Diabetic Ketoacidosis

Introduction

Diabetic ketoacidosis (DKA) is a life-threatening acute metabolic complication of diabetes mellitus characterised by hyperglycaemia, ketosis, and metabolic acidosis. It represents a medical emergency requiring immediate recognition, rapid assessment, and aggressive management to prevent significant morbidity and mortality.

🚨

Medical Emergency: DKA has a mortality rate of 1-5% in developed countries and requires immediate hospitalisation and intensive monitoring.

Definition and Diagnostic Criteria

DKA is diagnosed when all three of the following criteria are present:

Parameter	Diagnostic Threshold	Notes
Hyperglycaemia	Blood glucose >11.0 mmol/L	May be lower in euglycaemic DKA
Ketonaemia	Blood β-hydroxybutyrate ≥3.0 mmol/L OR urine ketones ≥2+ (moderate)	Blood ketones preferred over urine ketones
Metabolic acidosis	Venous pH <7.30 OR bicarbonate <15 mmol/L	Anion gap typically >12 mmol/L

Severity Classification

Mild DKA

pH 7.25-7.30

HCO₃⁻ 15-18 mmol/L
Alert mental state

Ward-based care possible

Moderate DKA

pH 7.00-7.24

HCO₃⁻ 10-14 mmol/L
Mild drowsiness

HDU monitoring required

Severe DKA

pH <7.00

HCO₃⁻ <10 mmol/L
Stupor/coma

ICU admission required

Epidemiology and Risk Factors

High-Risk Populations

New-onset Type 1 diabetes (20-40% present with DKA)
Adolescents and young adults with T1DM
Patients with recurrent DKA episodes
Socioeconomically disadvantaged populations
Aboriginal and Torres Strait Islander peoples

Common Precipitating Factors

Infection (35-40% of cases)
Insulin omission or inadequate dosing
New-onset diabetes
Cardiovascular events (MI, stroke)
Medications (corticosteroids, SGLT2 inhibitors)
Substance abuse (alcohol, cocaine)
Psychological stress

ℹ️

Euglycaemic DKA: Increasingly recognised with SGLT2 inhibitor use. Blood glucose may be <14 mmol/L but ketosis and acidosis are still present. Always check ketones in patients on SGLT2 inhibitors presenting with illness.

Pathophysiology Overview

DKA results from absolute or relative insulin deficiency combined with increased counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone). This leads to:

Insulin Deficiency

Decreased glucose uptake and increased hepatic glucose production

Lipolysis

Increased free fatty acid mobilisation and ketogenesis

Osmotic Diuresis

Dehydration and electrolyte losses (Na⁺, K⁺, PO₄³⁻, Mg²⁺)

Metabolic Acidosis

Ketoacid accumulation overwhelming buffering capacity

Aboriginal and Torres Strait Islander Health Considerations

Higher Incidence

ATSI populations have 2-4 times higher rates of T1DM and increased DKA presentation rates, particularly in remote communities.

Geographic Barriers

Remote location delays in recognition and transfer to appropriate facilities. Early telehealth consultation and retrieval planning essential.

Cultural Factors

Traditional healing practices may delay presentation. Engage with community health workers and provide culturally appropriate education.

Social Determinants

Food insecurity, medication access issues, and social stressors contribute to poor glycaemic control and recurrent DKA episodes.

✅

Key Learning Point: Early recognition and prompt treatment are crucial for optimal outcomes. Most DKA-related deaths are preventable with appropriate management and should prompt review of precipitating factors and diabetes education needs.

Clinical Presentation

MILD DKA

pH 7.25-7.30 / HCO₃ 15-18 mmol/L

Alert, minimal dehydration, able to tolerate oral fluids

• Emergency Department monitoring
• Consider short stay unit

MODERATE DKA

pH 7.00-7.24 / HCO₃ 10-15 mmol/L

Drowsy but rousable, moderate dehydration, vomiting

• Inpatient ward admission
• 4-6 hourly monitoring

SEVERE DKA

pH <7.00 / HCO₃ <10 mmol/L

Obtunded/comatose, severe dehydration, shock

• ICU/HDU admission
• Hourly monitoring required

🚨

Emergency Red Flags: GCS <12, systolic BP <90 mmHg, pH <7.00, K⁺ <3.5 or >6.0 mmol/L, anion gap >25 mmol/L, age >65 years with comorbidities.

