below 3.3HOLD INSULIN. Give 20-40 mmol/L KCl at 10-20 mmol/hr. Recheck hourly.
3.3-5.3Add 20-40 mmol KCl per litre of IV fluid. Target 4-5 mmol/L.
greater than 5.3Do not add K+ to fluids. Recheck every 2 hours.
greater than 6.5Treat hyperkalaemia. Consider ECG changes, calcium, insulin-dextrose.

Potassium Monitoring:

  • Every 1-2 hours initially
  • ECG monitoring for arrhythmias
  • Maximum peripheral IV rate: 10-20 mmol/hr
  • Central line required for rates greater than 20 mmol/hr

Phosphate Replacement

Routine phosphate replacement is NOT recommended but should be considered if: [1,16]

  • Serum phosphate below 0.3 mmol/L
  • Cardiac dysfunction, respiratory muscle weakness, or haemolytic anaemia
  • Patients at high risk (malnourished, chronic alcoholism)

If replacing: 20-30 mmol potassium phosphate over 6-12 hours, monitoring calcium levels (risk of hypocalcaemia).

Bicarbonate Therapy

Routine bicarbonate is NOT recommended in DKA.

Multiple randomised controlled trials have shown no benefit: [17,18,19]

  • Morris et al. (1986) [PMID: 3004246]: No difference in rate of pH or glucose recovery
  • Gamba et al. (1991) [PMID: 1933095]: No clinical benefit for pH 6.85-7.18
  • Chua et al. (2011) meta-analysis [PMID: 21411511]: No improvement in clinical outcomes; may increase risk of cerebral oedema in children

Potential Harms of Bicarbonate:

  • Paradoxical CNS acidosis (CO2 crosses blood-brain barrier faster than HCO3)
  • Hypokalaemia (H+/K+ exchange)
  • Delayed ketone clearance
  • Left shift of oxygen-haemoglobin dissociation curve

Consider Bicarbonate Only If:

  • pH below 6.9 with haemodynamic instability
  • Life-threatening hyperkalaemia
  • Give 100 mmol NaHCO3 (8.4%) in 400 mL over 2 hours if used

Osmolality Management in HHS

In HHS, the primary concern is preventing overly rapid correction of hyperosmolality, which can precipitate cerebral oedema: [5,6]

  • Target osmolality reduction: No faster than 3 mOsm/kg/hr
  • Calculate osmolality every 2-4 hours
  • Slower fluid rates if osmolality dropping too rapidly
  • Maintain serum sodium stable or gently rising with treatment
  • Consider 0.45% NaCl earlier if corrected sodium elevated

Treatment of Precipitating Factors

Simultaneously with metabolic correction, identify and treat the precipitating cause:

  • Sepsis: Broad-spectrum antibiotics, source control
  • Myocardial infarction: Cardiology consultation, antiplatelet therapy
  • Pancreatitis: Supportive care, NPO, analgesia
  • Medication review: Stop SGLT2 inhibitors, adjust diabetogenic medications
  • Non-adherence: Social work, diabetes education, insulin regimen review

Special Populations

Euglycemic DKA (SGLT2 Inhibitor-Associated)

Euglycemic DKA is an increasingly recognised complication of SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, ertugliflozin). [20,21,22]

Diagnostic Criteria:

  • Blood glucose below 14 mmol/L (below 250 mg/dL)
  • pH below 7.3 and HCO3 below 18 mmol/L
  • Positive ketones (serum β-OHB elevated)
  • Elevated anion gap

Risk Factors/Triggers:

  • Major surgery (SGLT2i should be stopped 3-4 days pre-operatively)
  • Severe illness or sepsis
  • Low carbohydrate/ketogenic diets
  • Reduction in insulin dose
  • Excessive alcohol consumption

Management Differences:

  • Stop SGLT2 inhibitor immediately
  • Start dextrose infusion (5% or 10%) EARLY - often from the beginning
  • Insulin is still required to suppress ketogenesis
  • Lower insulin doses may be appropriate (0.05-0.1 U/kg/hr)
  • Monitor ketones closely for resolution

Clinical Pearl: The Euglycemic Trap:

The "normal" blood glucose in SGLT2i-associated DKA masks the severity of the metabolic acidosis. Always check ketones and pH in any patient on an SGLT2 inhibitor presenting with nausea, vomiting, malaise, or abdominal pain - regardless of blood sugar level.

