This episode breaks down the two most high-stakes endocrine emergencies every nurse must be able to recognize and treat fast: diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS/HHNK). You’ll learn the core physiological differences, the hallmark diagnostic markers, and the exact priority steps for managing each crisis safely at the bedside. We walk through the DKA triad (hyperglycemia + metabolic acidosis + ketones) and contrast it with HHS (extreme hyperglycemia + severe dehydration + high osmolality without acidosis). You’ll also master the DKA FIK sequence (Fluids → Insulin → Potassium), the potassium pitfalls that change priority order, the life-threatening complication of cerebral edema in HHS, and why HHS insulin therapy must be slow and carefully titrated. Two real-world scenarios drive home exactly what to do first, what labs to watch, and how to avoid the classic NCLEX traps like “insulin before potassium.” The episode closes with high-impact prevention strategies, sick-day rules, and the growing role of diabetes technology — including closed-loop insulin systems and continuous glucose monitoring — that are dramatically reducing DKA readmissions.
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COMPREHENSIVE NOTES
No insulin → body burns fat → ketones formed → metabolic acidosis
Deep, rapid Kussmaul respirations
Total body potassium depleted though serum may appear high
State of starvation + dehydration
HHS (Type 2 diabetic, relative insulin deficiency)
Some insulin remains → prevents ketones → no significant acidosis
Extreme hyperglycemia (often 600–1200+)
Severe dehydration + high serum osmolality
Slow onset, often in older adults
Hyperglycemia > 250
Metabolic acidosis
pH < 7.30
Bicarb < 18
Anion gap elevated
Ketones moderate to large (blood or urine)
HHS Diagnostic Markers
Extreme hyperglycemia > 600 (often > 1000)
Serum osmolality > 320
Minimal or no ketones, pH > 7.3
This is a major NCLEX priority sequence.
F – Fluids first
Severe dehydration: 4–6 liters lost
Start aggressive normal saline
About 1 liter in the first hour
Goal: restore perfusion and blood pressure quickly
I – Insulin second
Only after fluids have begun
Regular insulin IV bolus → insulin infusion
Critical NCLEX rule: Check potassium FIRST
K – Potassium last
Insulin drives potassium into cells → serum potassium drops fast
If potassium < 3.3 → HOLD insulin and replace potassium immediately
Begin potassium replacement once potassium < 5.2 AND urine output is present
When glucose reaches 200–250
Switch to D5 ½ NS
Purpose: prevent hypoglycemia while continuing insulin to clear ketones and acidosis
Fluid loss often 9–12 liters
More aggressive initial resuscitation than DKA
Start 0.9% normal saline, often 1–2 liters in the first hour
Lower dose: ~0.05–0.1 units/kg/hr
Begin only after fluid resuscitation
Target glucose drop: 50–70 per hour
Purpose: prevent cerebral edema, caused by rapid osmotic shifts
Hyperosmolar blood → massive thrombosis risk
Early low molecular weight heparin unless contraindicated
Fluid transition
Switch fluids when glucose reaches 250–300
Use 0.45% sodium chloride
Priority:
Start normal saline
Hold insulin
Immediate aggressive potassium replacement
Once potassium rises above 3.3 → start insulin infusion
NCLEX trap: Giving insulin first.
Scenario 2: HHS elderly patient, glucose 1250, osmolality 400
Priority:
Aggressive normal saline
Insert Foley catheter for hourly urine output
Start LMWH for clot prevention
Delay insulin until hydration improves
Then start low-dose insulin infusion slowly
Type 1 diabetics
Young adults
Those experiencing diabetes burnout
Patients omitting insulin doses
Any illness that increases metabolic demand
Discharge teaching essentials
Sick-day rules: Never skip insulin
Check blood glucose 4–10 times/day
Check ketones when glucose > 250
Continuous glucose monitors (e.g., Eversense 365)
Automated insulin delivery systems
Omnipod 5
iLet / Twist system
These systems significantly reduce DKA admissions (40–60%)
Nurses increasingly become educators and system managers rather than crisis responders
Imagine walking into a patient's room and seeing a blood sugar of like, 1,000 or even worse 2,000. These are the stakes in a diabetic crisis. So, welcome to Think Like a Nurse, the show where we take these really complex clinical concepts and well, we turn them into the high impact knowledge you need to save a life and of course ace your exams. We are so glad you're here. And this whole approach, you know, simplifying this dense highstakes material, that's really the foundation that our creator Brooke Wallace laid for us. I mean, as a 20 veteran ICU nurse, an organ transplant coordinator, a clinical instructor, and a published author. She built this resource specifically to give nursing students the clinical clarity they really deserve.
