Hyperglycemia is defined as an excess of glucose in the bloodstream and is present when the blood glucose level is above 125 mg/dL after fasting for eight hours, or above 180 mg/dL two hours after eating. Hyperglycemia occurs due to three core reasons:

  • reduced insulin secretion (this is the main reason)
  • decreased ability to utilize glucose
  • increased glucose production

Insulin resistance is when the cells don't respond appropriately to insulin, and can't easily take up or utilize glucose. Experts believe visceral fat, family history of Type 2 DM, and being inactive are causes of insulin resistance.

While we typically associate hyperglycemia with diabetes mellitus, one does not have to have diabetes to have incidences of elevated blood glucose. Some common non-diabetic reasons a patient could have hyperglycemia are:

  • Stress-induced hyperglycemia – Any kind of trauma or significant illness is going to cause a stress response in the body. This causes activation of the SNS, elevated cortisol levels, elevated circulating catecholamines, enhanced gluconeogenesis and glycogenolysis (basically increased glucose production) and insulin resistance. The evidence shows that up to 30% of individuals who’ve suffered a trauma can have blood glucose levels greater than 200 mg/dL. Common causes of SIH are infection, sepsis, trauma, head injury, surgery and burns.
  • Cushing’s – Cushing’s Disease occurs when there’s an excess of cortisol hormone, which, in turn, leads to hyperglycemia. Read this post to learn more about Cushing’s Disease.
  • Polycystic ovarian syndrome (PCOS) – The higher-than-normal testosterone levels that occur with PCOS will stimulate insulin production leading to insulin resistance and hyperglycemia. Over time, individuals with PCOS can develop Type 2 diabetes mellitus.
  • Pancreatitis – In chronic pancreatitis patients have decreased insulin secretion, especially as the disease progresses. The pathophysiology of acute pancreatitis and how it relates to hyperglycemia is less clear. However, studies show correlations between elevated glucagon levels with insulin levels low in relation to the blood glucose.
  • Cancer – Pancreatic cancer has been shown to be a contributing factor in hyperglycemia. Additionally, therapies (such as chemotherapy) utilized in cancer treatment can cause hyperglycemia.
  • Cystic fibrosis – the thick mucus in cystic fibrosis leads to scarring of the pancreas, which impairs its ability to produce the appropriate amount of insulin. Read this post to learn more about cystic fibrosis.
  • Enteral or parenteral nutrition – Since most individuals receiving enteral or parenteral nutrition are hospitalized, the hyperglycemia is thought to be associated with the stress response. Additionally, these individuals are often on bedrest, which is associated with reduced glucose uptake and reduced insulin signaling in the tissues. Another consideration is the high amount of glucose in these therapies, especially parenteral (TPN). In fact, studies show that up to 88% of patients receiving TPN in the hospital setting have elevated blood glucose levels.
  • Obesity – The relationship between obesity and hyperglycemia is complex. The short version is that obesity leads to inflammation which leads to insulin resistance. As excess nutrition is consumed (and thereby, excess glucose), the body is going to try to keep blood sugar in the normal range by secreting insulin from the pancreas. Over time, the cells become less and less sensitive to insulin, meaning the insulin is not “unlocking” the cell to allow glucose to enter. 
  • Medications – There are quite a few medications that cause hyperglycemia. Common drug categories are corticosteroids (ex: prednisone), thiazide diuretics (ex: hydrochlorathiazide), beta-blockers (ex: metoprolol), fluoroquinolone antibiotics (ex: gatifloxacin) and second-generation antipsychotics (ex: olanzapine).

Complications of Hyperglycemia

There are many complications associated with hyperglycemia. Namely these are increased risk for infection, delayed wound healing, nerve damage leading to neuropathy, foot complications that can impair mobility, renal disease, hypertension, cardiovascular disease and stroke. Additionally, microvascular damage can ultimately result in retinopathy that can lead to significant visual impairment or blindness. Damage to nerves and reduced blood flow to the genitals and bladder can lead to sexual and bladder dysfunction as well. 

In the inpatient setting (especially the ICU), hyperglycemia is associated with increased morbidity and mortality. Managing blood glucose levels in these patients has shown to reduce the incidence of acute renal failure, sepsis, critical-illness polyneuropathy and the need for blood transfusions.

Additionally, studies show that hyperglycemia in patients with neurological injury is associated with much poorer outcomes, increased ICU stay and increased risk of significant disability and death. In ischemic stroke it is associated with expanding areas of infarction. And, if thrombolytics are given, a higher risk of hemorrhagic conversion.

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life-threatening emergencies that require immediate intervention.

Now that you have a baseline understanding of hyperglycemia, let’s explore it further using the Straight A Nursing LATTE method.

L: How does the patient LOOK?

