NCLEX review on Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) for nursing lecture exams and the NCLEX exam. HHNS is a life-threatening condition of diabetes mellitus.
It is important to know the differences between diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) because the two complications affect the diabetic patient. However, there are subtle difference between the two conditions.
Don’t forget to take the hyperglycemic hyperosmolar nonketotic syndrome quiz.
In these notes you will learn about:
- Key Player of HHNS
Causes of HHNS
Signs and Symptoms of HHNS
Nursing Interventions of HHNS
Lecture on Hyperglycemic Hyperosmolar Nonketotic Syndrome
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) NCLEX Review
A.K.A: Hyperosmolar Hyperglycemic State (HHS)
Definition of HHNS: a life-threatening condition of a hyperglycemic state that affects patients with diabetes mellitus. It presents with an extreme high blood glucose which causes the blood to become very concentrated “hyperosmolar” but without the breakdown of KETONES (fats)
Therefore, clinically the patient will have HEAVY-DUTY HYPERGlYCEMIA and DEHYDRATION (due to the hyperosmolar)
Key Players of HHS:
Glucose: fuels the cells so they can function. However, the body is not using the glucose because there isn’t enough insulin to take it into the cell or the cells are insulin RESISTANT. Glucose levels will >600 mg/dL. The blood becomes very concentrated a.k.a. “hyperosmolar” due to the extra glucose. This causes water to pull from inside the cells which will result in cell dehydration and an even higher glucose level.
Insulin: helps take glucose into the cell so the body can use it for fuel. In HHNS, the cells are not receptive to the insulin or there isn’t enough because of an illness which limits its availability. Therefore, GLUCOSE can NOT enter into the cell and glucose floats around in the blood. However, because it happens in mainly type 2 diabetes there is SOME insulin present (but not all cells are not receptive to use it but some do) which prevents the breakdown of fats (you will not see ketones).
Kidneys: plays a role in reabsorbing glucose in the renal tubules. However, there is too much glucose to be reabsorbed so it leaks into the urine. This causes OSMOTIC DIURESIS which causes polyuria and excretion of electrolytes (sodium, potassium, chloride). This leads to MAJOR DEHYDRATION.
Important take-aways: NO KETOSIS or ACIDOSIS in HHNS because there is just enough insulin present that prevents the body from breaking down fats for energy; therefore there is no build-up of ketones.
Patients are going to present with HYPERGLYCEMIA and DEHYRDATION.
CAUSES of Hyperglycemic Hyperosmolar Nonketotic Syndrome:
Illness or infection (the patient isn’t aware their blood glucose is high because they haven’t been monitoring it)…most common in OLDER ADULTS
IMPORTANT: Happens gradually….remember glucose is going to be VERY VERY high (higher than glucose levels in DKA)
Remember the Mnemonics: HHNS (Heavy-duty HYPERGLYCEMA)
Signs & Symptoms of HHNS
- High glucose >600 mg/dL
- Polyuria
- Polydipsia
- Dehydrated: dry mucous membranes
- Fever
- Fatigue
- Mental status changes (confusion, seizures)
- Coma
Nursing Interventions for HHNS
Goal: Hydrate, decrease blood glucose, monitor potassium levels and for cerebral edema, correct acid-base imbalance (similar to the treatment of DKA)
However, HYDRATION will helps just as well as insulin due to the severe hydration experienced in HHNS. The fluids will help hydrate the cell which will decrease glucose levels and help with electrolyte balance.
- Administering IV fluids: (depending on MD order) such as 0.9% Normal Saline (start out with a bolus of this) and progress with 0.45% NS to hydrate the cells (depends on how dehydrated the patient is)…see the lecture on hypotonic, isotonic, and hypertonic solutions.
- 5% dextrose may be added to the 0.45% NS when glucose is around 250 to 300 mg/dL. This will help gradually bring the blood sugar down and help the insulin do its job by removing the ketones.
- Administered insulin REGULAR (only type given IV) and make sure K+ is normal >3.3
- Typically started out by giving unit IV bolus…then start an infusion (checking blood glucose levels around the clock…hospital protocols)…you will be titrating the insulin base on blood glucose checks.
- NOTE: if you rapidly bring a patient’s blood glucose down (or up) the brain can’t cope and water will be moved from the blood to the CSF and you will get cerebral edema and increased intracranial pressure.
- Tip: when priming tubing for insulin infusion waste 50cc to 100cc (per institution protocol) because insulin absorbs into the plastic lining of the tubing.
- NOTE: if you rapidly bring a patient’s blood glucose down (or up) the brain can’t cope and water will be moved from the blood to the CSF and you will get cerebral edema and increased intracranial pressure.
- Typically started out by giving unit IV bolus…then start an infusion (checking blood glucose levels around the clock…hospital protocols)…you will be titrating the insulin base on blood glucose checks.
- Watch potassium levels very closely because insulin causes K+ to move back into the cell
- Administer Potassium solution IV to combat this….note renal function before administering.