Speaker 1: Today, we are diving into that um that terrifying duo of endocrine emergencies, diabetic ketoacidosis, you know, DKA, right? And hyperosmoler hypoglycemic state or HHS. These are guaranteed test staples. But honestly, more importantly, mastering the rapid management for DKA and HHS is just it's absolutely crucial for your bedside competency. And before we jump in, just a reminder, if you want more structured study guides or practice questions, all those resources designed for efficiency, you can find them over at think like a nurse.org. We are really committed to your success.
Speaker 2: Okay, so let's start with a really foundational question because being able to quickly tell the difference between DKA and HHS, that is the very first step to thinking like a nurse in this scenario. What is that fundamental sort of non-negotiable physiological difference that separates them?
Speaker 1: It all comes down to insulin.
Speaker 2: Mhm.
Speaker 1: And because of that, it comes down to acid.
Speaker 2: Acid. Okay.
Speaker 1: DKA, which you see mostly in type 1 diabetes. It results from an absolute lack of insulin. Zero, right? And if there's no insulin, the body thinks it's starving, so it starts burning fat.
Speaker 2: That fat breakdown, lipolysis, it creates these things called ketone bodies.
Speaker 1: And those ketones are strong acids.
Speaker 2: Ah, so that leads directly to the severe metabolic acidosis.
Speaker 1: Exactly. So, DKA is high sugar plus this runaway production of acid. You often see those patients with the Kussmaul respirations, right? That deep rapid breathing because their body is literally trying to blow off CO2, the acid to compensate.
Speaker 2: That's it. The lungs are trying to save the kidneys. Now, contrast that with HHS.
Speaker 1: Okay, HHS is most common in older patients, usually with type two diabetes. The thing is, they still have some insulin left, just a little bit, just enough to suppress that fat breakdown and prevent a ton of ketones. But that small amount of insulin It's not nearly enough to control the blood sugar, which is why their glucose just skyrockets.
Speaker 2: So, no acid, but these just astronomical sugar levels, which leads to incredible diaresis and massive, massive fluid loss.
Speaker 1: Precisely. So, to summarize for students, DKA has this key diagnostic triad.
Speaker 2: Yeah, you have to memorize this. First, hypoglycemia, glucose over 250. Okay. Second, acidosis. So, a pH less than 7.30 or a bicarb less than 18. And third, ketones. moderate to large amounts in the blood or urine, the anion gap will be wide open, too, confirming that acidosis.
Speaker 2: Got it. Now, let's look at the HHS markers, which are just the they're defined by their sheer scale, right?
Speaker 1: They really are. HHS has three defining features, and the numbers are way more shocking. First, extreme hypoglycemia. We're not talking 400 or 500. We're talking glucose, often greater than 600.
Speaker 2: Wow.
Speaker 1: And it's not unusual to see 800, 1200, or even higher. That's incredible. And that causes the second key marker elevated serum osmolality usually over 320. I mean the body is just screaming for water at that point.
Speaker 2: And the third pillar is the absence of acid. So their pH is relatively stable greater than 7.3. Yeah. And ketones are negative or you know minimal.
Speaker 1: Exactly. DKA is a crisis of acid HHS. That's a crisis of osmolality and volume depletion.
Speaker 2: And that core distinction I imagine drives the entire treatment plan.
Speaker 1: Oh absolutely. Because if you confuse the management you can cause devastating harm.
Speaker 2: Okay let's move to that. The most testable most life saving sequence in nursing DKA treatment priorities. We talked about FIK: fluids, insulin, potassium. Why is that sequence FIK not just a helpful pneummonic but a mandatory order of operations?
Speaker 1: The order is so so critical because of what happens with potassium. But first, let's focus on the F fluids first. These patients are severely hypovolemic. I mean, they've often lost four to six liters of fluid. We have to correct that and improve profusion immediately.
Speaker 2: So, we start with 0.9% sodium chloride, normal saline, and we give it fast. What kind of dose are we talking in that first hour?
Speaker 1: We're talking aggressive doses. One liter per hour or maybe 15 to 20 ml per kilogram just in that initial resuscitation hour. We need to fill that vascular space fast. You know, stabilize their blood pressure, get their profusion back.
Speaker 2: Okay. So once fluids are running, then we move to I insulin. Second, we use regular insulin, IV bololis, then a continuous infusion. The testable critical rule here, and this gets so many students in trouble, is the timing.
Speaker 1: Yes, you must confirm fluids have started and critically you must know the current serum potassium level.
Speaker 2: Why is that?
