Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)

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Nichole Weaver
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Included In This Lesson

Study Tools For Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)

HHNS Pathochart (Cheatsheet)
DKA vs HHNS (Cheatsheet)
Symptoms of Diabetes Mellitus (Image)
Treatment for DKA and HHNS (Image)
140 Must Know Meds (Book)
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Outline

Overview

  1. Severe Hyperglycemia without Ketoacidosis

Nursing Points

General

  1. Type II Diabetes Mellitus – Acute Exacerbation
    1. Body has just enough insulin to prevent fatty acid breakdown
  2. Gradual onset → Infection, Stress, Dehydration

Assessment

  1. Hyperglycemia
    1. Blood sugar > 600 mg/dL (usually higher)
    2. Negative Ketones
    3. Glycosuria (glucose dumps in urine)
  2. Hyperosmolarity
    1. PROFOUND Dehydration
    2. Altered LOC
    3. Dry mucous membranes
    4. ↑ BUN, Creatinine

Therapeutic Management

  1. Identify and treat cause
  2. #1 Priority = replace fluids
    1. MAY resolve the hyperglycemia as well
  3. Insulin Therapy
  4. Monitor neurological status
  5. Monitor and treat electrolyte imbalances

Nursing Concepts

  1. Fluid & Electrolytes
    1. 2 large bore IVs
    2. Replace IV fluids (IVF) with LR or NS
    3. Monitor electrolytes & replace as needed
    4. Potassium may ↓ with insulin therapy
      1. May add KCl to IVF
  2. Glucose metabolism
    1. Insulin drip IV (Regular Insulin)
    2. SubQ sliding scale protocol (Novolog)
    3. Monitor blood sugars frequently (q1-2h)

Patient Education

  1. Continue to monitor blood sugars and take meds even on a sick day
  2. Do not skip doses of medications
  3. Signs and symptoms of hyperglycemia (before HHNS) to alert to a problem earlier

 

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Transcript

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!

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Concepts Covered:

  • Test Taking Strategies
  • EENT Disorders
  • Prefixes
  • Suffixes
  • Disorders of the Adrenal Gland
  • Integumentary Disorders
  • Bipolar Disorders
  • Disorders of the Posterior Pituitary Gland
  • Hematologic Disorders
  • Immunological Disorders
  • Medication Administration
  • Musculoskeletal Disorders
  • Labor Complications
  • Musculoskeletal Trauma
  • Disorders of the Thyroid & Parathyroid Glands
  • Integumentary Important Points
  • Learning Pharmacology
  • Anxiety Disorders
  • Disorders of Pancreas
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  • Oncology Disorders
  • Somatoform Disorders
  • Dosage Calculations
  • Depressive Disorders
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  • Liver & Gallbladder Disorders
  • Upper GI Disorders
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  • Female Reproductive Disorders
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  • Shock
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Study Plan Lessons

12 Points to Answering Pharmacology Questions
Glaucoma
Glaucoma
54 Common Medication Prefixes and Suffixes
Addisons Disease
Burn Injuries
Burn Injuries
Cataracts
Cataracts
Nursing Care and Pathophysiology for Cushings Syndrome
Macular Degeneration
Macular Degeneration
Pressure Ulcers/Pressure injuries (Braden scale)
Pressure Ulcers/Pressure injuries (Braden scale)
Therapeutic Drug Levels (Digoxin, Lithium, Theophylline, Phenytoin)
Nursing Care and Pathophysiology for Diabetes Insipidus (DI)
Nursing Care and Pathophysiology for Disseminated Intravascular Coagulation (DIC)
Essential NCLEX Meds by Class
Nursing Care and Pathophysiology for Herpes Zoster – Shingles
Nursing Care and Pathophysiology for Herpes Zoster – Shingles
Nursing Care and Pathophysiology of Osteoarthritis (OA)
Nursing Care and Pathophysiology of Osteoarthritis (OA)
6 Rights of Medication Administration
Hearing Loss
Hearing Loss
Nursing Care and Pathophysiology of Osteoporosis
Nursing Care and Pathophysiology of Osteoporosis
Thrombocytopenia
Blood Transfusions (Administration)
Fractures
Fractures
Nursing Care and Pathophysiology for Hyperthyroidism
Integumentary (Skin) Important Points
Integumentary (Skin) Important Points
Nursing Care and Pathophysiology for Hypothyroidism
The SOCK Method – Overview
The SOCK Method – S
The SOCK Method – O
The SOCK Method – C
The SOCK Method – K
Anxiety
Basics of Calculations
Nursing Care and Pathophysiology of Diabetes Mellitus (DM)
Dimensional Analysis Nursing (Dosage Calculations/Med Math)
Generalized Anxiety Disorder
Leukemia
Diabetes Management
Lymphoma
Oral Medications
Post-Traumatic Stress Disorder (PTSD)
Nursing Care and Pathophysiology of Diabetic Ketoacidosis (DKA)
Injectable Medications
Oncology Important Points
Somatoform
Hyperglycaemic Hyperosmolar Non-ketotic syndrome (HHNS)
IV Infusions (Solutions)
Complex Calculations (Dosage Calculations/Med Math)
Mood Disorders (Bipolar)
Depression
Paranoid Disorders
Personality Disorders
Cognitive Impairment Disorders
Eating Disorders (Anorexia Nervosa, Bulimia Nervosa)
Alcohol Withdrawal (Addiction)
Grief and Loss
Suicidal Behavior
Nursing Care and Pathophysiology for Acquired Immune Deficiency Syndrome (AIDS)
Nursing Care and Pathophysiology for Anaphylaxis
Benzodiazepines
MAOIs
SSRIs
TCAs
Insulin
Histamine 1 Receptor Blockers
Histamine 2 Receptor Blockers
Renin Angiotensin Aldosterone System
ACE (angiotensin-converting enzyme) Inhibitors
Angiotensin Receptor Blockers
Calcium Channel Blockers
Cardiac Glycosides
Metronidazole (Flagyl) Nursing Considerations
Ciprofloxacin (Cipro) Nursing Considerations
Vancomycin (Vancocin) Nursing Considerations
Anti-Infective – Penicillins and Cephalosporins
Atypical Antipsychotics
Autonomic Nervous System (ANS)
Sympathomimetics (Alpha (Clonodine) & Beta (Albuterol) Agonists)
Parasympathomimetics (Cholinergics) Nursing Considerations
Parasympatholytics (Anticholinergics) Nursing Considerations
Diuretics (Loop, Potassium Sparing, Thiazide, Furosemide/Lasix)
Epoetin Alfa
HMG-CoA Reductase Inhibitors (Statins)
Magnesium Sulfate
NSAIDs
Corticosteroids
Hydralazine (Apresoline) Nursing Considerations
Nitro Compounds
Vasopressin
Dissociative Disorders
Proton Pump Inhibitors
Schizophrenia
Nursing Care and Pathophysiology for SIADH (Syndrome of Inappropriate antidiuretic Hormone Secretion)