DKA vs HHS

Two diabetic emergencies. Both have sky-high glucose. One will kill with acid. The other with syrup.

Type 1 vs 2 background · Anion-gap acidosis · Hypoglycemia counterpart

Before we start · a patient just rolled in.

22-year-old with Type 1 diabetes. Found confused. Breathing deep and fast. Glucose is 480. pH is 7.1. Serum osmolality is 310.

What are you treating?

The One Thing to Remember

Both DKA and HHS are hyperglycemic emergencies. Both can kill. But they kill in completely different ways:

DKA · Death by Acid

No insulin at all. Body can't use glucose, so it burns fat instead. Fat breakdown produces ketone bodiesBeta-hydroxybutyrate, acetoacetate, and acetone. They're acids. Too many of them overwhelm the body's buffering capacity and tank the pH.. Ketones are acids. They accumulate. pH drops. The body is literally dissolving in its own acid.

Fruity breath = acetone being exhaled. Deep, fast breathing = Kussmaul respirations, desperately blowing off CO2.

HHS · Death by Syrup

Some insulin, but not enough. Enough to prevent ketosis (fat doesn't get burned), but not enough to handle glucose. Glucose climbs and climbs · 600, 800, 1200. The blood becomes thick as syrup.

Massive osmotic diuresis. Profound dehydration · often 8-10L depleted. Hyperosmolarity causes altered mental status, seizures, coma.

DKA = no insulin = ketoacidosis. HHS = some insulin = no ketosis but extreme hyperglycemia. 🔑 DKA Drops the pH. HHS Hikes the osmolality. The amount of insulin determines which emergency you get.

The Full Comparison

Every row is a potential board question. The differences are consistent and testable.

Feature DKA HHS
Diabetes type Usually Type 1 Usually Type 2
Onset Hours (rapid) Days to weeks (insidious)
Glucose 250-500 mg/dL >600 mg/dL (often >1000)
pH < 7.3 (acidotic) > 7.3 (normal-ish)
Ketones Elevated (positive) Minimal or absent
Serum osmolality Variable (~300-320) >320 (often >350)
Anion gap Elevated (AG metabolic acidosis) Normal
Mental status Usually alert (unless severe) Altered · confusion, seizures, coma
Breathing Kussmaul (deep, fast) Normal or shallow
Breath Fruity (acetone) Normal
Dehydration Moderate (3-5L deficit) Severe (8-10L deficit)
Mortality ~1-5% ~10-20% (higher)
Board Trap: DKA CAN happen in Type 2 diabetes. It's called "ketosis-prone Type 2" or "Flatbush diabetesOriginally described in African-American patients in Flatbush, Brooklyn. These patients present with DKA but are actually Type 2 · they can eventually come off insulin. The exam tests this to see if you automatically rule out DKA when you see "Type 2."." If the vignette says Type 2 but gives you pH 7.1 and positive ketones · it's DKA. Don't let the diabetes type fool you. 😀 The board LOVES putting "Type 2" at the top of the stem and waiting for you to rule out DKA. Don't do it. pH plus ketones plus AG makes the call. Diabetes type is just a label.

Sort the Features

Drag each feature into the correct bucket. Some belong to both.

Sorted: 0 / 0

DKA

HHS

Both

Treatment · The Steps That Save Lives

The treatment order matters. Get it wrong and you kill the patient a different way.

Fluids FIRST

Normal saline (0.9% NaCl) · 1-1.5L in the first hour. Both DKA and HHS are profoundly dehydrated. Fluids restore perfusion, improve renal function, and start lowering glucose before you even touch insulin. HHS is worse · 8-10L deficit. DKA is 3-5L. Both need fluids before anything else.

🔑 Fluids First. Always. Before insulin. Before potassium. Before anything.

Check Potassium BEFORE Insulin

Insulin drives K+ into cells. If K+ is already low (<3.3), giving insulin will tank it further → fatal arrhythmia. Always check K+ before starting insulin.

  • K+ < 3.3: Hold insulin. Replace K+ first.
  • K+ 3.3-5.3: Start insulin + give K+ simultaneously.
  • K+ > 5.3: Start insulin, hold K+ replacement.

Insulin Drip

Regular insulin IV · continuous infusion. Start at 0.1 units/kg/hr (after K+ is safe). Goal: lower glucose by 50-70 mg/dL per hour. Not faster · dropping glucose too fast causes cerebral edemaRapid glucose correction creates an osmotic gradient that pulls water into brain cells. Most dangerous in pediatric DKA. This is why we don't bolus insulin and rush the correction..

Switch to D5 + Insulin When Glucose Hits 200-250

In DKA, glucose will normalize before ketosis resolves. If you stop insulin when glucose normalizes, ketosis comes right back. So: add dextrose (D5) to the fluids and keep the insulin running until the anion gap closesThe anion gap reflects circulating ketoacids. When it normalizes (typically <12), the ketosis is resolved. That's when you can safely transition to subcutaneous insulin..

Monitor Everything

Glucose every hour. BMP every 2-4 hours (K+, bicarb, anion gap). Watch for complications: hypokalemia (most common cause of death during treatment), cerebral edema (especially peds DKA), hypoglycemia (overcorrection).

Board Trap: "The glucose is normal, stop the insulin!" · WRONG. In DKA, you keep insulin running until the anion gap closes, even if glucose is 150. Add dextrose to prevent hypoglycemia. Glucose normalizes before ketosis resolves. Stopping insulin early = rebound DKA. 💥 Glucose is a proxy. The anion gap is the actual disease marker. A normalized glucose with an open gap is like extinguishing the smoke alarm while the fire is still burning. The gap closes when the ketoacids are gone.

