Assessment & Treatment of Five Diabetic Emergencies

Common emergencies encountered in diabetics are important due to both their frequency and that they're often life-threatening. The complications include 1) diabetic ketoacidosis (DKA); 2) hyperosmolar hyperglycemic state (HHS); 3) hyperglycemia without obvious acidosis; 4) hypoglycemia; and 5) other selected medical emergencies in diabetes.
Patients experiencing a diabetic emergency should be placed on a cardiac monitor due to the potential for severe electrolyte disturbances. Photos courtesy Nashville Fire Department

Patients experiencing a diabetic emergency should be placed on a cardiac monitor due to the potential for severe electrolyte disturbances. Photos courtesy Nashville Fire Department

EMS calls for patients with diabetes are common for many reasons, including their increased risk for cardiac disease, cerebrovascular disease, pneumonia, infection and their many diabetic complications. Knowing and recognizing common emergencies encountered in diabetics is important due to both their frequency and that they are often life-threatening.

In this article, we focus on five diabetic emergencies: 1) diabetic ketoacidosis (DKA); 2) hyperosmolar hyperglycemic state (HHS); 3) hyperglycemia without obvious acidosis; 4) hypoglycemia; and 5) other selected medical emergencies in diabetes.

Learning Objectives

1. Know the five primary actions of insulin on the body.

2. Understand the causes of common diabetic emergencies often encountered in the prehospital setting.

3. Recognize the signs and symptoms of common diabetic emergencies.

Key Terms

Diabetes: A metabolic disorder that primarily results from absent or diminished insulin secretion by the pancreas or from defects of insulin receptors in the body. This causes an inability for the body to utilize glucose properly.

Hyperglycemia: Increased glucose in the blood, typically linked to diabetes.

Hypoglycemia: Decreased glucose in the blood, usually caused by excessive insulin or low food intake.

Insulin: Hormone released by the pancreas in response to increased levels of sugar in the body. It promotes transport and entry of sugar into muscle cells and other tissues, resulting in lower blood sugar levels.

Ketoacidosis: The presence of excessive amounts of organic acid and an increase of ketones in the blood, often occurring as a complication of diabetes. Symptoms are hyperventilation, a fruity odor of the breath, altered levels of consciousness, nausea, vomiting and dehydration.

Type 1 & Type 2 Diabetes

The pathophysiology of Type 1 and Type 2 diabetes are actually quite different, although their names suggest two subtypes of the same disease.

Type 1 diabetes, previously called juvenile-onset diabetes, usually begins in childhood and is often familial. In Type 1 diabetes, the body has an absolute lack of insulin.

Type 2 diabetes, previously referred to as adult-onset diabetes, is distinct from Type 1 in that cells in the body become resistant to insulin, but there are still some cells that still produce insulin. Most patients with Type 2 diabetes are older and have comorbid conditions such as obesity and hypertension.1,2 Unfortunately, there are a growing number of obese adolescents who are developing this “adult-onset” disease relatively early in their lives.

Patients with Type 2 diabetes usually take oral medications vs. insulin for treatment, whereas patients with Type 1 diabetes require insulin replacement therapy. In both types of diabetes, uncontrolled hyperglycemia is damaging to virtually all body tissue.

Severe hypoglycemia usually occurs when glucose is < 50 mg/dL and can lead to rapid deterioration and death if not corrected promptly.

Severe hypoglycemia usually occurs when glucose is < 50 mg/dL and can lead to rapid deterioration and death if not corrected promptly.

Diabetic Ketoacidosis (DKA)

Insulin is a hormone produced in the pancreas by beta cells. Although insulin has innumerable roles throughout the body, we find it best to focus on five main actions. (See Table 1.)

Table 1: Five major actions of insulin


Drives glucose into cells


Drives potassium into cells




Blocks fat breakdown


Blocks protein breakdown

The primary role of insulin is to facilitate the movement of glucose across cell membranes for use as an energy source. Additionally, it moves potassium into the cell, is anabolic and blocks the breakdown of proteins and fats.

Thus, lack of insulin results in hyperglycemia, hyperkalemia and a catabolic state where proteins are broken down into ketoacids, and fats are broken down into free fatty acids. All of these combined is what we know as DKA. (See Figure 1.)

Causes: Any situation arising in a diabetic that requires increased insulin without that demand being met can result in DKA.