The signs/symptoms of hyperglycemia are typically more subtle than those of hypoglycemia, and aren’t usually present until blood glucose levels are significantly elevated. In most cases, the patient will be unaware of the elevated blood glucose unless the level are in the 270-360 mg/dL range for an extended period of time. The classic signs of hyperglycemia are polyphagia, polydipsia, and polyuria. Patients may also complain of blurred vision, nausea, vomiting, abdominal pain, weakness. In DKA the patient may have fruity-smelling breath and rapid, deep breathing called kussmaul respirations.

A: How do you ASSESS the patient?

Assess all patients with blood glucose abnormalities for altered level of consciousness and confusion. Additionally:

  • Assess intake and output – these patients will have increased thirst and increased urine output
  • Assess for polyphagia – inquire how much the patient eats or if they feel “always hungry”
  • Assess for risk factors for developing hyperglycemia such as critical illness, parenteral nutrition, culprit medications, etc..
  • Assess for complications of hyperglycemia such as wounds that are not healing, impaired vision, neuropathy, and neuropathic pain.
  • Assess the patient’s feet as many patients with chronic hyperglycemia easily develop wounds that go unnoticed due to the neuropathy.
  • Monitor vital signs as many times hyperglycemia accompanies a severe infection or can progress into DKA or HHS. These patients will be very ill and likely require intensive care.

T: What TESTS will be conducted? 

  • Blood glucose – Blood glucose can be measured at the bedside with a glucometer, which is capable of reading levels within a specific range. This range will vary by the device used. If the blood glucose level falls below or above this range, the device simply displays a value of “low” or “high”. If the blood glucose level is not detectable by the glucometer, it will need to be measured via a traditional lab draw.
    • Fasting blood glucose – This test measures the glucose level after a period of not eating (typically overnight). A fasting blood glucose less than or equal to 99 mg/dL is normal, a level between 100 and 125 mg/dL is considered prediabetes, and a level above 125 mg/dL is considered to be diabetes.
    • Random blood glucose – This test measures the glucose level at a random time not related to meal times. A level above 200 mg/dL is diagnostic for diabetes.
    • Glucose tolerance test – This test measures your blood glucose level after ingesting a specified amount of glucose. Tests are typically conducted 1, 2 and maybe also 3 hours after ingesting the glucose. If, at the 2-hr check, the blood glucose is below 140 mg/dL this is a normal result. If it is between 140 to 199 mg/dL at that two hour mark, this is considered prediabetes, and anything at 200 mg/dL and above is diabetes.
  • HbA1c (also known as glycosylated hemoglobin) tells us about the level of blood glucose present in the bloodstream over the past 120-days (which is the lifespan of a red blood cell). A normal level is < 5.7%, a level between 5.7 and 6.4% indicates prediabetes is present, and a level above 6.5% is indicative of diabetes.
  • DKA and HHS are unique circumstances that require intensive care and monitoring. To learn more about those conditions and the many lab tests that are conducted, check out this episode.

T: What TREATMENTS are provided?

The main treatment for elevated blood glucose is insulin. In the clinical setting, we typically don’t give any insulin until the blood glucose gets above 150 mg/dL. However, this can vary drastically based on MD practice and patient condition. For example, neuro patients and those who have had open heart surgery will typically have their blood glucose more closely managed. 

To learn more about medications used to treat hyperglycemia, check out this post.

E: How do you EDUCATE and EVALUATE?

Education for hyperglycemia will be tailored to the patient and the cause. For patients with diabetes, there will be a wealth of teaching such as: 

  • How to measure blood glucose levels
  • Proper nutrition for diabetes
  • Diabetes foot care
  • When to seek medical care (such as with DKA)
  • How to manage blood glucose when ill (a “sick-day” protocol).

For patients with transient or non-diabetic hyperglycemia, teaching will be focused on avoiding future occurrences (if possible) and on the treatments being provided in the in-patient setting. For example, a question many patients with stress-induced hyperglycemia will ask is “Why am I getting insulin? I don’t have diabetes.” so your teaching will be focused on the need for blood glucose management as a way to prevent complications.

How do you evaluate the effectiveness of your interventions? In hyperglycemia, the goal is euglycemia (a normal blood glucose level). Other indicators that your intervention has been effective could be: 

  • The patient is free of hyperglycemic complications after surgery
  • The patient states an understanding of the need for insulin while receiving TPN
  • HbA1c < 5.7%


The information, including but not limited to, audio, video, text, and graphics contained on this website are for educational purposes only. No content on this website is intended to guide nursing practice and does not supersede any individual healthcare provider’s scope of practice or any nursing school curriculum. Additionally, no content on this website is intended to be a substitute for professional medical advice, diagnosis or treatment.