Classical Triad Symptoms

Polyuria and Polydipsia: Osmotic diuresis from hyperglycaemia
Nausea and Vomiting: Present in 75-90% of cases
Abdominal Pain: May mimic surgical abdomen (pseudoperitonitis)

Progressive Clinical Features

Early

Hyperglycaemic symptoms: Thirst, polyuria, polydipsia, fatigue, blurred vision, weight loss over days to weeks

Developing

Ketosis symptoms: Nausea, vomiting, anorexia, abdominal pain, fruity breath odour (acetone)

Advanced

Dehydration/acidosis: Kussmaul breathing, altered mental state, hypotension, tachycardia, hypothermia

Physical Examination Findings

Dehydration Assessment

Mild (3-5%): Dry mucous membranes, decreased skin turgor
Moderate (6-9%): Sunken eyes, prolonged capillary refill, orthostatic hypotension
Severe (>10%): Shock, altered consciousness, cool extremities

Respiratory Signs

Kussmaul breathing: Deep, rapid respirations (pH <7.20)
Acetone breath: Sweet, fruity odour
Respiratory rate: Often 20-40 breaths/min

⚠️

Abdominal Pain Caution: Severe abdominal pain in DKA may resolve with treatment. Avoid unnecessary surgical consultation unless pain persists after initial fluid resuscitation and pH improvement.

Mental State Changes

pH 7.25-7.30

Alert, mild confusion

pH 7.10-7.24

Drowsy, moderate confusion

pH 7.00-7.09

Obtunded, difficult to rouse

pH <7.00

Coma (5-10% of cases)

Common Precipitating Factors

Infection (40%): UTI, pneumonia, sepsis, gastroenteritis
Medication non-adherence (25%): Insulin omission, especially in young adults
New-onset diabetes (15-20%): First presentation of Type 1 DM
Medical illness: MI, stroke, pancreatitis, hyperthyroidism
Medications: Corticosteroids, thiazides, β-blockers, atypical antipsychotics
Alcohol or drug abuse: Including cocaine use

ℹ️

Euglycaemic DKA: May occur with SGLT2 inhibitors, pregnancy, or prolonged starvation. Glucose may be <14 mmol/L but ketosis and acidosis still present.

👶

Paediatric Considerations:

• More likely to present with new-onset diabetes
• Higher risk of cerebral oedema
• May present with bed-wetting, behavioural changes
• Often misdiagnosed as viral gastroenteritis

🤰

Pregnancy Considerations:

• Lower glucose threshold for ketosis
• Euglycaemic DKA more common
• Kussmaul breathing may be attributed to normal pregnancy
• Urgent obstetric consultation required

Aboriginal and Torres Strait Islander Health

Geographic Access

Remote communities may present later due to distance from healthcare. Ensure early recognition training for community health workers and telehealth support.

Cultural Factors

Traditional healing practices may delay presentation. Engage with community elders and traditional healers to promote early medical intervention.

Communication

Use interpreter services when required. Explain symptoms in culturally appropriate language, avoiding medical jargon.

Investigations

🚨

Time-Critical Testing: DKA diagnosis requires immediate laboratory confirmation. Do not delay treatment while awaiting results if clinical suspicion is high.

Essential Immediate Investigations

Essential

Blood Gas Analysis (VBG/ABG)

pH, bicarbonate, base excess, lactate. VBG adequate for pH assessment. Repeat q2-4h initially.

Essential

Blood Glucose Level

Bedside glucometer + laboratory glucose. May be normal or mildly elevated in euglycaemic DKA.

Essential

Blood Ketones (β-hydroxybutyrate)

Preferred over urine ketones. >3.0 mmol/L diagnostic. Bedside meter available in most EDs.

Essential

Electrolytes (UEC)

Na⁺, K⁺, Cl⁻, HCO₃⁻, urea, creatinine. Calculate anion gap. Monitor K⁺ closely.

Essential

Full Blood Count

WCC may be elevated due to stress response. Look for evidence of infection.

Available

Urine Ketones

If blood ketones unavailable. Qualitative only. Less reliable than blood ketones.

Additional Investigations

Available

HbA1c

Assess long-term glycaemic control. May guide management decisions.