Speaker 1: If you start insulin too early or if the potassium is already low, you risk causing ventricular arhythmias and that can be lethal.
Speaker 2: So why does insulin drop the potassium level so quickly?
Speaker 1: Because insulin is basically the key that unlocks the cell door. And when that insulin is running, it quickly drives both glucose and potassium back into the intracellular space.
Speaker 2: Ah, okay.
Speaker 1: And remember that paradox we talked about? DKA causes potassium to leak out of the cells. So it looks high in the bloodstream, but the total body store is actually depleted.
Speaker 2: So as the insulin starts working,
Speaker 1: the serum potassium level will plummet rapidly often to dangerous levels, which is why we hold insulin if the K+ is below 3.3 until we get that replacement running.
Speaker 2: Which brings us right to K potassium replacement third. So we have to monitor that serum potassium constantly. When do we actually start the potassium replacement?
Speaker 1: We start K plus replacement usually K L once the serum potassium falls below 5.2 and this is a big ang we have confirmed the patient has urine output.
Speaker 2: that makes sense urine output is vital because if the kidneys aren't working you can quickly build up toxic levels of the potassium you're giving them. Okay let's talk about the fluid transition you don't just keep giving normal saline forever right or you'd risk rebound hypoglycemia or other issues.
Speaker 1: exactly when the blood glucose reaches about 200 to 250 we have to change the IV solution to dextrose 5% in 0.45% sodium chloride, D5 half normal saline.
Speaker 2: And the goal there is just to keep them safe from hypoglycemia while you keep the insulin drip going.
Speaker 1: That's it. Because you often need to continue that insulin drip to clear the remaining ketones and fix the acidosis even after the glucose looks better.
Speaker 2: Let's run a quick scenario. We have a 25-year-old with type 1 diabetes. PH is 7.15 by carb 14, glucose 410, and their potassium is 3.0. What's the immediate overriding priority?
Speaker 1: Okay, so that K+ is 3.0. That's low. The overriding priority is potassium replacement. Full stop.
Speaker 2: So, you delay the insulin.
Speaker 1: You have to. Since their K plus is already below 3.3, we must delay the insulin infusion and start immediate aggressive potassium replacement while we're also starting those initial liters of .9% normal saline.
Speaker 2: And only then once the potassium is stable and climbing,
Speaker 1: then we introduce the insulin trip. That low K+ is a huge deviation from the standard FIK sequence. And honestly, it's a critical thinking trap on exams. the depth we need. Okay, now let's pivot to HHS management. You said HHS patients have a fluid deficit of like 9 to 12 L. I mean that's astronomical volume loss. How does that change our priorities?
Speaker 1: Well, the treatment for HHS is just
Speaker 2: yeah,
Speaker 1: it's hyperfocused on volume and osmolality correction and and it requires a much slower approach to glucose management to avoid a really deadly risk.
Speaker 2: And what's the number one priority?
Speaker 1: Priority one is still aggressive fluid replacement. Often even more aggressive than DKA. because of that sheer volume deficit. So we start with 0.9% sodium chloride sometimes 1 to 2 liters in the very first hour and the insulin is the dose different and what's the key complication we're trying to avoid by managing it differently.
Speaker 2: The insulin dose is generally lower than DKA something like 0.05 to 0.1 units per kilogram per hour and again you only start it after the fluids are running well but the vital difference is the target rate of the glucose drop. We need a slower drop rate here
Speaker 1: slower generally no more than 50 to 70 milligrams per deciliter per hour. M and the reason the whole reason is we are actively trying to avoid cerebral edema.
Speaker 2: Cerebral edema is yeah that's terrifying. It's caused by that rapid change in osmolality. Right. If we drop the blood sugar too fast in someone who's been profoundly hyper osmoler fluid just rushes into the brain cells.
Speaker 1: Exactly. The brain adapted to that high osmolality. If you drop it too fast you create this sudden concentration gradient and the brain it swells. This slower target is an HHS specific priority. And their fluid transition threshold is also higher I assume.
Speaker 2: Yes, it is. For DKA, we switch at 200 to 250. For HHS, we wait until the glucose gets down to 250 to 300 before we switch the IV fluid to 0.45% sodium chloride.
Speaker 1: The hyper viscosity of the blood in HHS also creates a specific major risk that you don't see as much in DKA. We're talking about clots.
Speaker 2: That's right. The extreme dehydration in that thick, sludgy blood, it greatly increases the risk of both Venus and arterial flosis.
Speaker 1: So, what do we do about that? low molecular weight heparin or LMWH. It has to be started early in the protocol for pretty much every HHS patient unless there's a specific contraindication that is a critical differentiating intervention.