Paediatric DKA

Paediatric DKA requires modified management due to the higher risk of cerebral oedema (0.5-1% incidence, 21-24% mortality). [23,24,25]

Key Differences:

  • Slower fluid resuscitation: 10-20 mL/kg bolus (not 15-20 mL/kg/hr)
  • Lower insulin rate: 0.05-0.1 U/kg/hr (no bolus in children)
  • More cautious fluid replacement over 24-48 hours
  • Lower threshold for hypoglycaemia concern

Risk Factors for Cerebral Oedema:

  • Young age (below 5 years)
  • New diagnosis of diabetes
  • Severe acidosis (pH below 7.1)
  • Low pCO2 at presentation
  • Elevated BUN at presentation
  • Bicarbonate administration
  • Failure of sodium to rise with treatment
  • Large fluid volumes in first 4 hours (greater than 40 mL/kg)

Recognition of Cerebral Oedema:

  • Headache
  • Decreasing level of consciousness
  • Bradycardia
  • Hypertension
  • Irritability or behavioural changes
  • Cranial nerve palsies
  • Pupillary changes

Treatment of Cerebral Oedema:

  1. Reduce IV fluid rate by 50%
  2. Elevate head of bed to 30 degrees
  3. Mannitol 20%: 0.5-1 g/kg IV over 10-15 minutes
  4. OR Hypertonic Saline 3%: 2.5-5 mL/kg IV over 10-15 minutes
  5. Consider intubation if GCS below 8 (avoid hyperventilation)
  6. Urgent CT head and neurosurgical consultation

Pregnancy

DKA in pregnancy carries significant maternal and foetal risks: [26]

  • Foetal mortality 10-35% (higher with severe DKA)
  • Foetal heart rate abnormalities common during DKA
  • Lower threshold for diagnosis (pregnant women have lower HCO3 baseline)
  • Risk of precipitating preterm labour

Management Considerations:

  • Lower threshold for ICU admission
  • Continuous foetal monitoring after viability (greater than 24 weeks)
  • Similar fluid and insulin protocols
  • Obstetric and neonatal team involvement
  • Consider delivery if foetal distress not responding to maternal treatment

Elderly Patients with HHS

Elderly patients with HHS require careful attention to: [5,6]

  • Cardiac status: Risk of fluid overload, pulmonary oedema
  • Renal function: Slower fluid rates if AKI present
  • Cerebral oedema risk: Slow osmolality correction
  • Thromboembolism risk: Consider DVT prophylaxis early
  • Underlying precipitant: Often MI, stroke, or infection
  • Cognitive assessment: Delirium is common

Complications

Hypoglycaemia

Incidence: 5-25% of DKA episodes Prevention:

  • Add dextrose when glucose below 14 mmol/L (DKA) or below 16.7 mmol/L (HHS)
  • Monitor glucose hourly during insulin infusion
  • Reduce insulin rate if glucose falling too rapidly

Hypokalaemia

Incidence: Nearly universal if potassium not replaced Prevention:

  • Do not start insulin if K+ below 3.3 mmol/L
  • Replace potassium in all IV fluids when K+ below 5.3 mmol/L
  • Monitor K+ every 1-2 hours initially
  • Target serum K+ 4-5 mmol/L

Cerebral Oedema

Incidence: 0.5-1% in children, rare in adults Risk Factors: Young age, new diagnosis, severe acidosis, excessive fluids, bicarbonate use Mortality: 21-24% Management: Osmotic therapy (mannitol or hypertonic saline), reduce fluids, elevate HOB

Venous Thromboembolism

DKA is a prothrombotic state due to: [27,28]

  • Dehydration and hyperviscosity
  • Endothelial dysfunction from hyperglycaemia
  • Elevated procoagulant factors (Factor VIII, vWF, fibrinogen)
  • Decreased natural anticoagulants (Protein C, Protein S)
  • Central venous catheter use

Prevention: Consider prophylactic anticoagulation (LMWH) in high-risk patients.

