DKA:
- Typically younger adults with T1DM
- Onset: hours to days
- Polyuria, polydipsia, weight loss, tachypnoea (Kussmaul respiration), abdominal pain, acetone breath, nausea/vomiting, confusion
- Often triggered by infection, missed insulin doses, or myocardial infarction
HHS:
- Typically older adults with type 2 diabetes
- Onset: days to weeks
- Profound dehydration, polydipsia, polyuria, confusion, lethargy, potential hypovolaemic shock
- Higher risk of neurological sx due to increased osmolality (e.g., coma, seizures)
- Less severe abdominal pain compared to DKA

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Pathophysiology

DKA:
- Severe insulin deficiency → lipolysis → ketone production → metabolic acidosis
- Associated with hyperglycaemia and dehydration
HHS:
- Partial insulin deficiency → marked hyperglycaemia (>30 mmol/L) → osmotic diuresis → severe dehydration
- Minimal or absent ketone production due to residual insulin activity

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Diagnosis

DKA:
- Blood glucose: ≥11 mmol/L (but may be lower in SGLT2 inhibitor-induced euglycaemic DKA)
- Arterial pH: ≤7.3
- Serum bicarbonate: ≤15 mmol/L
- Ketones: ≥3 mmol/L in blood or large in urine
HHS:
- Blood glucose: ≥30 mmol/L
- Serum osmolality: ≥320 mOsm/kg
- Little or no ketonaemia (blood ketones <1 mmol/L)

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Treatment

DKA:
- Start with 0.9% NaCl; replace deficits over 24–48 hours
- IV insulin infusion (0.05–0.1 units/kg/hour), adjust to maintain glucose reduction of 3–5 mmol/L per hour
- Add K+ if serum K+ <5.0 mmol/L; avoid insulin if K+ <3.5 mmol/L until corrected
- Correct underlying triggers (e.g., infection, missed insulin doses)
HHS:
- Initial 0.9% NaCl to restore circulating volume; consider 0.45% saline if osmolality remains high
- Start insulin only after adequate fluid replacement; use at a lower rate (0.05 units/kg/hour)
- Thromboprophylaxis: High risk of thromboembolism, start LMWH
- Address precipitating factors (e.g., infection, medications)
Both:
- Regular monitoring of blood glucose, ketones, and electrolytes
- Avoid rapid shifts in osmolality to prevent cerebral oedema
- Transition to subcutaneous insulin once stable

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Notes:

SLOW correction in HHS vs DKA
Always need endocrinologist input and transfer to nearest tertiary hospital
Never bolus and only do IV fluid / insulin in consultation w specialist
Monitor K and administer KCl if K is low (K lower in DKA, hold insulin if you are doing this)

DKA vs HHS

Diabetic Ketoacidosis

Causes and Pathophysiology

Insulin Deficiency

Prevents glucose from entering cells, leading to hyperglycaemia.
Lipolysis increases, producing fatty acids for ketone production as an alternate fuel source, resulting in acidosis.

Mechanisms in DKA

Osmotic Diuresis and Hypovolemia: Insulin deficiency → hyperglycaemia → hyperosmolarity → osmotic diuresis → hypovolaemia.
Metabolic Acidosis with Anion Gap: Insulin deficiency → increased lipolysis → free fatty acids → ketone production → ketones in blood → bicarbonate consumption.
Intracellular Potassium Deficit: Insulin deficiency → K+ moves extracellularly → hypokalaemia on total body level, though serum levels may appear normal or elevated.

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Clinical Features

General Symptoms

Acute onset (<24 hours).
Dehydration: polyuria, polydipsia, vomiting, weight loss.

Specific Signs

Kussmaul Respiration: Deep, laboured breathing due to metabolic acidosis.
Fruity Breath: Due to exhaled acetone.
Abdominal Pain: Common, related to acidosis and possible gastroparesis.

Additional Signs: Acetone breath, hypotension, tachycardia, altered mental status (in severe cases).

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Diagnosis

Criteria for DKA:

Hyperglycaemia: Blood sugar levels >13.9 mmol/L (250 mg/dL), typically <44 mmol/L.
Metabolic Acidosis: pH <7.3, HCO3 <15.
Ketosis: Serum ketones >3 mmol/L or positive urine ketones.

Severity Classification (Mild, Moderate, Severe):

Mild: pH 7.25–7.3, HCO3 15–18.
Moderate: pH 7.00–7.24, HCO3 10–15.
Severe: pH <7.00, HCO3 <10.

