- Severe Hyperglycemia without Ketoacidosis
- Type II Diabetes Mellitus – Acute Exacerbation
- Body has just enough insulin to prevent fatty acid breakdown
- Gradual onset → Infection, Stress, Dehydration
- Blood sugar > 600 mg/dL (usually higher)
- Negative Ketones
- Glycosuria (glucose dumps in urine)
- PROFOUND Dehydration
- Altered LOC
- Dry mucous membranes
- ↑ BUN, Creatinine
- Identify and treat cause
- #1 Priority = replace fluids
- MAY resolve the hyperglycemia as well
- Insulin Therapy
- Monitor neurological status
- Monitor and treat electrolyte imbalances
- Fluid & Electrolytes
- 2 large bore IVs
- Replace IV fluids (IVF) with LR or NS
- Monitor electrolytes & replace as needed
- Potassium may ↓ with insulin therapy
- May add KCl to IVF
- Glucose metabolism
- Insulin drip IV (Regular Insulin)
- SubQ sliding scale protocol (Novolog)
- Monitor blood sugars frequently (q1-2h)
- Continue to monitor blood sugars and take meds even on a sick day
- Do not skip doses of medications
- Signs and symptoms of hyperglycemia (before HHNS) to alert to a problem earlier
Cornell Note-Taking System Instructions:
- Record: During the lecture, use the note-taking column to record the lecture using telegraphic sentences.
- Questions: As soon after class as possible, formulate questions based onthe notes in the right-hand column. Writing questions helps to clarifymeanings, reveal relationships, establish continuity, and strengthenmemory. Also, the writing of questions sets up a perfect stage for exam-studying later.
- Recite: Cover the note-taking column with a sheet of paper. Then, looking at the questions or cue-words in the question and cue column only, say aloud, in your own words, the answers to the questions, facts, or ideas indicated by the cue-words.
- Reflect: Reflect on the material by asking yourself questions, for example: “What’s the significance of these facts? What principle are they based on? How can I apply them? How do they fit in with what I already know? What’s beyond them?
- Review: Spend at least ten minutes every week reviewing all your previous notes. If you do, you’ll retain a great deal for current use, as well as, for the exam.
For more information, visit www.nursing.com/cornell
This lesson is going to talk about HHNS.
HHNS stands for hyperglycemic hyperosmolar nonketotic syndrome. So that gives us a bit of a hint as to what’s going on, right? This is a state of severe hyperglycemia, except WITHOUT Ketoacidosis. It’s considered an acute exacerbation of Type 2 Diabetes Mellitus. Remember that the cell has two options for getting energy. One is through glucose and one is by breaking down fatty acids. Using glucose requires insulin, and breaking down fatty acids produces ketones. Remember from DKA that without any insulin, the body is forced to use the fatty acid route – causing acidosis. In Type 2 Diabetes, the body has JUST ENOUGH insulin, to prevent the body from using this option. BUT – still not enough to deal with the extremely high levels of blood glucose. So they get severely hyperglycemic, which sends them into a very hyperosmolar state because of the high concentration of glucose in the blood. It’s usually a gradual onset caused by infection, stress, or dehydration – or by them not taking their meds or making poor diet choices.
We’ll see in HHNS that these patients sugars are at least over 600, but the average is 1100, and I actually saw someone with a sugar over 1300 just last week. They’re usually VERY high. Now, the big thing you’ll notice is that they’re much higher than what we see with DKA, which is usually below 600. Why is that? Honestly, it’s because these HHNS patients don’t have acidosis. Once the acidosis hits in DKA, those patients start to feel very ill and they are very sick – so they go to the ER. In HHNS, these patients may feel a bit tired, or they may be extra thirsty, but since there’s no acidosis, their sugars just keep going higher and higher before they feel sick enough to be seen. Now, remember that in HHNS they will have negative ketones in their urine, but since their kidneys begin dumping the excess sugar, we’re going to see glycosuria or glucose in the urine. Fun fact, the threshold for glucose in the kidneys is about 180 mg/dL. Anything above that will dump glucose into the urine. When that happens, the water follows and we see polyuria or osmotic diuresis.
The other issue we see in HHNS, is the hyperosmolarity. Remember with all that extra sugar in the bloodstream, fluids are going to shift out of the cells and into the bloodstream to balance it out. So we see PROFOUND dehydration. And in HHNS, the sugars tend to be MUCH higher – so this osmotic shift is even more severe and the dehydration is much more significant in HHNS than it is in DKA. They will have dry mucous membranes and likely an elevated temp, and they’ll probably have an altered level of consciousness. The profound dehydration in the brain cells can cause confusion, agitation, lethargy, or even a coma. And, of course because of this severe dehydration and the stress on the kidneys, we’ll see their BUN and Creatinine elevate.
So, just like DKA we want to identify and treat the cause, especially if it was infectious. But our TOP priority in this case is going to be replacing those IV fluids. The dehydration and osmotic diuresis is profound in HHNS, so replacing lost fluids is the most important thing we can do. This may even correct the blood sugar for us, but most patients will need some insulin therapy. We either give Regular insulin IV OR we give Novolog SubQ, depending on the severity. So when it comes to NCLEX questions, you’ll see things like “start two large bore IVs” as part of your priorities, because fluids are so important. We also want to monitor their neuro status and their electrolytes. Again, insulin can drive potassium into the cells and they could become hypokalemic, so we need to consider replacing potassium if necessary. DKA patients may start hyperkalemic because of the acidosis and shift down, but HHNS patients aren’t acidotic – so their potassium starts from normal levels – so it will go down much faster. So we usually check chemistries every 2-4 hours on these patients, and we can add KCl to their IV fluids if needed.
Our top priority nursing concepts for a patient with hyperglycemic hyperosmolar nonketotic syndrome are fluid & electrolytes and glucose metabolism. Fluid replacement is #1, insulin is #2. Check out the care plan attached to this lesson to see more detailed nursing interventions and rationales.
Let’s recap. In HHNS, there is hyperglycemia and hyperosmolarity, but NO ketoacidosis because the body has JUST enough insulin to prevent the breakdown of fatty acids for energy. We see severe hyperglycemia, leading to glucose being dumped in the urine and causing a hyperosmolar state. This leads to osmotic diuresis and profound dehydration. Patients will be dry and hot and possible have an altered LOC. Our #1 priority is to correct the dehydration by replacing IV fluids. If needed, we’ll also give insulin therapy and monitor and replace potassium as needed.
So those are the things you need to know for HHNS – you can see how DKA and HHNS are similar, but the priorities are different, so, if you haven’t watched the DKA lesson yet, check that out as well. Don’t miss all the resources attached to this lesson, including a cheatsheet on the differences between DKA and HHNS. Now, go out and be your best selves today. And, as always, happy nursing!