There are several causes of DKA, which we remember by the “five I’s” of: 1) infection; 2) infarction; 3) infant on board (i.e., pregnancy); 4) indiscretion with sugar or alcohol; and 5) insulin lack. (See Table 2.)

Table 2: The “five I’s” that cause diabetic ketoacidosis and hyperosmolar hyperglycemic state


Urinary, respiratory, skin


Myocardial infarction, stroke, bowel, bone, skin

Infant on board


Indiscretion with diet

Non-compliance with diabetic diet (e.g., sugar, carbohydrates or alcohol)

Insulin lack

Pump failure, skipping insulin doses

The most common external cause of DKA is infection–usually a urinary tract infection, but diabetics are also at risk for pneumonia, cellulitis and more invasive skin infections.3

Infarction of any type of tissue can also lead to DKA. These include myocardial infarctions (MIs) and cerebral infarctions (i.e., strokes). Less commonly, bowel ischemia can lead to DKA. Thus, adult patients over the ages of 30—40 with suspected DKA should be questioned for any symptoms consistent with myocardial ischemia or infarction.

Type 1 diabetics may not have chest pain with acute MI, and may present with shortness of breath, weakness or other subtler symptoms, such as isolated nausea and vomiting, and should have a 12-lead ECG performed when appropriate.

A rapid stroke exam should also be performed in patients with weakness, visual changes, and any other stroke-like symptoms or altered mental status.

Pregnancy can cause DKA due to an increased insulin requirement. All females of childbearing age should be questioned about their pregnancy status.

Indiscretion with sugar, going off a diabetic diet, or use of alcohol can cause DKA when patients take in too many calories without accounting for them with appropriate doses of increased insulin.

The single most common cause of DKA, however, is simply skipping insulin doses. This may occur when patients miss meals and erroneously believe that they don’t need to take their insulin because they’re not eating. In fact, a certain level of insulin is always required by the body for basic metabolic functions, even in the absence of food intake.

Insulin lack can also occur unintentionally in patients with insulin pumps who have pump failure or dislodgement of their pump, sometimes unrecognized by the patient. Patients with new-onset Type 1 diabetes can be grouped in this insulin-lack category, as their initial presentation is frequently DKA.

As insulin levels decline, blood glucose levels increase, because cells can’t transport glucose across their membranes without insulin.

Signs and symptoms: Understanding insulin deficiency as the cause of DKA is key to understanding all subsequent downstream effects. As insulin levels decline, blood glucose levels increase, because cells can’t transport glucose across their membranes without insulin. Increasing blood glucose levels cause the plasma to become hyperosmolar.

High levels of glucose in the kidneys draw large amounts of water and electrolytes into the urine through an osmotic effect.1 This results in large-volume diuresis (i.e., polyuria). Classically, patients in DKA report polyuria and polydipsia (i.e., increased thirst).

Unchecked, this increased diuresis due to increased osmolality will result in severe dehydration. On average, a patient with DKA has fluid deficit of 4—6 L. Not only does this diuretic effect result in loss of water, it also causes loss of electrolytes, particularly potassium and phosphorus.

With lack of glucose as an energy source, fat begins to break down into free fatty acids, which are metabolized into ketoacids. The rise in ketoacids produces a metabolic acidosis. One ketoacid, acetone, can sometimes be smelled by providers and is said to have a “fruity” odor.

In an attempt to compensate for the metabolic acidosis, patients may take deep and labored breaths to lower their carbon dioxide (CO2), and they will develop a secondary or compensatory respiratory alkalosis.

Blowing off CO2 helps offset the metabolic acidosis by raising the pH of the blood. This respiratory pattern is classically referred to as “Kussmaul respirations,” and describes the deep breathing often observed in DKA patients.

The acidosis, for reasons not entirely clear, may also lead to generalized abdominal discomfort, a common symptom reported by DKA patients. However, providers should be cautious not to dismiss intra-abdominal processes such as bowel ischemia and other surgical abdominal issues, which can also cause abdominal pain and lead to DKA.3 Abdominal discomfort, nausea and vomiting may also be a sign of acute MI in a diabetic patient.

Electrolyte emergencies may arise in patients with severe DKA. Due to the osmotic diuresis, total body potassium levels are decreased. However, serum potassium concentrations may actually be high initially as potassium is shifted out of cells in acidotic low insulin states.

When insulin is administered, it will begin to correct the acidosis along with stimulating the glucose transport pump that also transports potassium, and serum potassium concentrations may rapidly plummet. This can result in life-threatening hypokalemic-induced arrhythmias. For this reason, insulin should never be administered in the field (or in the hospital) until potassium values are known.