Acute Respiratory Distress Syndrome (ARDS)

Rare but reported complication, particularly with:

  • Aggressive fluid resuscitation
  • Underlying sepsis
  • Aspiration

Rhabdomyolysis

May occur due to:

  • Hypophosphataemia
  • Hypokalaemia
  • Severe dehydration

Rebound Hyperglycaemia/Ketosis

Cause: Premature discontinuation of IV insulin or inadequate overlap with SC insulin Prevention: Continue IV insulin 1-2 hours after first SC insulin dose

Resolution Criteria and Transition

Criteria for DKA Resolution

DKA is considered resolved when: [1]

  • Blood glucose below 11 mmol/L (below 200 mg/dL)
  • AND two of the following:
    • Serum bicarbonate ≥15 mmol/L
    • Venous pH greater than 7.30
    • Anion gap ≤12 mmol/L
  • β-hydroxybutyrate below 0.6 mmol/L (if available)

Criteria for HHS Resolution

HHS is considered resolved when:

  • Osmolality below 310 mOsm/kg
  • Glucose below 16.7 mmol/L
  • Normal mental status
  • Able to eat and drink

Transition to Subcutaneous Insulin

The 1-2 Hour Overlap Rule: [1,29,30]

Continue IV insulin infusion for 1-2 hours after the first dose of subcutaneous basal insulin. This ensures adequate plasma insulin levels as the short-acting IV insulin is cleared (half-life of only minutes).

Transition Protocol:

  1. Ensure DKA resolution criteria met
  2. Patient able to tolerate oral intake
  3. Calculate total daily insulin dose:
    • Insulin-naïve: 0.5-0.6 U/kg/day (0.3-0.4 U/kg/day if insulin-sensitive)
    • Previously on insulin: Restart home dose (or adjust based on current requirements)
  4. Give as basal-bolus regimen:
    • 50% as basal (glargine, detemir, or degludec)
    • 50% as rapid-acting divided before meals
  5. Give first SC insulin dose with a meal
  6. Continue IV insulin infusion for 1-2 hours after SC basal
  7. Discontinue IV insulin infusion
  8. Monitor glucose before meals and at bedtime

Early Basal Insulin Administration:

Some protocols advocate giving basal insulin early during the IV insulin infusion (before resolution) to:

  • Simplify transition
  • Reduce rebound hyperglycaemia
  • Allow more flexible timing of IV insulin cessation

Studies suggest 0.3 U/kg glargine given within 12 hours of starting IV insulin is safe and may improve outcomes. [30]

Monitoring During Treatment

Frequency of Monitoring

ParameterFrequencyTarget
Blood glucoseHourlyDecrease 3-4 mmol/L/hr
Serum potassiumEvery 1-2 hours4-5 mmol/L
Venous pH/HCO3Every 2-4 hourspH greater than 7.30, HCO3 ≥15
Electrolytes (full)Every 2-4 hoursCorrect abnormalities
Anion gapEvery 2-4 hours≤12 mmol/L
β-hydroxybutyrateEvery 2-4 hoursbelow 0.6 mmol/L
Serum osmolality (HHS)Every 2-4 hoursbelow 310 mOsm/kg
Urine outputHourlygreater than 0.5 mL/kg/hr
Fluid balanceHourlyAssess hydration status
Conscious levelHourlyGCS improving
ECGContinuous or 4-hourlyK+ abnormalities

ICU Flowsheet Parameters

Maintain an ICU flowsheet documenting:

