Key Differences Between DKA and HHS
DKA and HHS are distinct hyperglycemic emergencies that differ primarily in the degree of ketoacidosis, glucose elevation, and osmolality—with DKA characterized by severe acidosis and ketosis at lower glucose levels, while HHS presents with extreme hyperglycemia and hyperosmolarity without significant ketosis. 1
Laboratory Diagnostic Criteria
Glucose Levels
- DKA: Plasma glucose typically >250 mg/dL 2, 1
- HHS: Plasma glucose markedly elevated, usually >600 mg/dL 2, 1
Acid-Base Status (The Critical Distinguishing Feature)
- DKA: Arterial pH ranges from <7.00 (severe) to 7.25-7.30 (mild), with serum bicarbonate <10 to 15-18 mEq/L 2, 1
- HHS: Arterial pH typically >7.30 with serum bicarbonate >15 mEq/L 2, 1
Ketone Bodies
- DKA: Positive serum and urine ketones (the defining feature) 2, 1
- HHS: Small or absent ketones in serum and urine 2, 1
Osmolality and Anion Gap
- DKA: Variable effective serum osmolality; anion gap elevated (>10-12 mEq/L) 2, 1
- HHS: Effective serum osmolality >320 mOsm/kg (calculated as 2[measured Na+] + glucose/18); anion gap variable 2, 1
Clinical Presentation Differences
Time Course of Development
- DKA: Develops rapidly, typically within 24 hours 2, 1
- HHS: Evolves slowly over several days to weeks 2, 1
Physical Examination Findings
- DKA: Kussmaul respirations (deep, rapid breathing to compensate for acidosis), abdominal pain and vomiting in up to 25% of patients (may include coffee-ground emesis from hemorrhagic gastritis) 2, 1
- HHS: More profound dehydration with poor skin turgor, absence of Kussmaul respirations, less frequent abdominal pain 2, 1
Mental Status Alterations
- DKA: Ranges from alert to stupor/coma, but alertness more common 2, 1
- HHS: Stupor/coma significantly more frequent due to extreme hyperosmolarity 2, 1, 3
Pathophysiologic Mechanisms
Insulin Deficiency Severity
- DKA: Absolute or severe relative insulin deficiency leads to uncontrolled lipolysis, release of free fatty acids, and hepatic ketogenesis 2, 4
- HHS: Residual insulin action sufficient to prevent significant ketogenesis but inadequate to control hyperglycemia 1, 5
Counterregulatory Hormones
Both conditions involve elevated glucagon, catecholamines, cortisol, and growth hormone, leading to increased hepatic/renal glucose production and impaired peripheral glucose utilization 2, 4
Management Approach Differences
Fluid Therapy Priority
- DKA: Fluid therapy important but insulin is the cornerstone of treatment 5
- HHS: Fluid replacement is the cornerstone of therapy, generally requiring more aggressive volume resuscitation (15-20 mL/kg/hr initially) 1, 5
Bicarbonate Therapy
- DKA: May require bicarbonate therapy in severe cases with pH <7.0 1
- HHS: Bicarbonate therapy rarely needed 2
Rate of Correction
- DKA: Can correct metabolic abnormalities more rapidly in adults 5
- HHS: Requires slower, more cautious correction to avoid complications, particularly in elderly patients 5
Mortality and Prognosis
- DKA mortality: Approximately 5% in experienced centers, <1% in some series 1, 3
- HHS mortality: Approximately 15%, roughly 10-fold higher than DKA 1, 3
- Prognosis worsened by extremes of age, coma, hypotension, and severity of dehydration 1
Mixed Presentations
Up to one-third of patients may present with overlapping features of both DKA and HHS, requiring tailored management based on the prominent clinical features present 5, 6. These mixed cases are managed using the same three-pronged approach (fluids, insulin, electrolytes) but with adjustments based on the severity of acidosis, dehydration, and osmolarity 5, 6.
Critical Pitfall to Avoid
The most common precipitating factor for both conditions is infection, which must be actively identified and treated 2, 1, 4. Patients can be normothermic or even hypothermic despite infection due to peripheral vasodilation; hypothermia is a poor prognostic sign 2.