Speaker 2: Okay, so let's run that second scenario. We have an 82-year-old history of type 2. He's lethargic, disoriented, glucose is, 1250, osmolality is 400, ketones are trace. What are your immediate bedside actions?
Speaker 1: Okay, immediate actions are start aggressive 0.9% normal saline. Insert a fully catheter for hourly urine output monitoring and administer that LMWH subcutaneously for thrombosis prophylaxis.
Speaker 2: and the insulin.
Speaker 1: We will hold or at least delay the insulin until the fluids have significantly lowered the osmolality and we've confirmed a stable fluid status. It's fluids, then anti-coagulation, then slow insulin.
Speaker 2: These acute protocols are obviously life-saving. But let's shift now into the real world and well prevention. Who are the most common patients you see walking through the ER doors with DKA and why? Okay.
Speaker 1: You know, in the trenches, you see a lot of type 1 patients who are young adults, college students, new parents, people under just significant stress. And this is often the manifestation of what we call diabetes burnout. They just get tired of the constant monitoring, the testing, the calculating, the injecting and they start omitting insulin doses or just stop monitoring altogether because they're completely overwhelmed.
Speaker 2: That's a huge psychological component that I think future nurses really need to understand. It's not just a physiological failure. It's a chronic disease management crisis.
Speaker 1: Exactly. And then when they get a minor illness like a cold or the flu, that stress response raises counter regulatory hormones which drives the glucose up even higher. And since they already miss their insulin, the DKA just spirals out of control so fast.
Speaker 2: So this is where education becomes prevention.
Speaker 1: It's everything.
Speaker 2: So if we're doing discharge teaching after we've stabilized them, what are the like three essential takeaways we need to drill into them to prevent a readmission?
Speaker 1: Okay, so first First and foremost, sick day rules are non-negotiable. They must never skip insulin even when they aren't eating because the body still produces glucose. Second, they have to check their blood glucose frequently. I mean, at least four, maybe up to 10 times daily.
Speaker 2: Okay?
Speaker 1: And third, and this is maybe the most vital for prevention, they must check for ketones if their glucose is consistently over 250. Checking for ketones is the early warning system that stops DKA before it requires an ICU bed.
Speaker 2: And this is where where the future of acute care and chronic care really intersect and where our sources get really exciting. We're moving from a system focused on managing the crisis to a system focused on preventing it with technology.
Speaker 1: Exactly.
Speaker 2: And the shift is it's revolutionary for nursing practice. We have seen DKA admissions drop significantly by like 40 to 60% in some groups precisely because of this advanced tech.
Speaker 2: Like what?
Speaker 1: Well, think about the implantable continuous glucose monitors like the Eversense 365. It lasts a full year and gives proactive And then there's the power of the closed loop systems, the automated insulin delivery systems.
Speaker 2: Yes, the Omnipod 5 or the Twist system. They're essentially acting as an artificial pancreas. They aren't just reading the glucose. They are actively adjusting and delivering micro doses of insulin based on predictive trends.
Speaker 1: Wow. This fundamentally changes the bedside nurse's role, especially in the outpatient setting. We move from being these reactive crisis managers who implement FIK when a patient's crashing to being high level systems managers and educators.
Speaker 2: So, we have to teach patients how to trust and troubleshoot the technology. The skills we need are expanding so fast from just pure physiology, the acid, the fluids, the potassium to integrating technological data streams, managing algorithms, and providing that profound psychological support to combat the burnout.
Speaker 1: It's about empowering the patient to keep themselves out of the hospital. You know, the success of the FIK protocol means you saved a life in the moment. That's huge. But the success of prevention technology, that means you gave them back months or years of quality unbburdened living. That's the bigger picture we need to focus on.
Speaker 2: That's the perfect distinction. And it leaves us with, I think, a provocative thought. As you master these rapid life-saving protocols like FIK, which is essential, how will you also leverage technology to shift your focus toward long-term management and truly prevent these crises from ever happening in the first place? You know, moving nursing practice forward. It's a challenge every future nurse is going to face. Your mastery of these topics really relies on recognizing those critical differences. DKA's acid versus HHS's osmolality and then correctly executing that DKA fluid insulin potassium sequence versus the HHS approach of aggressive fluids and that slower careful insulin. That knowledge is what gives you clinical confidence.
Speaker 1: That is the knowledge that truly helps you think like a nurse. Thank you so much for tuning in to this conversation and joining us. We invite you to check in for more conversations each week as we continue to break down these complex clinical topics. And remember to Visit think like a nurse.org for all the high yield resources you need to succeed.