Diabetic Emergencies (DKA and HHS)
<3.3
Critical K+
Replace potassium BEFORE insulin at this level
<7.30
DKA pH
Acidotic threshold
>320
HHS Osmolality
mOsm/kg defines HHS
DKA vs HHS Comparison
same family, very different presentationsDKA
- Type Usually Type 1
- Glucose 250-600 mg/dL
- pH Less than 7.30
- Ketones Present (positive)
- Osmolality Variable
- Signs Kussmaul breathing, fruity breath, abdominal pain
HHS
- Type Usually Type 2
- Glucose Often greater than 600 mg/dL
- pH Usually greater than 7.30
- Ketones Minimal to absent
- Osmolality Greater than 320 mOsm/kg
- Signs Severe dehydration, altered mental status, seizures
Treatment Priorities
Replace potassium BEFORE starting insulin if K+ is less than 3.3 mEq/L. Insulin drives K+ intracellularly and can cause fatal hypokalemia.
Aggressive IV fluid resuscitation (NS 1-1.5 L/hr initially, then adjust)
Check potassium immediately
If K+ <3.3, replace potassium BEFORE insulin. If 3.3-5.3, give K+ with insulin. If >5.3, hold K+ and recheck in 2 hours
Continuous insulin infusion (0.1-0.14 units/kg/hr)
When glucose reaches 200-250, add dextrose to IVF and continue insulin until anion gap closes
Overlap subQ insulin 1-2 hours before stopping drip
Key Values to Memorize
K+ <3.3 = replace first
DKA pH <7.30
HHS osmolality >320
Add D5 at glucose 200-250
Anion gap guides insulin drip
Overlap subQ 1-2 hrs
potassium timing is the #1 tested concept, get it right
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Practice CCRN QuestionsExam Traps
Potassium BEFORE insulin if K+ is less than 3.3
Insulin drives potassium intracellularly. Starting insulin when potassium is already critically low can cause fatal hypokalemia with cardiac arrest. The exam LOVES this question. Replace potassium to at least 3.3 before initiating the insulin drip.
Do not stop the insulin drip when glucose normalizes
The insulin drip treats the acidosis, not just the hyperglycemia. When glucose drops to 200-250 mg/dL, add dextrose to the IV fluids and continue the drip until the anion gap closes. Stopping insulin prematurely causes acidosis rebound.
HHS has HIGHER mortality despite less acidosis
HHS presents with extreme hyperosmolarity (>320 mOsm/kg) and severe dehydration. Patients are often older with more comorbidities. The lack of significant acidosis is deceptive because the mortality is actually higher than DKA.
Potassium Timing
The exam LOVES asking about potassium timing. If K+ is less than 3.3, replace BEFORE starting insulin. This is non-negotiable.
Anion Gap Guides the Drip
Switch from drip to subQ when anion gap closes, NOT when glucose normalizes. The gap matters more than the glucose number.
The body cannot use glucose for fuel (no insulin key to unlock the cells). It burns fat instead, creating acidic ketone byproducts. Think of it like battery acid leaking everywhere. The blood becomes dangerously acidic, the patient breathes fast (Kussmaul) trying to blow off the acid, and the breath smells fruity from ketones.
The battery is not leaking acid (minimal ketones) but it is completely drained of water. Glucose climbs to extreme levels (often >600 mg/dL), pulling massive amounts of water out of cells through osmosis. The blood becomes thick and concentrated. Patients develop severe dehydration and altered mental status.
Both need the same first step: fluids, fluids, fluids. Aggressive IV normal saline rehydrates the patient and starts bringing glucose down even before insulin. Then check potassium. Then start insulin. The order matters because insulin without potassium or fluids can be fatal.
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