EMS providers should be aware of a rare but highly lethal complication of DKA seen in children. Cerebral edema is seen in up to 1% of severe cases of DKA in children and has a mortality of up to 50%. Its cause is still unclear, but it’s associated with the severity of the acidosis and also with the administration of bicarbonate.4 It presents with signs of increased intracranial pressure such as headache, pupil changes, alteration of mental status, and bradycardia.3

Management: EMS providers should always consider DKA in the differential in diabetic patients, particularly Type 1 diabetes who present with hyperglycemia. Providers should look for signs of DKA, such as dehydration (e.g., dry skin, dry mucous membranes, tachycardia), Kussmaul respirations and abdominal pain.

Providers should perform a 12-lead ECG and stroke exam when appropriate, especially as patients approach 40 years of age or complain of chest pain, shortness of breath or any neurologic symptoms. Causes of DKA, particularly infection, should be sought.

The most important prehospital treatment is to begin isotonic IV fluids. In the ED, the current standard of care for patients in DKA is to receive about 20 cc/kg bolus (1—1.5 L) of normal saline and then 500 cc/hr. for four hours. Thus, EMS providers should aim for this as the patient’s initial therapy. Lactated Ringers solution can be substituted for normal saline at the same rate.

DKA patients ultimately need insulin therapy and often require an insulin drip, which isn’t usually administered by EMS providers.

All patients should be placed on a cardiac monitor, due to the potential for severe electrolyte disturbances such as hyperkalemia, which commonly occurs prior to insulin administration.

Sodium bicarbonate administration has been associated with cerebral edema in children and can paradoxically make the central nervous system more acidotic in both children and adults. Therefore, empiric administration of bicarb shouldn’t be used in the prehospital setting unless a patient has impending cardiac arrest, including life-threatening ECG changes of hyperkalemia.

In patients who are unresponsive, severely altered, or who are at risk for aspiration with swallowing, IV dextrose should be administered.

In patients who are unresponsive, severely altered, or who are at risk for aspiration with swallowing, IV dextrose should be administered.

Hyperglycemic Hyperosmolar State

Diabetic hyperglycemic hyperosmolar state (HHS) occurs in patients with Type 2 diabetes and has a markedly higher mortality rate than DKA.5

Similar to DKA, patients experience hyperglycemia (with glucose levels generally greater than 600 mg/dL) with a hyperosmolar-induced diuresis and dehydration.

Although there’s a relative insulin deficiency present in HHS, the degree of deficiency isn’t as great as in DKA and the disease is in great part due to insulin resistance.

Thus, the cells have enough insulin for some energy production, which prevents ketoacid production and thus ketoacidosis. However, glucose accumulates in the body.3

In fact, the degree of hyperglycemia is typically much greater in HHS than DKA and is often above 1,000 mg/dL, resulting in an even greater osmotic diuresis.5 Thus, patients with HHS are profoundly dehydrated with an average fluid deficit of 8—12 L.2

Dehydration is often compounded by the high number of HHS patients who are bedridden and thus have poor water intake.5

Causes: The same causes of DKA also cause HHS, and the five I’s should be considered here as well. Infection remains the most common cause of HHS and is present in about half of all patients with HHS, particularly pneumonia and urinary tract infections.5 Myocardial infarction and stroke are also common precipitants. Medications, especially steroids, may be the underlying cause of a patient developing HHS.

Signs and symptoms: Providers should look for signs of severe dehydration. Patients are often hypotensive and tachycardic. Because patients with HHS don’t develop severe metabolic acidosis like in patients with DKA, they won’t have Kussmaul respirations and don’t usually develop abdominal pain unless they have actual intra-abdominal pathology.3

Unlike patients with DKA, patients with HHS are much more likely to present with neurological effects, including coma in up to 20%, and may present with focal neurological deficits and seizures.3,5

Management: The same treatments of DKA should occur in HHS. Although a 12-lead ECG isn’t mandatory for younger hyperglycemic patients and those in presumed DKA, prehospital providers should always obtain a 12-lead ECG in all presumed HHS patients and screen them for stroke. This is because both acute MI and cerebrovascular accident (CVA) may be either the cause or complication of this syndrome. Providers should strongly consider and examine for sources of infection.

