Diabetic Ketoacidosis (DKA) Clinical Overview

I. The "On-Call" Snapshot

Clinical Significance in Malaysia: This is one of the most common reasons for admission to a medical ward for a young person with diabetes, and a life-threatening complication you need to identify and treat immediately in the Emergency Department.

High-Yield Definition: DKA is a state of absolute or relative insulin deficiency resulting in a triad of:

1. Hyperglycemia: Capillary or venous blood glucose >14 mmol/L.

2. Ketosis: Presence of significant ketones in urine (2+ or more) or blood (serum beta-hydroxybutyrate >3.0 mmol/L).

3. Metabolic Acidosis: Venous pH <7.3 or serum bicarbonate <15 mmol/L.

   (Source: Malaysian CPG Management of Type 1 Diabetes Mellitus, 4th Ed. 2020)

Clinical One-Liner: Basically, the body has no insulin, so it starts burning fat for fuel. This produces acid (ketones), making the blood dangerously acidic and causing massive dehydration.

II. Etiology & Risk Factors

Etiology: Caused by an absolute or severe relative deficiency of insulin. This leads to uncontrolled gluconeogenesis and ketogenesis.

Risk Factors (Remember the 5 'I's):

• Infection: Most common precipitant (e.g., UTI, pneumonia, dengue). Always hunt for a source.

• Inadequate Insulin: Patient stopped or reduced their insulin dose. This is a very common cause due to non-compliance, financial issues, or incorrect sick-day management.

• Infarction/Ischemia: MI, stroke, or other vascular events can trigger DKA, especially in older patients.

• Initial Presentation: This is the first presentation of new-onset Type 1 Diabetes in about 20-40% of cases.

• Inflammation: Pancreatitis, for example.

III. Quick Pathophysiology

No insulin means glucose can't enter cells. The body thinks it's starving.

1. Hyperglycemia: The liver pumps out more glucose (gluconeogenesis). This high sugar level acts as an osmotic diuretic, pulling water out of the body into the urine, leading to severe dehydration and electrolyte loss.

2. Ketogenesis: The body breaks down fat into fatty acids, which are converted in the liver to ketone bodies (acetoacetate, beta-hydroxybutyrate). These are acidic.

3. Acidosis: As ketones accumulate, they overwhelm the body's buffering system, causing a high anion gap metabolic acidosis. The body tries to compensate by breathing fast and deep (Kussmaul breathing) to blow off CO2.

IV. Clinical Assessment

Red Flags & Immediate Actions:

• Altered Mental Status (GCS <15): Alert senior immediately. Risk of cerebral edema. Prepare for possible intubation and consider IV Mannitol on specialist advice.

• Severe Acidosis (pH <7.0): Alert senior/ICU. May need more aggressive resuscitation. Bicarbonate therapy is controversial and should only be given on consultant advice.

• Hypokalemia on presentation (K+ <3.3 mmol/L): Alert senior. DO NOT START INSULIN. You will cause a fatal arrhythmia. You must replace potassium first.

• Hypotension (SBP <90 mmHg) unresponsive to initial fluid bolus: Alert senior. Consider sepsis and need for vasopressors.

History:

• Common (>50%): Polyuria, polydipsia, lethargy, nausea, vomiting, significant weight loss over days.

• Less Common (10-50%): Abdominal pain (can mimic an acute abdomen), deep, sighing respiration (Kussmaul's).

• Pertinent Negatives: Ask about insulin compliance, recent illness or fever, and any chest pain or focal weakness to rule out MI/stroke.

Physical Examination:

• General: Looks unwell, dehydrated (dry mucous membranes, reduced skin turgor), pear-drop smell on breath (ketones).

• Vitals: Tachycardia, hypotension, tachypnea (Kussmaul breathing). May or may not have fever; absence of fever does not rule out infection.

• Systems: Abdominal tenderness is common but be wary of a surgical cause. Perform a full exam to look for a source of infection.