Available

Blood Cultures

If fever, elevated WCC, or clinical suspicion of sepsis. Take before antibiotics.

Available

Urinalysis & Microscopy

Exclude UTI as precipitant. Ketones, glucose, protein, nitrites, leucocytes.

Available

ECG

Assess for cardiac arrhythmias secondary to electrolyte abnormalities (especially K⁺).

Available

Chest X-ray

If respiratory symptoms or signs suggesting pneumonia as precipitant.

Specialist

C-peptide & Anti-GAD

For newly diagnosed diabetes to differentiate Type 1 vs Type 2. Not urgent.

Diagnostic Criteria

Parameter	Mild DKA	Moderate DKA	Severe DKA
pH	7.25-7.30	7.00-7.24	<7.00
Bicarbonate (mmol/L)	15-18	10-14	<10
Blood Ketones (mmol/L)	>3.0	>3.0	>3.0
Anion Gap	>10	>12	>12
Mental Status	Alert	Alert/drowsy	Stupor/coma

Monitoring Frequency

0-2 hours

Every 1-2 hours: BGL, blood ketones, VBG, electrolytes

2-6 hours

Every 2-4 hours: Continue monitoring as resolution occurs

6+ hours

Every 4-6 hours: Once stable and ketones clearing

💡

Anion Gap Calculation: [Na⁺ + K⁺] - [Cl⁻ + HCO₃⁻]. Normal range 8-16 mmol/L. Elevated anion gap with ketosis confirms DKA diagnosis.

Special Considerations

Euglycaemic DKA

SGLT2 inhibitor use
Pregnancy
Recent insulin administration
Reduced oral intake
BGL may be <14 mmol/L

Precipitant Investigation

Infection screen if indicated
Cardiac enzymes if chest pain
Drug screen if suspected
Medication compliance review

⚠️

Point-of-Care Testing: Bedside ketone and glucose meters are acceptable for initial assessment and monitoring. Confirm with laboratory values when clinically indicated.

Treatment

🚨

Emergency Management: DKA is a life-threatening emergency. Immediate IV access, fluid resuscitation, and insulin therapy are critical. Consider HDU/ICU admission for severe cases.

Initial Emergency Management

ABC Assessment

Airway, breathing, circulation. IV access (2 large bore cannulas). Cardiac monitoring. Urinary catheter if unconscious.

Fluid Resuscitation

0.9% NaCl 1L over first hour if haemodynamically unstable. Then transition to replacement therapy.

Insulin Therapy

IV insulin infusion 0.1 units/kg/hour after initial fluid bolus. Continue until ketosis resolves.

Fluid Management

Phase	Fluid Type	Rate	Target
Initial Resuscitation	0.9% NaCl	1L over 1 hour	Haemodynamic stability
Replacement Phase	0.9% NaCl or Hartmann's	250-500mL/hour	Replace 50% of deficit over 24h
When glucose <15 mmol/L	5% Dextrose + 0.45% NaCl	125-250mL/hour	Prevent hypoglycaemia

⚠️

Fluid Overload Risk: Monitor closely in elderly, cardiac, or renal impairment. Consider central venous pressure monitoring if indicated.

Insulin Protocol

💉

Human Insulin (Short-acting)

Actrapid® · Humulin R® · IV Infusion

Initial Dose 0.1 units/kg/hour IV infusion

Preparation 50 units in 50mL 0.9% NaCl (1 unit/mL)

Target Glucose fall 3-5 mmol/L/hour

PBS Status ✔ PBS General Benefit

Glucose Level	Insulin Rate	Dextrose	Action
>15 mmol/L	0.1 units/kg/hour	None	Continue 0.9% NaCl
10-15 mmol/L	0.05-0.1 units/kg/hour	5% dextrose	Add dextrose to fluids
6-10 mmol/L	0.05 units/kg/hour	5-10% dextrose	Increase dextrose concentration
<6 mmol/L	Reduce or stop insulin	10% dextrose	Urgent glucose correction

Electrolyte Management

Potassium Replacement

⚡

Potassium Chloride

IV Replacement · Monitor ECG

K+ >5.5 mmol/L No KCl initially

K+ 3.5-5.5 mmol/L 20-40 mmol/L in IV fluids

K+ <3.5 mmol/L 40-60 mmol/L + delay insulin if <3.3

PBS Status ✔ PBS General Benefit

🚨

Hypokalaemia Risk: Insulin drives K+ intracellularly. Monitor K+ every 2-4 hours initially. Delay insulin if K+ <3.3 mmol/L until corrected.

