DKA vs HHS
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DKA (Diabetic Ketoacidosis) occurs primarily in T1DM, with absolute insulin deficiency driving ketone production, metabolic acidosis, and moderate hyperglycemia. HHS (Hyperosmolar Hyperglycemic State) occurs in T2DM with enough residual insulin to suppress ketosis but not hyperglycemia, leading to extreme glucose levels and severe dehydration without acidosis.
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I now have extensive information from both Goldman-Cecil Medicine and Rosen's Emergency Medicine. Here is the full comparison:
DKA vs HHS
Overview
| Feature | DKA | HHS |
|---|---|---|
| Typical patient | Type 1 DM (any age) | Type 2 DM, elderly |
| Onset | Hours to days | Days to weeks (longer prodrome) |
| Core defect | Absolute insulin deficiency | Relative insulin deficiency (enough to block ketosis, not hyperglycemia) |
| Mortality | ~5% | 8-25% (historically up to 40-70%) |
Pathophysiology
DKA: Absolute insulin deficiency + counter-regulatory hormone excess (glucagon, cortisol, epinephrine) drives three simultaneous processes:
- Hepatic gluconeogenesis and glycogenolysis → hyperglycemia
- Peripheral lipolysis → free fatty acids → hepatic ketone production (beta-hydroxybutyrate, acetoacetate, acetone)
- Osmotic diuresis → profound dehydration and electrolyte loss
The result is the classic triad: hyperglycemia + ketosis + metabolic acidosis.
HHS: Residual insulin is enough to suppress lipolysis and block significant ketone production, but not enough to control glucose. Extreme hyperglycemia drives a massive osmotic diuresis. The elderly/infirm cannot drink enough to compensate. Declining GFR eventually halts glucose excretion, compounding hyperglycemia. The profound dehydration produces the defining feature: severe hyperosmolality. - Goldman-Cecil Medicine, 26e; Rosen's Emergency Medicine, 10e
Diagnostic Criteria / Lab Findings
| Parameter | DKA | HHS |
|---|---|---|
| Blood glucose | >250 mg/dL (may be lower in euglycemic DKA) | >600 mg/dL (often >1000 mg/dL) |
| Arterial pH | <7.3 (mild 7.20-7.30; severe <7.00) | >7.30 (rarely drops below 7.30) |
| Serum bicarbonate | <18 mmol/L | >18 mmol/L |
| Serum osmolality | Mildly elevated | >320 mOsmol/L (markedly elevated) |
| Ketones | Strongly positive (urine 2+ or serum ≥3.0 mmol/L) | Absent or trace |
| Anion gap | Elevated (ketoacid accumulation) | Normal or mildly elevated |
| Sodium | Low/normal (dilutional from osmotic shift) | Normal or HIGH (severe dehydration) |
| Potassium | Normal/high at presentation, but total body depleted | More accurately reflects total body stores (less acidosis to shift K+ out of cells) |
Ketone testing caveat: Nitroprusside strips detect acetoacetate only - not beta-hydroxybutyrate (the dominant ketone in DKA). Results can be misleadingly low initially, then appear to worsen as treatment converts beta-hydroxybutyrate back to acetoacetate. Bedside capillary ketone monitors are preferred. - Goldman-Cecil Medicine, 26e
Clinical Features
| Feature | DKA | HHS |
|---|---|---|
| Kussmaul breathing | Yes (deep, rapid breathing to compensate acidosis) | No |
| Fruity/acetone breath | Yes | No |
| Abdominal pain | Common (can mimic acute abdomen) | Less common |
| GI symptoms (N/V) | Very common | Less common |
| Altered mental status | Present (correlates with osmolality) | Prominent - up to 10% in frank coma |
| Focal neurologic signs | Less typical | Common (hemisensory deficits, aphasia, extensor plantar reflexes) |
| Dehydration signs | Present | Profound (orthostatic hypotension, tachycardia, fever) |
| Seizures | Possible | Occur; phenytoin is CONTRAINDICATED (impairs endogenous insulin) |
| Thrombosis | Less common | Frequent - arterial and venous (hyperviscosity + dehydration) |
Precipitants (shared)
- Infections (most common)
- Inadequate insulin or non-adherence
- New-onset diabetes
- Acute coronary syndrome
- Drugs: corticosteroids, SGLt-2 inhibitors (euglycemic DKA), clozapine, olanzapine, thiazides, cocaine
- Other illness: CVA, PE, pancreatitis, thyrotoxicosis, Cushing syndrome
- ~20% of HHS patients have no prior diabetes diagnosis
Fluid & Electrolyte Deficits
| DKA | HHS | |
|---|---|---|
| Water | 3-5 L (adult) | Greater - often 8-10 L |
| Sodium | 5-10 mmol/kg | 5-10 mmol/kg or more |
| Potassium | Up to 7 mmol/kg (masked by acidosis) | Variable |
Treatment
Both conditions: Fluids first
- Volume restoration and adequate tissue perfusion is the top priority in both
- Isotonic crystalloid (NS or balanced crystalloid) for hemodynamic instability
- If in shock: fluids as fast as possible (adults) or 20 mL/kg boluses (children) until SBP ≥80 mmHg
Insulin
DKA: Continuous IV insulin infusion at 0.1 units/kg/hr is standard. Switch IV fluid to D5W/0.45% NS when glucose ≤300 mg/dL to prevent hypoglycemia while continuing insulin to clear ketones. Insulin must be continued until ketosis resolves (not just until glucose normalizes).
HHS: IV insulin infusion is NOT routinely required because residual insulin function exists. However, consider 0.1 units/kg/hr IV for very high glucose (>700 mg/dL) or in severely hypoperfused patients with erratic SC/IM absorption. Treatment is primarily directed at the underlying precipitant.
Electrolytes (both)
- Potassium: Replace before starting insulin if K+ <3.5 mEq/L (insulin drives K+ intracellularly and can cause life-threatening hypokalemia)
- Phosphate: Correct as needed
- Magnesium: 1-2 g MgSO₄ if low
Other HHS-specific points
- Subcutaneous heparin to reduce thrombosis risk (from hyperviscosity + dehydration)
- Phenytoin is contraindicated for seizures
- Treat the underlying precipitant aggressively
- Cerebral edema is a feared complication (especially fatal in children)
Intubation in DKA
- Avoid intubation if possible - patients have tremendous respiratory drive and matching their minute ventilation on a ventilator is challenging
- Intubate only if comatose or vomiting
- Once intubated, maintain hyperventilation to prevent worsening acidosis
Mixed DKA/HHS
A subset of T2DM patients with depressed endogenous insulin secretion present with features of both - high glucose AND mild-moderate ketoacidosis. Because portal insulin is still higher than in pure DKA, ketone production is quantitatively less. pH rarely drops below 7.30 in this overlap picture. - Goldman-Cecil Medicine, 26e
Key Mnemonic Summary
| DKA | HHS | |
|---|---|---|
| Who | T1DM, young | T2DM, elderly |
| Glucose | >250 | >600 |
| pH | <7.3 | >7.3 |
| Ketones | Yes | No |
| Osmolality | Mildly up | Markedly up (>320) |
| Bicarb | <18 | >18 |
| Kussmaul | Yes | No |
| Abdominal pain | Yes | No |
| CNS | Mild-moderate | Severe (coma in 10%) |
| Mortality | ~5% | 8-25% |
| Insulin Rx | Mandatory, continuous IV | Often not required; treat cause |
Sources: Goldman-Cecil Medicine, 26e; Rosen's Emergency Medicine, 10e
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