DKA vs HHS

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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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