Bicarbonate Therapy

⚠️

Limited Indication: Generally NOT recommended. Consider only if pH <6.9 or severe hyperkalemia with cardiac arrhythmias. Risk of cerebral oedema and hypokalaemia.

🧪

Sodium Bicarbonate 8.4%

Rarely Used · pH <6.9 Only

Indication pH <6.9 or severe acidosis with shock

Dose 50-100 mmol in 200mL water over 1 hour

Monitoring Repeat ABG after infusion

PBS Status ✔ PBS General Benefit

Monitoring Protocol

Parameter	Initial Frequency	Stable Phase	Target
Blood Glucose	Hourly	2-4 hourly	Decrease 3-5 mmol/L/hour
Ketones (βOHB)	2-4 hourly	4-6 hourly	Decrease 0.5 mmol/L/hour
Electrolytes	2-4 hourly	6-8 hourly	K+ 4-5 mmol/L
ABG/VBG	4-6 hourly	8-12 hourly	pH >7.3, HCO₃⁻ >15
Fluid Balance	Hourly	4 hourly	Positive balance initially

Resolution Criteria

✅

DKA Resolution: All criteria must be met: Glucose <11.1 mmol/L, β-hydroxybutyrate <0.6 mmol/L (or urine ketones negative/trace), venous pH >7.3, HCO₃⁻ >15 mmol/L.

Transition to Subcutaneous Insulin

Overlap Period

Give first SC insulin dose 30-60 minutes before stopping IV insulin infusion to prevent rebound ketosis.

Insulin Regimen

Calculate total daily dose based on weight (0.5-1 units/kg/day).

Special Populations

🤰

Pregnancy

Risk Factors: Hyperemesis gravidarum, infection, poor compliance, gestational diabetes progression

Physiological Changes: Lower bicarbonate baseline (18-22 mmol/L), respiratory alkalosis compensation

DKA Criteria (Pregnancy-specific):

Blood glucose >11 mmol/L OR known diabetes
Venous pH <7.30 OR bicarbonate <15 mmol/L
Ketonaemia >3.0 mmol/L OR ketonuria ≥2+

Insulin Management

Continue usual insulin regime plus IV insulin infusion. Target glucose 4-7 mmol/L to prevent fetal hypoglycaemia.

Fluid Management

Careful fluid balance - risk of pulmonary oedema. Initial 1L normal saline over 1 hour, then 250-500 mL/hour based on assessment.

🚨

Urgent Obstetric Review: Continuous fetal monitoring if viable (>24 weeks). Consider delivery if maternal condition deteriorating or fetal compromise.

👶

Paediatric (Under 18 years)

Presentation: Often new-onset Type 1 diabetes (40-50% of cases). High risk of cerebral oedema.

Severity Assessment:

Mild: pH 7.25-7.30, bicarbonate 15-18 mmol/L
Moderate: pH 7.10-7.24, bicarbonate 10-14 mmol/L
Severe: pH <7.10, bicarbonate <10 mmol/L

Insulin (Actrapid)

0.05-0.1 units/kg/hour IV infusion (lower than adult dose). Reduce to 0.02-0.05 units/kg/hour once glucose <15 mmol/L.

Fluid Replacement

Calculate deficit: mild 5%, moderate 7%, severe 10% dehydration. Replace over 48 hours. Initial bolus 10-20 mL/kg if shocked, otherwise start maintenance + deficit replacement.

⚠️

Cerebral Oedema Risk: Headache, altered consciousness, bradycardia. Treat with mannitol 0.5-1 g/kg IV or hypertonic saline 2.5-5 mL/kg of 3% solution. Transfer to PICU immediately.

👴

Elderly (Over 65 years)

Complications: Higher mortality, increased cardiovascular events, prolonged recovery

Comorbidities: Heart failure, chronic kidney disease, cognitive impairment affecting self-management

Insulin Dosing

Start conservatively at 0.05 units/kg/hour, titrate slowly. Monitor for hypoglycaemia - target glucose 8-12 mmol/L may be appropriate.