Clinical Pearl: DKA can present with a raised white cell count and C-reactive protein even without infection, due to the stress response. Don't be fooled, but maintain a high index of suspicion for sepsis.

V. Diagnostic Workflow

Differential Diagnosis:

• Hyperosmolar Hyperglycemic State (HHS):

  • Points For: Severe hyperglycemia, dehydration, altered mental status.

  • Points Against: Minimal or no ketosis, no significant acidosis (pH >7.3, Bicarb >18). Glucose is typically much higher (>33 mmol/L).

  • How to Differentiate: The venous blood gas (VBG/ABG) is key. The absence of acidosis points away from DKA.

• Alcoholic Ketoacidosis (AKA):

  • Points For: Ketoacidosis, nausea, vomiting, abdominal pain.

  • Points Against: Blood glucose is often low, normal, or only mildly elevated. Strong history of recent alcohol binge and poor oral intake.

  • How to Differentiate: History and a normal/low glucose level.

• Sepsis with Lactic Acidosis:

  • Points For: High anion gap metabolic acidosis, tachycardia, hypotension.

  • Points Against: Ketones are absent or only mildly elevated.

  • How to Differentiate: Check serum lactate. While DKA can have a mildly elevated lactate, a very high level points towards sepsis or tissue hypoperfusion.

Investigations Plan:

• Bedside / Initial (First 15 Mins):

  • Capillary Blood Glucose (CBG): Will be high.

  • Urine Dipstick for Ketones: Will be strongly positive (e.g., +++).

  • Venous/Arterial Blood Gas (VBG/ABG): Essential to confirm acidosis (low pH, low bicarb) and check electrolytes. VBG is usually sufficient.

  • ECG: Look for signs of hyperkalemia (peaked T waves) or hypokalemia (U waves, flattened T waves).

• First-Line Labs & Imaging:

  • Renal Profile/BUSE: Crucial for initial potassium level, creatinine (to assess renal function), and to calculate the anion gap: (Na+) - (Cl- + HCO3-). A gap >12 suggests DKA.

  • Full Blood Count (FBC): Look for leukocytosis suggesting infection.

  • Serum Ketones (Beta-hydroxybutyrate): Gold standard if available. More accurate than urine ketones.

  • Infectious Workup: Blood cultures, urine FEME & culture, CXR if indicated.

• Confirmatory / Gold Standard: The diagnosis is made clinically and biochemically based on the initial blood gas and lab results showing the triad of hyperglycemia, ketosis, and acidosis.

VI. Staging & Severity Assessment

Severity is based on the degree of acidosis. This determines the level of care required.

• Mild DKA: pH 7.25 – 7.30, Bicarbonate 15 – 18 mmol/L

• Moderate DKA: pH 7.00 – <7.25, Bicarbonate 10 – <15 mmol/L

• Severe DKA: pH <7.00, Bicarbonate <10 mmol/L

Impact on Management: All patients require admission. Moderate and Severe DKA should ideally be managed in a high-dependency unit (HDU) or ICU for continuous monitoring.

VII. Management Plan

Management revolves around three pillars: Fluids, Insulin, and Potassium (FIP). Follow a strict protocol.

Immediate Stabilisation (The ABCDE Plan):

• A/B: Ensure airway is patent. Give high-flow oxygen via face mask (10-15L/min) if patient is hypoxic (SpO2 <94%) or critically ill.

• C: Start IV fluids immediately. Secure two large-bore IV cannulas.

  • Give 1 Litre of 0.9% Normal Saline over the first hour.

  • Subsequent fluid management depends on hydration status but is typically 1L over 2 hours, then 1L over 4 hours.

• D: Assess GCS. If low, see red flags above.

• E: Expose to assess for rashes, signs of infection.

Definitive Treatment (The Ward Round Plan - The DKA Protocol):

1. Fluids: After the initial bolus, continue with 0.9% Normal Saline. Once blood sugar falls to <14 mmol/L, change the IV fluid to 0.45% Saline + 5% Dextrose (D5NS/2) to prevent hypoglycemia and allow the insulin infusion to continue.