All patients should be placed on cardiac monitors and isotonic IV fluids initiated. A volume bolus should be administered until adequate perfusion is achieved. The exact amount of this bolus is variable, but EMS providers should be aggressive with fluids until the patient has a strong pulse or the systolic BP is above approximately 110—120 mmHg.

Hyperglycemia Without Obvious Acidosis

Patients with either Type 1 or Type 2 diabetes can present with hyperglycemia without ketosis or signs of HHS. These patients may be encountered early in the course of their DKA or HHS, and thus haven’t yet developed acidosis or hyperosmolarity, or they may just be chronically hyperglycemic.

It’s also possible for patients to be hyperglycemic for a long period of time yet be unaware. For example, an undiagnosed Type 2 diabetic may develop hyperglycemia, polydipsia and polyuria over several weeks; although their blood glucose level may be well over 200 mg/dL, they may have no other symptoms or laboratory abnormalities.

Once diagnosed, it’s very important for diabetics to maintain euglycemia (i.e., a normal level of blood glucose), since long-term hyperglycemia can lead to multiple complications including heart attack, stroke, blindness, neuropathy and extremity infections leading to amputations.

Causes: The causes of hyperglycemia without acidosis are the same as the causes with acidosis–namely the five I’s.

Signs and symptoms: What’s important to note in hyperglycemia without acidosis is the lack of symptoms. Patients won’t have Kussmaul breathing and their breath won’t take on a “fruity” odor. Unless there’s a CVA, there should be no neurologic abnormality and patients are generally well-appearing. The only clue may be polydipsia and polyuria, or just nonspecific complaints like weakness and fatigue.

Diabetic patients who monitor their own glucose levels might note that their blood glucose has been elevated. Hyperglycemia without obvious acidosis may be incidentally found by EMS providers when responding for a patient with another primary complaint.

Management: In the prehospital setting, it’s generally not known whether a patient is in DKA or HHS unless there are obvious signs or symptoms. Therefore, the initial approach to hyperglycemia is very similar in most cases.

It’s important to consider whether the patient has signs or symptoms of an infection.

In older patients who are found to be hyperglycemic, a 12-lead ECG and stroke evaluation are important parts of the assessment. Even though these patients show no signs of DKA or HHS, they may still be volume depleted, and IV fluids should be initiated if at all possible in patients with blood glucose above 250 mg/dL, though a fluid bolus isn’t generally indicated.

Once at the hospital, hyperglycemia is generally treated with a combination of IV crystalloids and subcutaneous insulin doses, depending on the underlying cause.


Although hyperglycemia doesn’t always represent an emergency in diabetics, symptomatic hypoglycemia is always an emergency and can lead to rapid deterioration and death if not corrected promptly. Severe hypoglycemia usually occurs when glucose is < 50 mg/dL.1

Causes: Hypoglycemia isn’t a direct complication of diabetes, but rather a complication of its treatment. We remember the causes of hypoglycemia with the mnemonic “re-explained.” (See Table 3.)

Table 3: Causes of hypoglycemia “˜Re-ExPLAINeD’


Renal failure


Exogenous insulin or oral hypoglycemic


Pituitary dysfunction


Liver disease (e.g., hepatitis, hepatoma, acetaminophen overdose)


Adrenal insufficiency, alcohol (especially in children)


Infection (especially in children) or insulinoma (very rare)




Drugs (often aspirin, oral hypoglycemic agents and beta-blockers)

Hypoglycemia most often occurs in Type 1 diabetics on insulin. It can be due to an increase in the patient’s insulin dose, skipping meals or heavy exercise.1

Hypoglycemia can also occur in Type 2 diabetics who take oral hypoglycemic medications, particularly the sulfonylureas.

The sulfonylureas, including glipizide, glimepiride and glyburide, act by increasing insulin release from the pancreas. Non-sulfonylurea oral diabetic medications, such as metformin, don’t usually cause hypoglycemia.2

It should be noted that infection in both Type 1 and Type 2 diabetics can present as hypoglycemia, and that hypoglycemia can also occur in non-diabetic patients.

Signs and symptoms: Hypoglycemia should always be considered and immediately excluded in the diabetic patient presenting with altered mental status, weakness or stroke symptoms.

Signs and symptoms can be divided into neuroglycopenic and autonomic manifestations.2

Neuroglycopenic manifestations are those that result from low levels of glucose in the brain. This includes confusion, agitation, focal neurological deficits, seizures and coma. Focal neurologic deficits may mimic stroke and are the reason all potential stroke patients must have their glucose checked as soon as possible.