Evidence Base

Landmark Studies and Guidelines

Study/GuidelinePMIDKey Finding
ADA Hyperglycemic Crises 200919564476Gold standard consensus statement
Morris Bicarbonate Trial 19863004246No benefit of bicarbonate pH 6.9-7.14
Gamba Bicarbonate Trial 19911933095No benefit of bicarbonate pH 6.85-7.18
Chua Bicarbonate Meta-analysis 201121411511No clinical benefit, potential harm
PECARN Fluid Trial 201829897851Fluid rate/type does not affect neurologic outcomes in paediatric DKA
SMART/SALT-ED DKA Subgroup 202033026410Balanced crystalloids faster DKA resolution
Ramanan Fluid Meta-analysis 202133509176Balanced crystalloids superior time to resolution
Glaser Cerebral Oedema 200111172153Risk factors for paediatric cerebral oedema
Peters euDKA 201526078479SGLT2i-associated euglycemic DKA case series
Fayfman Hyperglycemic Crises 201728351451Comprehensive review of management
Dhatariya DKA Review 202032409410Modern pathophysiology review

Areas of Ongoing Research

  1. Optimal fluid type: Ongoing trials comparing balanced crystalloids to saline
  2. Closed-loop insulin delivery: Automated glucose management in DKA
  3. Point-of-care ketone monitoring: Integration into management algorithms
  4. Prevention strategies: Technology for early detection of DKA
  5. SGLT2i perioperative management: Optimal cessation timing

Indigenous Health Considerations

Australian Aboriginal and Torres Strait Islander Peoples

Aboriginal and Torres Strait Islander peoples experience significantly higher rates of diabetes and hyperglycemic crises due to: [7,31]

Culturally Safe Care Principles:

New Zealand Māori and Pacific Islander Peoples

Similar health disparities exist for Māori and Pacific Islander populations in New Zealand: [32]

Remote and Rural Considerations

Initial Management in Resource-Limited Settings

Rural and remote emergency departments may have limited access to:

Practical Adaptations:

Retrieval Medicine Considerations (Australia)

Royal Flying Doctor Service (RFDS) and state-based retrieval services regularly transfer patients with hyperglycemic crises: [33]

Pre-Retrieval Optimisation:

In-Flight Considerations:

Telemedicine Support

Remote clinicians should utilise telehealth for:

SAQ Practice Questions

SAQ 1: DKA Fluid and Electrolyte Management

Exam Focus: Question: A 24-year-old woman with Type 1 diabetes presents to the emergency department with nausea, vomiting, and abdominal pain. She has not taken her insulin for 2 days due to a gastroenteritis illness. Her observations are: HR 118, BP 95/60, RR 32 (Kussmaul breathing), SpO2 99% on air, GCS 15.

Investigations:

a) Calculate the anion gap and corrected sodium. (2 marks) b) Outline your initial fluid resuscitation strategy for the first 4 hours. (4 marks) c) When would you commence insulin and at what rate? What parameter must you monitor closely and why? (4 marks)

Model Answer:

a) Calculations (2 marks)

b) Fluid Resuscitation Strategy (4 marks)

c) Insulin Therapy (4 marks)

SAQ 2: Euglycemic DKA

Exam Focus: Question: A 58-year-old man with Type 2 diabetes is day 2 post laparoscopic cholecystectomy. He develops nausea, vomiting, and increasing shortness of breath. His medications include metformin, empagliflozin, and atorvastatin. Observations: HR 105, BP 110/70, RR 24, SpO2 94% on 2L O2.

Investigations:

a) What is the diagnosis? Calculate the anion gap. (2 marks) b) Explain the pathophysiology of this condition in the context of the patient's medications. (4 marks) c) Outline your management approach, highlighting key differences from standard DKA management. (4 marks)

Model Answer:

a) Diagnosis (2 marks)

b) Pathophysiology (4 marks)

c) Management (4 marks)

Viva Scenarios

Viva 1: Severe DKA with Hypokalaemia

Exam Focus: Scenario: A 19-year-old male with Type 1 diabetes is brought to the emergency department unresponsive. He has been unwell for 3 days with vomiting. GCS 8 (E2V2M4), HR 130, BP 80/50, RR 36, SpO2 97% on air.