American Diabetes Association. (n.d.). Foot Complications. Retrieved January 10, 2022, from https://www.diabetes.org/diabetes/foot-complications

American Diabetes Association. (n.d.). Hyperglycemia (High blood glucose). American Diabetes Association. https://www.diabetes.org/healthy-living/medication-treatments/blood-glucose-testing-and-control/hyperglycemi

Basile, L. M. (n.d.). The Link Between PCOS and Diabetes—Polycystic ovary syndrome is associated with increased risk for diabetes. Here, learn why that is—And how you can help prevent it. Retrieved January 16, 2022, from https://www.endocrineweb.com/polycystic-ovary-syndrome-pcos/link-between-pcos-diabetes

Donahue, A. (n.d.). 10 Causes of Blood Sugar Rises in Non-Diabetics [Non-Diabetic Hyper and Hypoglycemia]. Retrieved January 16, 2022, from https://www.nutrisense.io/blog/what-causes-blood-sugar-to-rise-in-non-diabetics

Drugs.com. (n.d.). Nondiabetic Hyperglycemia—What You Need to Know. Retrieved January 16, 2022, from https://www.drugs.com/cg/nondiabetic-hyperglycemia.html

Frontera, J. A., Fernandez, A., Claassen, J., Schmidt, M., Schumacher, H. C., Wartenberg, K., Temes, R., Parra, A., Ostapkovich, N. D., & Mayer, S. A. (2006). Hyperglycemia After SAH. Stroke, 37(1), 199–203. https://doi.org/10.1161/01.STR.0000194960.73883.0f

Gosmanov, A., & Umpierrez, G. (n.d.). Management of Hyperglycemia During Enteral and Parenteral Nutrition Therapy. Retrieved January 10, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746491/

Goyal, N., Kaur, R., Sud, A., Ghorpade, N., & Gupta, M. (2014). Non Diabetic and Stress Induced Hyperglycemia [SIH] in Orthopaedic Practice What do we know so Far? Journal of Clinical and Diagnostic Research : JCDR, 8(10), LH01–LH03. https://doi.org/10.7860/JCDR/2014/10027.5022

Hwangbo, Y., & Lee, E. K. (2017). Acute Hyperglycemia Associated with Anti-Cancer Medication. Endocrinology and Metabolism, 32(1), 23–29. https://doi.org/10.3803/EnM.2017.32.1.23

Kahn, B. B., & Flier, J. S. (2000). Obesity and insulin resistance. Journal of Clinical Investigation, 106(4), 473–481.

Kahn, S. E., Hull, R. L., & Utzschneider, K. M. (2006). Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature, 444(7121), 840–846. https://doi.org/10.1038/nature05482

Mecott, G. A., Al-Mousawi, A. M., Gauglitz, G. G., Herndon, D. N., & Jeschke, M. G. (2010). The Role of Hyperglycemia in Burned Patients: Evidence-Based Studies. Shock (Augusta, Ga.), 33(1), 10.1097/SHK.0b013e3181af0494. https://doi.org/10.1097/SHK.0b013e3181af0494

Obesity Medicine Association. (n.d.). Obesity & Insulin Resistance—How Are They Connected? OMA. Retrieved January 10, 2022, from https://obesitymedicine.org/obesity-and-insulin-resistance/

Pasquel, F. J., Spiegelman, R., McCauley, M., Smiley, D., Umpierrez, D., Johnson, R., Rhee, M., Gatcliffe, C., Lin, E., Umpierrez, E., Peng, L., & Umpierrez, G. E. (2010). Hyperglycemia During Total Parenteral Nutrition. Diabetes Care, 33(4), 739–741. https://doi.org/10.2337/dc09-1748

Rehman, A., Setter, S., & Vue, M. (n.d.). Drug-Induced Glucose Alterations Part 2: Drug-Induced Hyperglycemia | Diabetes Spectrum. Retrieved January 10, 2022, from https://diabetesjournals.org/spectrum/article/24/4/234/31830/Drug-Induced-Glucose-Alterations-Part-2-Drug

Sampayo, V., & Tofthagen, C. (2017). Hyperglycemia and Cancer: An Algorithm to Guide Oncology Nurses. Clinical Journal of Oncology Nursing, 21(3), 345–352. https://doi.org/10.1188/17.CJON.345-352

Solomon, S. S., Duckworth, W. C., Jallepalli, P., Bobal, M. A., & Iyer, R. (1980). The Glucose Intolerance of Acute Pancreatitis. 29, 5.

Stehouwer, C. D. A. (2018). Microvascular Dysfunction and Hyperglycemia: A Vicious Cycle With Widespread Consequences. Diabetes, 67(9), 1729–1741. https://doi.org/10.2337/dbi17-0044