The autonomic manifestations occur due to counter-regulatory hormones, such as epinephrine, which are released during a hypoglycemic state. These signs and symptoms include palpitations, tachycardia, anxiety and sweating.

Note that the rapidity at which hypoglycemia develops usually determines which type of symptoms predominate. In patients with a sudden drop in glucose, the autonomic manifestations predominate. However, in patients with a slower decline in glucose levels, neuroglycopenic signs predominate.1,2

Management: Securing the ABCs (i.e., airway, breathing and circulation) is always the most important first step. The first-line treatment of hypoglycemia is glucose. In an alert patient who’s able to swallow, oral glucose can be given, or, if not available, foods rich in sugar.

In patients who are unresponsive, severely altered, or at risk for aspiration with swallowing, IV dextrose should be administered. A dose of 50 cc of 50% (25 grams) dextrose is usually administered and is expected to raise serum glucose by 225—250 mg. Although about three-quarters of all EMS services use D50, this hyperosmolar solution may be less safe than using 100 cc of D10W.6

Glucagon is a second-line agent that can be administered intramuscularly (IM) in patients where IV access isn’t possible; however, it’s slower than IV glucose in reversing symptoms of hypoglycemia.

Glucagon can be given at a dose of 1 mg IM, subcutaneously or intranasally, though IM is preferred due to its more rapid onset. Glucagon acts by releasing glycogen stores from the liver, which can then be converted to glucose.

Keep in mind that in malnourished patients, particularly alcoholics and those with severe liver disease, glucagon is often ineffective due to low glycogen stores. Common adverse effects of glucagon include nausea and vomiting.

Particular caution should be taken when a hypoglycemic patient is encountered who uses oral hypoglycemic medications. These patients are at high risk of hypoglycemia recurrence.

Unintentional ingestion of sulfonylureas by children–even one pill–can result in severe hypoglycemia and death if not recognized. Although not available in the prehospital setting, octreotide is used in the ED as an alternative treatment for sulfonylurea overdose.

Accepting refusals from hypoglycemic patients on oral hypoglycemic medications is dangerous and should be avoided if possible.

Common Medical Emergencies

Long-term hyperglycemia is very damaging to organ systems, placing diabetics at higher risk for many other disease processes including infections, strokes and MIs. Presentations of these disease processes may be atypical compared to the non-diabetic patient. This is most notable in MIs where diabetics may not complain of chest pain, but rather, may have other atypical symptoms such as dyspnea, nausea, vomiting, syncope or weakness.

Considering these symptoms as the typical MI presentation in diabetics will help reduce the chance of missing an MI. Providers should have a low threshold to obtain a 12-lead ECG in diabetics with any of these complaints.

Infections are common in diabetics, particularly infections of the urine, respiratory tract and skin. Performing a thorough history and physical exam, and paying close attention to vital signs to screen for sepsis will help identify infections.

Finally, patients with altered mental status or other neurological complaints should have a stroke exam performed.

Glucagon is a second-line agent that can be administered intramuscularly in patients where IV access isn't possible; however, it's slower than IV glucose in reversing symptoms of hypoglycemia.

Glucagon is a second-line agent that can be administered intramuscularly in patients where IV access isn’t possible; however, it’s slower than IV glucose in reversing symptoms of hypoglycemia.


Diabetic patients frequently utilize the prehospital care system. Common problems in this group include DKA, HHS, hypoglycemia, hyperglycemia without acidosis, and other common medical problems which may manifest with atypical presentations.

Careful consideration of these diagnoses in all diabetic patients will result in earlier diagnosis and treatment.


1. Cydulka RK, Maloney Jr. GE, Diabetes mellitus and disorders of glucose homeostasis. In Marx JA, Hockberger RS, Walls RM, et al (Eds.): Rosen’s emergency medicine: Concepts and clinical practice, 8th edition. Saunders: Philadelphia, 2014, pp. 1652—1666, 2014.

2. Tintinalli JE, Stapcyzynski JS, Ma OJ, et al. Tintinalli’s emergency medicine: A comprehensive study guide, 8th edition. McGraw-Hill Education: New York, 2016.

3. Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335—1343.

4. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344(4):264—269.

5. Paquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis and treatment. Diabetes Care. 2014;37(11):3124—3131.

6. Hern HG, Kiefer M, Louie D, et al. D10 in the treatment of prehospital hypoglycemia: A 24 month observational cohort study. Prehosp Emerg Care. 2017;21(1):63—67.

No posts to display