Investigations:

Examiner Questions and Model Answers:

Q1: How would you classify this DKA and what are your immediate priorities?

This is severe DKA based on:

Immediate priorities (within first 15-30 minutes):

  1. Airway protection - GCS 8 requires consideration of intubation
  2. IV access - two large bore cannulae
  3. Aggressive fluid resuscitation - 0.9% NaCl 1-1.5 L in first hour
  4. Potassium replacement - K+ 2.8 mmol/L is critically low
  5. DO NOT give insulin yet - will worsen hypokalaemia
  6. ECG - assess for hypokalaemic changes
  7. IDC for urine output monitoring
  8. Identify precipitant - sepsis screen, cardiac enzymes

Q2: The serum potassium is 2.8 mmol/L. How does this affect your management?

Critical principle: K+ below 3.3 mmol/L is a contraindication to starting insulin.

Management:

Q3: The pH is 6.92. Would you give sodium bicarbonate?

This is controversial and at the threshold for consideration.

Arguments against:

Arguments for consideration:

My approach:

Q4: What are the indications for intubation in this patient?

This patient (GCS 8) is at high risk and requires consideration of airway protection.

Indications for intubation:

Considerations:

Viva 2: HHS in Elderly Patient

Exam Focus: Scenario: An 78-year-old woman is brought from a nursing home with confusion and reduced oral intake over 5 days. Background: Type 2 diabetes, hypertension, ischaemic heart disease, CKD stage 3. HR 100, BP 100/60, RR 18, Temp 38.2°C, GCS 12 (E3V4M5).

Investigations:

Examiner Questions and Model Answers:

Q1: What is the diagnosis and what distinguishes this from DKA?

Diagnosis: Hyperosmolar Hyperglycemic State (HHS) with features of sepsis

Distinguishing features from DKA:

FeatureThis PatientDKA Criteria
Glucose58 mmol/L (greater than 33.3)greater than 11 mmol/L
Osmolality378 mOsm/kg (greater than 320)Often below 320
pH7.28 (borderline low but greater than 7.3 threshold)below 7.3
HCO320 mmol/L (borderline)below 18 mmol/L
Ketones1.2 mmol/L (mild)greater than 3 mmol/L

This is predominantly HHS with some acidosis (likely mixed with AKI and possible lactic acidosis from sepsis). The mild ketosis and borderline acidosis suggest a mixed state but HHS features predominate.

Q2: What is the likely precipitant and how would you investigate?

Likely precipitant: Sepsis (fever 38.2°C, nursing home resident, reduced intake)

Investigations:

Common HHS precipitants in elderly:

Q3: How does fluid management differ in HHS compared to DKA?

Key differences:

  1. More profound dehydration:

  2. Risk of rapid osmolality correction:

  3. Elderly/cardiac patient considerations:

  4. Sodium correction:

My approach:

Q4: What insulin rate would you use and why?

JBDS recommendation for pure HHS: 0.05 U/kg/hr (lower than DKA)

Rationale:

My approach:

Important: If significant ketosis/acidosis present (mixed state), use DKA protocol (0.1 U/kg/hr).

References

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  2. Lizzo JM, Goyal A, Gupta V. Diabetic Ketoacidosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing. 2023. [PMID: 29262232]

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  22. Handa A, Narasimhan B, Chhabra L. Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors: a case report and clinical review. Acta Diabetol. 2020;57(11):1409-1416. [PMID: 32204367]

  23. 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]

  24. Edge JA, Ford-Adams ME, Dunger DB. Causes of death in children with insulin dependent diabetes 1990-96. Arch Dis Child. 1999;81(4):318-323. [PMID: 10589559]

  25. Kuppermann N, Ghetti S, Schunk JE, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378(24):2275-2287. [PMID: 29897851]

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  29. Umpierrez GE, Latif K, Stoever J, et al. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis. Am J Med. 2004;117(5):291-296. [PMID: 15336577]