Fluid Management

Cautious fluid replacement - risk of fluid overload. Consider 0.5L over 2 hours initially, then 200-300 mL/hour with frequent reassessment.

Monitoring: Hourly neurological observations, cardiac monitoring if indicated, early involvement of cardiology/nephrology if comorbidities present

⚠️

Goals of Care: Consider patient preferences and functional status. May require less aggressive targets and longer duration of treatment.

🫘

Renal Impairment

Risk Factors: Diabetic nephropathy, dehydration, nephrotoxic medications (ACE inhibitors, diuretics, NSAIDs)

Assessment: Baseline creatinine may be elevated. Calculate eGFR. Distinguish pre-renal (dehydration) from intrinsic renal disease.

Fluid Management

Monitor fluid balance carefully. May need slower rehydration if oliguric. Target urine output >0.5 mL/kg/hour.

Insulin Dosing

No dose adjustment required for insulin. Monitor glucose closely as clearance may be reduced in severe renal failure.

Electrolyte Management

Careful potassium replacement - risk of hyperkalaemia if oliguric. Consider phosphate restriction if eGFR <30 mL/min/1.73m².

ℹ️

Renal Replacement: Consider dialysis if severe acidosis (pH <7.0) not responding to treatment, fluid overload, or severe hyperkalaemia (K+ >6.5 mmol/L).

🫀

Hepatic Impairment

Associations: Non-alcoholic fatty liver disease (NAFLD), medication-induced hepatitis, concurrent alcohol use

Complications: Impaired glucose regulation, altered drug metabolism, coagulopathy risk

Insulin Management

No dose adjustment required. Monitor glucose closely - hepatic glucose production may be impaired, increasing hypoglycaemia risk.

Monitoring

Check LFTs, INR/PT if cirrhosis suspected. Avoid hepatotoxic medications. Consider reduced protein intake if hepatic encephalopathy risk.

⚠️

Drug Interactions: Review all medications for hepatic metabolism. Paracetamol dose reduction may be required in severe hepatic impairment.

🦠

Immunocompromised

Risk Factors: Corticosteroids, chemotherapy, transplant recipients, HIV, underlying malignancy

Infectious Triggers: Higher risk of atypical organisms. Broader antimicrobial coverage may be required.

Infection Screening

Blood cultures, urine culture, chest X-ray mandatory. Consider fungal cultures, viral PCR if indicated. Early ID consultation.

Empirical Antibiotics

Consider broader spectrum: piperacillin-tazobactam 4.5g IV 8-hourly OR meropenem 1g IV 8-hourly if severe sepsis/neutropenic.

Steroid Management: Continue essential steroids (replacement doses). Avoid high-dose steroids unless life-threatening condition.

🚨

Neutropenic Fever: If neutrophils <1.0 × 10⁹/L and fever >38°C, treat as neutropenic sepsis with urgent broad-spectrum antibiotics.

Aboriginal and Torres Strait Islander Health Considerations

Higher Disease Burden

Type 2 diabetes prevalence 3-4 times higher in ATSI populations. Younger onset, more complications. Consider screening for diabetes complications (nephropathy, retinopathy) at presentation.

Geographic Access

Remote communities may have delayed presentation. Telehealth support for ongoing management. Early transfer protocols for severe cases. Ensure adequate supplies of insulin and monitoring equipment.

Cultural Safety

Involve Aboriginal Health Workers/Practitioners. Respect cultural practices around food and family involvement in care. Explain treatment clearly with interpreters if needed. Consider family preferences for care location.

Discharge Planning

Coordinate with local health services and Aboriginal Medical Services. Ensure reliable supply of medications and monitoring equipment. Education materials in appropriate language/format. Consider social determinants affecting ongoing care.

Rheumatic Heart Disease

Higher prevalence in ATSI populations. Assess for RHD if cardiac symptoms present. Penicillin allergy documentation important for prophylaxis considerations. Involve cardiology if valvular disease suspected.

📋

Multidisciplinary Care: All special populations benefit from early involvement of diabetes educators, dietitians, social workers, and subspecialists as appropriate. Consider discharge planning from admission to ensure safe transition and prevent readmission.