Additional Diagnostics:

Electrolytes: Check for hyperkalaemia or hypokalaemia, hyponatraemia.
Serum Osmolality: Helps differentiate from Hyperosmolar Hyperglycemic State (HHS).
ECG: Monitor for arrhythmias related to electrolyte imbalance.
Additional Tests: Infection screen (FBC, blood cultures, urine cultures, CXR), autoantibodies for T1DM.

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Management

Initial Steps (ABC)

Airway, Breathing, Circulation: Stabilise vitals, and transfer to a tertiary hospital if needed.
Fluid Resuscitation:
- IV Normal Saline 0.9% (500 mL over 10–15 min if hypotensive).
- Gradual replacement with 5% Dextrose when blood glucose <12 mmol/L.

Electrolyte Correction

Potassium Replacement:
- Monitor and replace K+ based on serum levels.
- Caution: insulin lowers serum K+, increasing hypokalaemia risk.
Bicarbonate: Reserved for severe acidosis (pH <6.9) due to risk of cerebral oedema.
Phosphate: Generally not replaced unless severe hypophosphatemia.

Insulin Therapy

Initiate IV insulin infusion (Actrapid 0.1 units/kg/hr).
Aim to reduce serum glucose by 3-6 mmol/hr.
Transition to subcutaneous insulin once stable.

Monitoring

Blood glucose and electrolytes every 1–2 hours.
Monitor for signs of cerebral oedema, especially if rapid correction is needed.

Search for Precipitating Factors

Common triggers: infection, non-compliance with insulin, new onset of diabetes.
Investigate underlying causes, e.g., infection (urine M/C/S, blood cultures), AMI (ECG), pancreatitis (lipase), etc.

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Complications

Cerebral Oedema

Typically presents 6–12 hours after initiation of therapy.
Symptoms: Headache, altered mental status.
Management: Head elevation, reduce IV fluids, 20% mannitol if necessary.

Electrolyte Imbalance

Hyperkalaemia/hypokalaemia.
Hypoglycaemia due to insulin therapy.

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Notes:

Mortality Rate: <5% with prompt management.
Patient Education: Reinforce the importance of regular insulin use, monitoring, and sick day management to prevent recurrence.

DKA is a medical emergency that requires prompt recognition and management.

Close monitoring and electrolyte management are essential to prevent complications.
Treatment may require additional adjustments based on underlying triggers or concurrent infections.

Hyperosmolar Hyperglycaemic State (HHS)

Presentation

Predominantly occurs in older adults with Type 2 Diabetes Mellitus (T2DM).

Develops over several days to weeks.
Due to a relative insulin deficiency:
- Causes marked hyperglycaemia → increased serum osmolality.
- Leads to severe dehydration as water is drawn from cells to balance osmotic pressure.

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Key clinical features:

Severe dehydration with significant polyuria and polydipsia.
No abdominal pain (as acidosis, seen in DKA, is generally absent).
High risk of neurological symptoms (confusion, lethargy) due to elevated osmolality.
Requires slow rehydration to mitigate the risk of cerebral oedema.

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Diagnosis

pH: Normal (>7.3).
Blood Glucose Levels (BSL): Usually >30 mmol/L.
Serum Ketones: Absent or only mildly elevated.
Plasma Osmolality: Elevated (>320 mOsm/kg).

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Treatment

Transfer & Monitoring

Arrange urgent transfer to the nearest tertiary hospital.
Establish access with two large-bore cannulas to facilitate simultaneous IV fluid and insulin administration.
Regular monitoring of serum osmolality and blood glucose hourly.

Fluid Management

Start IV normal saline for rehydration, aiming for gradual correction to avoid cerebral oedema.
Slow correction preferred in HHS vs. DKA due to increased risk of osmotic shifts causing cerebral oedema.

Insulin Therapy

Commence IV insulin infusion in consultation with a specialist or according to local protocol.
Avoid bolus doses and adhere to slow, careful titration.

Electrolyte Monitoring & Correction

Monitor potassium levels frequently and administer potassium chloride if potassium is low.
Insulin may need to be withheld if potassium is low, as insulin administration can further reduce serum potassium levels.

Infection Management

Investigate for and manage any underlying infection, which could be a precipitating factor.

Venous Thromboembolism Prophylaxis

High risk of thrombotic events due to hyperosmolarity and dehydration; initiate chemoprophylaxis for venous thromboembolism (VTE).

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Notes:

SLOW correction is critical in HHS compared to DKA to avoid complications such as cerebral oedema.
Always require input from an endocrinologist and transfer to a tertiary hospital for management.
Electrolyte Considerations:
- Potassium: Monitor closely as rehydration and insulin therapy can deplete potassium levels

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