  30. Shankar V, Haque A, Churchwell KB, Russell W. Insulin glargine supplementation during early management phase of diabetic ketoacidosis in children. Intensive Care Med. 2007;33(7):1173-1178. [PMID: 17468847]

  31. O'Dea K, Rowley KG, Brown A. Diabetes in Indigenous Australians: possible ways forward. Med J Aust. 2007;186(10):494-495. [PMID: 17516893]

  32. Robson B, Purdie G, Cram F, Simmonds S. Age standardisation - an indigenous standard? Emerg Themes Epidemiol. 2007;4:3. [PMID: 17433116]

  33. Royal Flying Doctor Service. RFDS Clinical Manual: Diabetic Emergencies. RFDS Australia. 2024.

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  36. Decourcey DD, Steil GM, Wypij D, Agus MS. Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year retrospective analysis of mortality. Pediatr Crit Care Med. 2013;14(7):694-700. [PMID: 23833444]

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  40. Pasquel FJ, Tsegka K, Wang H, et al. Clinical Outcomes in Patients With Isolated or Combined Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State: A Retrospective, Hospital-Based Cohort Study. Diabetes Care. 2020;43(2):349-357. [PMID: 31852727]

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Appendix: Management Algorithms

DKA Management Algorithm

┌─────────────────────────────────────────────────────────────────────┐
│                    DIABETIC KETOACIDOSIS                            │
│                    Management Algorithm                              │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  DIAGNOSIS: Glucose greater than 11 mmol/L + pH below 7.3 + HCO3 below 18 + Ketones greater than 3   │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  INITIAL RESUSCITATION (First Hour)                                 │
│  • IV access × 2 large bore                                         │
│  • 0.9% NaCl 15-20 mL/kg (1-1.5 L)                                  │
│  • Check K+ before insulin                                          │
│  • ECG, sepsis screen, identify precipitant                        │
└─────────────────────────────────────────────────────────────────────┘
                              │
              ┌───────────────┴───────────────┐
              ▼                               ▼
┌─────────────────────────┐     ┌─────────────────────────┐
│  K+ below 3.3 mmol/L         │     │  K+ ≥3.3 mmol/L         │
│  • HOLD INSULIN         │     │  • Start insulin        │
│  • KCl 20-40 mmol/hr    │     │    0.1 U/kg/hr          │
│  • Recheck hourly       │     │  • Add K+ to fluids     │
│  • Start insulin when   │     │    if K+ below 5.3           │
│    K+ greater than 3.3              │     │                         │
└─────────────────────────┘     └─────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  ONGOING MANAGEMENT                                                  │
│  • Glucose hourly, K+ 1-2 hourly, VBG 2-4 hourly                   │
│  • Target glucose drop 3-4 mmol/L/hr                                │
│  • Continue 0.9% or 0.45% NaCl based on corrected Na               │
│  • Add dextrose when glucose below 14 mmol/L                            │
│  • Reduce insulin to 0.02-0.05 U/kg/hr when dextrose added         │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  RESOLUTION CRITERIA                                                 │
│  • Glucose below 11 mmol/L                                               │
│  • pH greater than 7.30                                                          │
│  • HCO3 ≥15 mmol/L                                                  │
│  • Anion gap ≤12 mmol/L                                             │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  TRANSITION TO SC INSULIN                                            │
│  • Patient eating and drinking                                       │
│  • Give SC basal insulin (0.5-0.6 U/kg/day)                         │
│  • Continue IV insulin 1-2 hours after first SC dose               │
│  • Diabetes education before discharge                              │
└─────────────────────────────────────────────────────────────────────┘