2. Insulin: Start a Fixed Rate Intravenous Insulin Infusion (FRIII).

   • Dose: 0.1 units/kg/hour. (e.g., 50 units of Actrapid in 50mL of Normal Saline, run at a rate based on patient's weight).

   • DO NOT give a stat IV bolus of insulin. This is an outdated practice.

   • DO NOT start insulin until you have confirmed the initial potassium level is ≥3.3 mmol/L.

3. Potassium: This is critical to prevent fatal arrhythmias.

   • If initial K+ <3.3 mmol/L: HOLD INSULIN. Give 20-40mmol of KCl replacement per hour until K+ is >3.3.

   • If initial K+ 3.3 – 5.5 mmol/L: Add 20-40mmol of KCl to each litre of IV fluid.

   • If initial K+ >5.5 mmol/L: Do not add potassium, but recheck levels within 1-2 hours as they will fall rapidly with insulin treatment.

4. Monitoring:

   • Hourly capillary blood glucose.

   • 2-4 hourly renal profile to monitor potassium and acidosis resolution.

   • Strict fluid balance chart.

Resolution of DKA & Discharge Plan:

• Criteria for resolution: pH >7.3, Bicarbonate >15 mmol/L, and blood ketones <0.6 mmol/L (or urine ketones cleared). The patient must also be able to eat and drink.

• Transition to Subcutaneous (SC) Insulin: Once resolved, plan for conversion to the patient's usual SC insulin regimen. CRITICAL: You must give the first SC dose and wait at least 1-2 hours before stopping the IV insulin infusion to prevent a relapse into ketosis.

• Discharge: Involve the Diabetes Educator. Ensure patient understands sick-day rules (never stop insulin, monitor glucose/ketones, stay hydrated).

VIII. Complications

• From Treatment:

  • Hypoglycemia: Management: If conscious, give oral glucose. If unconscious, give IV Dextrose 50%. Caused by not adding dextrose to fluids once CBG falls.

  • Hypokalemia: Management: Proactive and aggressive potassium replacement as per protocol.

• From Disease:

  • Cerebral Edema: Rare in adults, more common in children. Presents with headache, worsening GCS. Management: Alert senior/ICU immediately, consider IV Mannitol. High mortality.

  • Thromboembolism: DKA is a pro-thrombotic state. Consider VTE prophylaxis for admitted patients.

IX. Prognosis

With proper protocol-based management, mortality in Malaysia is low (<1%). Prognosis is worse in the elderly, those with severe acidosis at presentation, and those with severe underlying comorbidities like MI or sepsis.

X. How to Present to Your Senior

"Dr, for your review please. This is Patient [Name] in [Bed Location], a [Age]-year-old, known [Type 1/2] diabetic, who presented with vomiting and lethargy.

On assessment, she is dehydrated and tachypneic. Her CBG is 'high' at 25, urine ketones are +++, and her VBG shows a pH of 7.1 with a bicarbonate of 8.

My working diagnosis is moderate to severe DKA, likely precipitated by a suspected UTI.

I have already started 1L of Normal Saline, sent off the urgent labs including cultures, and obtained an ECG. Her initial potassium is 4.2. I would like to start the DKA insulin infusion protocol now."

XI. Summary & Further Reading

Top 3 Takeaways:

1. Fluids First, Fast: Aggressive rehydration with Normal Saline is the first step.

2. Check Potassium Before Insulin: Never start an insulin infusion if the patient's potassium is <3.3 mmol/L.

3. Find and Treat the Precipitant: DKA doesn't happen in a vacuum. Hunt for the underlying cause, most commonly infection or insulin non-compliance.

Key Resources:

• Primary Guideline: Malaysian CPG: Management of Type 1 Diabetes Mellitus (4th Edition, 2020)

• UpToDate: Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment

• Key Review Article: Kitabchi, A. E., et al. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes care, 32(7), 1335-1343. (Landmark paper, principles still hold).