Follow-Up & Prevention

Post-DKA

Immediate Follow-Up

24-48 hours post-resolution

GP/Endocrinologist

Short-term

1-2 Weeks

Diabetes education review

Diabetes Team

Long-term

Ongoing Care

Regular monitoring plan

Multidisciplinary

Immediate Post-DKA Management (First 48 Hours)

Monitor for Complications

• Cerebral oedema (especially paediatric) • Hypoglycaemia from insulin overlap • Hypokalaemia rebound • Thromboembolism risk

Transition to Subcutaneous Insulin

• Continue IV insulin 1-2 hours after first SC dose • Resume usual regimen or establish new regimen • Monitor BGL 4-hourly initially

Identify Precipitating Factors

• Review infection screen results • Medication compliance assessment • Social/psychological stressors

Discharge Planning Checklist

✓

Blood glucose stable

BGL 4-10 mmol/L on subcutaneous insulin for ≥12 hours

✓

Electrolytes normalised

K⁺ >3.5 mmol/L, normal anion gap

✓

Tolerating oral intake

No nausea/vomiting, adequate fluid intake

✓

Patient education completed

Sick day management, ketone testing, when to seek help

✓

Follow-up arranged

GP within 24-48 hours, diabetes team within 1-2 weeks

Prevention Strategies

Patient Education Priorities

Recognition of early DKA symptoms
Proper insulin storage and administration
Blood and urine ketone monitoring
Sick day management protocol
When to contact healthcare providers
Importance of medication adherence

System-Level Prevention

Regular diabetes team reviews
Structured education programs
Psychological support services
Accessible after-hours advice
Community pharmacy support
Culturally appropriate resources

Sick Day Management Protocol

💡

Key Message: Never stop insulin during illness. "When sick, check more, take more."

Blood Glucose	Ketones	Action Required	Monitoring Frequency
>15 mmol/L	Any level	Extra rapid-acting insulin, increase fluids	BGL & ketones 2-hourly
Any level	Blood >1.5 mmol/L or Urine >2+	Extra rapid-acting insulin, seek medical advice	BGL & ketones 2-hourly
Any level	Blood >3.0 mmol/L or Urine >3+	Urgent medical attention - potential DKA	Immediate assessment

Follow-Up Schedule

24-48 hours

GP Review: Clinical stability, electrolytes if indicated, insulin adjustment, psychosocial assessment

1 week

Diabetes Educator: Equipment check, education reinforcement, sick day plan review

2-4 weeks

Endocrinologist: Insulin regimen optimisation, complication screening, long-term management plan

3 months

Comprehensive Review: HbA1c, diabetes complications screen, medication review, quality of life assessment

Special Population Considerations

👶

Paediatric

Extended monitoring: 72 hours observation for cerebral oedema

Family education: Age-appropriate diabetes management skills

School liaison: Management plan for educational settings

🤱

Pregnancy

Obstetric review: Fetal monitoring, delivery planning if near term

Tighter control: Target BGL 3.5-5.5 mmol/L fasting, <7.8 mmol/L post-meal

Multidisciplinary: Endocrinology, obstetrics, diabetes educator

👴

Elderly

Cognitive assessment: Impact on self-management capacity

Medication review: Polypharmacy interactions, adherence aids

Social support: Family involvement, community services

Aboriginal and Torres Strait Islander Health

Cultural Safety

Involve Aboriginal health workers, respect cultural practices, family-centred approach to diabetes education.

Geographic Access

Telemedicine follow-up, extended supply medications, local health service coordination, transport assistance.

Education Resources

Culturally appropriate materials, visual aids, involvement of community leaders, peer education programs.

Prevention Programs

Community-based diabetes programs, traditional food integration, physical activity initiatives, regular health checks.

⚠️

Red Flags for Recurrent DKA: Non-adherence to insulin, eating disorders, psychiatric comorbidities, substance abuse, socioeconomic barriers, inadequate diabetes education.

Quality Improvement Measures

DKA Prevention Rate

Education Program Completion

>90% of patients receive structured education

Readmission Rate

30-day DKA Readmission

<5% target rate

Follow-up Compliance

Scheduled Appointments

>80% attendance within 1 week

HbA1c Improvement

3-month Post-DKA

≥0.5% reduction in HbA1c