HHS Management Algorithm

┌─────────────────────────────────────────────────────────────────────┐
│              HYPEROSMOLAR HYPERGLYCEMIC STATE                        │
│                    Management Algorithm                              │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  DIAGNOSIS: Glucose greater than 33.3 mmol/L + Osmolality greater than 320 + pH greater than 7.3       │
│             + Minimal ketones (below 1.5 mmol/L)                         │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  KEY DIFFERENCES FROM DKA                                            │
│  • More severe dehydration (10-15% body weight)                     │
│  • Slower osmolality correction (below 3 mOsm/kg/hr)                     │
│  • Lower insulin rate (0.05 U/kg/hr for pure HHS)                   │
│  • High mortality (10-20%) - often elderly with comorbidities      │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  FLUID RESUSCITATION                                                 │
│  • Hour 1: 0.9% NaCl 1-1.5 L                                        │
│  • Subsequent: 0.45% NaCl 250-500 mL/hr (corrected Na usually high)│
│  • Add dextrose when glucose below 16.7 mmol/L                           │
│  • Replace deficit over 24-48 hours (not aggressively)             │
│  • Calculate osmolality every 2-4 hours                            │
└─────────────────────────────────────────────────────────────────────┘
                              │
                              ▼
┌─────────────────────────────────────────────────────────────────────┐
│  RESOLUTION CRITERIA                                                 │
│  • Osmolality below 310 mOsm/kg                                          │
│  • Glucose below 16.7 mmol/L                                             │
│  • Normal mental status                                              │
│  • Able to eat and drink                                            │
└─────────────────────────────────────────────────────────────────────┘

Potassium Replacement Protocol

┌─────────────────────────────────────────────────────────────────────┐
│              POTASSIUM REPLACEMENT IN DKA/HHS                        │
└─────────────────────────────────────────────────────────────────────┘

Serum K+ Level              Action Required
─────────────────────────────────────────────────────────────────────
below 3.3 mmol/L                 ⚠️ CRITICAL - HOLD INSULIN
                            • Give KCl 20-40 mmol/hr (central line)
                            • Recheck K+ every 30-60 min
                            • Start insulin only when K+ greater than 3.3

3.3-5.3 mmol/L              ✓ SAFE TO START INSULIN
                            • Add KCl 20-40 mmol/L to IV fluids
                            • Monitor K+ every 1-2 hours
                            • Target K+ 4-5 mmol/L

greater than 5.3 mmol/L                 ✓ SAFE TO START INSULIN
                            • Do NOT add K+ to fluids
                            • Monitor K+ every 2 hours
                            • Expect K+ to fall with treatment

greater than 6.5 mmol/L                 ⚠️ TREAT HYPERKALAEMIA
                            • ECG for arrhythmia
                            • Calcium gluconate 10 mL IV
                            • Consider insulin-dextrose
                            • Exclude haemolysis
─────────────────────────────────────────────────────────────────────

Maximum K+ Replacement Rates:
• Peripheral IV: 10-20 mmol/hr
• Central line: Up to 40 mmol/hr (with cardiac monitoring)

CICM Second Part Exam Tips

Exam Focus: Frequently Tested Concepts:

  1. Calculations - Be able to rapidly calculate:

  2. Potassium Management - This is the most common "gotcha" in DKA scenarios:

  3. Bicarbonate Controversy - Be prepared to discuss:

  4. Euglycemic DKA - Increasingly examined topic:

  5. Cerebral Oedema - Know the paediatric risk factors and treatment:

  6. Resolution Criteria - Be precise:

  7. Transition to SC Insulin:

Common Examiner Questions:

Summary

Diabetic ketoacidosis and hyperosmolar hyperglycemic state are life-threatening complications of diabetes mellitus requiring prompt recognition and systematic management. The four pillars of treatment - fluid resuscitation, insulin therapy, electrolyte replacement, and treatment of the precipitating cause - must be applied simultaneously. Key principles include avoiding insulin until potassium is adequate (greater than 3.3 mmol/L), adding dextrose when glucose falls to allow continued insulin for ketone clearance, and maintaining a slow rate of osmolality correction in HHS. The 1-2 hour overlap rule when transitioning to subcutaneous insulin prevents rebound hyperglycaemia. Special populations including paediatric patients, those on SGLT2 inhibitors with euglycemic DKA, pregnant women, and elderly patients with HHS require modified approaches. Australian and New Zealand clinicians should be aware of the increased burden of hyperglycemic crises in Indigenous populations and the need for culturally safe, accessible care.

Learning map

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