Decision Tree · Hyperglycemic Emergency Workup

A patient arrives with glucose >250. Walk through the algorithm.

Step 1: The glucose is 450. You check a pH and it comes back 7.18. Is this more consistent with DKA or HHS?

Right. pH < 7.3 = acidotic. DKA produces an anion gap metabolic acidosis from ketoacids. HHS has a pH > 7.3 (or normal). The acid is always the first branch point. Check pH, check ketones, check anion gap.
Not quite. pH of 7.18 is severely acidotic. HHS does NOT produce significant acidosis · there are enough insulin traces to prevent ketone production. If the pH is tanked, it's DKA. That's the first fork in every algorithm.

Step 2: Different patient. Glucose is 1100. pH is 7.38. Osmolality is 380. Ketones are trace. What is this?

Yes. The triad: glucose >600, osmolality >320, pH >7.3. Trace ketones are a trap · HHS CAN have mild ketosis. But "trace" is not the same as the significant ketosis of DKA. The pH is the tiebreaker. 7.38 is normal. This is HHS.
That's the trap. Yes, ketones are technically positive · but "trace" ketones can appear in HHS. The pH is 7.38 (normal), osmolality is 380 (massively elevated), and glucose is 1100. Every single number screams HHS. Don't let trace ketones distract you from the full picture.

Step 3: You've confirmed DKA. Glucose is 380, pH is 7.15. The patient is severely dehydrated. What do you do FIRST?

Always. Fluids first. 1-1.5L normal saline in the first hour. The dehydration is killing them as fast as the acid. Fluids restore perfusion, improve renal clearance, and start lowering glucose on their own. Insulin comes after K+ is checked.
Understandable impulse, but fluids first. Insulin without fluid resuscitation is dangerous · hypoperfused kidneys can't clear the ketoacids, and insulin drives K+ into cells when you don't even know the K+ level yet. The order is: fluids → check K+ → insulin.

Step 4: You're treating DKA. Glucose has come down to 220, but the anion gap is still 22. What do you do?

Exactly. The anion gap is still elevated = ketosis is still active. Stopping insulin now means rebound DKA. The move: add dextrose to the IV fluids (prevents hypoglycemia) and keep the insulin drip going until the gap closes (<12). Glucose is a number. The gap is the disease.
This is the classic board trap. Glucose normalizes before ketosis resolves. If you stop insulin when glucose hits 200, the ketones come right back. The anion gap is still 22 · the disease is still active. Add D5 to prevent hypoglycemia, keep insulin running until the gap closes.

Step 5: You're about to start insulin in DKA. The potassium comes back at 2.9. What now?

Critical. K+ < 3.3 = hold insulin until you replace it. Insulin drives K+ into cells. Starting insulin on a K+ of 2.9 could drop it to <2.0 → fatal cardiac arrhythmia. The K+ rules: <3.3 hold insulin, 3.3-5.3 start both, >5.3 start insulin alone.
Close, but not when K+ is this low. Simultaneous is correct for K+ 3.3-5.3. But at 2.9, you MUST replace K+ first before touching insulin. Insulin shifts K+ intracellularly · on an already depleted K+, that can be fatal. The cutoff is 3.3. Below that: hold. Above that: go.

Elimination Game · 5 Patients, 5 Diagnoses

Each clue eliminates a diagnosis. When only one remains, that's your answer.

Tap "Next Clue" to begin.

Clinical Vignettes

Eight patients just stumbled into the ED. Figure out what's killing them and how to stop it.

You got 0 out of 8.

The Lineup

Four hyperglycemic emergencies. Tap each card to flip.

⚡
DKA
The acidotic one. Glucose + ketones + anion gap.

DKA

  • Type: T1DM mostly
  • Glucose: >250 mg/dL
  • pH: <7.3 (acidosis)
  • HCO3: <18 mEq/L
  • Ketones: positive
  • Anion gap: >12
  • Breathing: Kussmaul (deep, labored)
  • Board pearl: Low serum Na is dilutional, not real salt loss
😶
HHS
The syrupy one. Extreme glucose, no ketones, obtunded.

HHS

  • Type: T2DM mostly
  • Glucose: >600 mg/dL
  • pH: normal (no acidosis)
  • Ketones: none/minimal
  • Osmolality: >320 mOsm/kg
  • Mental status: obtunded, seizures
  • Board pearl: Mortality higher than DKA because patients present late
💊
Euglycemic DKA
Normal glucose, but still acidotic. The sneaky SGLT2i trap.

Euglycemic DKA

  • Cause: SGLT2 inhibitors (canagliflozin, empagliflozin)
  • Glucose: normal or near-normal (<250)
  • Ketones: positive
  • Acidosis: present (anion gap)
  • Board pearl: SGLT2i must be stopped; glucose-based DKA criteria will miss this
  • Action: check ketones in any patient on SGLT2i who is ill
💩
Lactic Acidosis
High anion gap mimic. Check lactate, not just glucose.

Lactic Acidosis

  • Mimics: high anion gap acidosis like DKA
  • Differentiator: elevated lactate, not ketones
  • Causes: metformin toxicity, shock, ischemia, sepsis
  • Glucose: variable (not necessarily high)
  • Board pearl: metformin-associated lactic acidosis in renal failure is a classic stem
  • Action: stop metformin, treat underlying cause

Clinical Images

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Insulin syringe IV insulin infusion: 0.1 units/kg/hr for DKA/HHS treatment
Type 1 diabetes pathophysiology T1DM: absolute insulin deficiency drives DKA via unopposed lipolysis
Board-Style Walkthrough

Board-Style Walkthrough

Original board-style vignettes. Shuffled, never-repeat, full explanations for every choice.