- 1What Is Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
- 2What Are the Symptoms of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
- 3What Are the Causes of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
- 4How Are Hyperglycemic Conditions Evaluated?
- 5How to Manage the Hyperglycemic Condition?
Introduction
Hyperglycemia is a condition that causes high levels of sugar (glucose) in the blood, above 200 mg/dL (milligrams per deciliter) or 11.1 millimoles per liter (mmol/L). It mainly affects diabetic people or can even develop in a non-diabetic person. In diabetes, when food is taken, it is broken into sugar, and these sugars cannot be converted into energy by the insulin, which is secreted by the pancreas. This condition occurs due to the body's inability to secrete enough insulin or use it effectively.
Diabetes has various types, such as type 1 DM (juvenile or insulin-dependent diabetes), which occurs due to the pancreas's inability to produce insulin, and type 2 DM (adult-onset diabetes or non-insulin-dependent diabetes), which occurs when the body cannot use insulin well. The other type is gestational diabetes, which occurs during pregnancy.
The complications of high blood sugar (hyperglycemia) can lead to diabetic ketoacidosis (DKA) in type 1 DM in young patients and cause the body to produce excess ketones (blood acids), electrolyte balance, and fluid. Hyperglycemia also causes hyperglycemic hyperosmolar state (HHS) in type 2 diabetes patients and leads to high blood sugar levels for a prolonged period. In some patients, both complications can also be present. These complications of hyperglycemia require emergency evaluation and management.
What Is Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
Diabetic ketoacidosis (DKA) occurs when the body lacks insulin and has more than 250 mg/dL of sugar. When this occurs, the body cannot utilize the sugar for energy. Instead, it breaks down the fat in the body. But, when fat is broken, a toxic product called ketones is released called ketones, which gets piled up in the blood and urine. If this condition is not treated, the person can go into a severe life-threatening condition called a diabetic coma. It consists of triads of ketonemia (abnormal levels of ketones), hyperglycemia, and metabolic acidosis (when the potential of hydrogen or pH is less than 7.3, and the HCO3 or bicarbonate level is also low).
The hyperglycemic hyperosmolar state (HHS) occurs when insulin does not work properly, and sugar levels exceed 600 mg/dL. There are increased sugar levels in the blood but no increased levels of ketones. Therefore, the body does not use fat or glucose for energy. If not treated, the person can experience severe dehydration and coma.
What Are the Symptoms of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
The symptoms of diabetic ketoacidosis develop quickly within 24 hours which are:
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Increased frequency of urination.
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Polydipsia (extreme thirst).
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Nausea.
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Stomach pain.
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Weakness and tiredness.
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Fruity-scented breath.
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Confusion.
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Shortness of breath.
The symptoms of a hyperglycemic hyperosmolar state occur slowly (days to weeks), which are:
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State of confusion, hallucinations, and delirium.
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Loss of consciousness.
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Polydipsia.
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Loss of vision or blurred vision.
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Paralysis affects one side of the body.
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Frequent urination.
What Are the Causes of Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State?
The precipitating causes of diabetic ketoacidosis and hyperglycemic hyperosmolar states are:
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Urinary tract infections (UTIs).
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Pneumonia (lung infection).
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Poor insulin treatment.
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Acute myocardial infarction (heart attack).
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Neurovascular accidents.
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Pancreatitis (inflammation of the pancreas).
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Alcohol use.
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Psychological disorders, such as eating disorders or depression.
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Insulin pumps malfunction.
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Medications include beta-blockers, glucocorticoids, atypical antipsychotics (Olanzapine and Risperidone), specific chemotherapeutic agents, and thiazide diuretics. Other drugs, such as sodium-glucose co-transporter 2 (SGLT2) inhibitors, a type of oral antidiabetic, can also cause DKA.
How Are Hyperglycemic Conditions Evaluated?
Diabetic Ketoacidosis Evaluation:
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Patients with DKA have short-onset symptoms, such as polydipsia, polyuria, loss of weight, nausea, vomiting, abdominal pain, and lethargy, and about 25 percent of patients have a loss of consciousness. In the case of severe DKA, the patient undergoes a coma or stupor (near-unconsciousness).
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Physical examination includes dehydration with poor skin turgor (the skin takes a long time to return to its normal position when lifted) and dry mucous membrane. Dehydration causes increased serum sodium concentration. Apart from these, the patients also present with an increased heartbeat and blood pressure. Patients also show Kussmaul respirations (rapid, deep breathing) and a fruity breath odor.
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Blood sugar levels are more than 250 mg/dl in case of severe DKA.
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In severe DKA, blood sugar levels are more than 250 mg/dl, and serum bicarbonate levels are less than ten milliequivalents per liter (mEq/L).
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Arterial pH (potential hydrogen, which measures acidity or alkalinity) is less than seven.
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Increased serum ketone levels. A nitroprusside test is done to estimate the acetone levels.
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Anion gap blood test (measure the acid-base balance) is more than 12 in severe DKA.
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Urine or serum β-hydroxybutyrate is more than three millimoles per liter (mmol/L).
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Leukocytosis (increased white blood cells) due to infection.
Hyperglycemic Hyperosmolar State Evaluation:
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Patients (older than 60) with HHS have symptoms such as weakness, extreme thirst, increased frequency of urination, and blurred vision. Apart from these, they have signs of dehydration, too.
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Plasma glucose levels are more than 600 mg/dl.
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There are absent or small amounts of ketone bodies in the urine.
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Serum bicarbonate levels are less than 18 mEq/L.
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The arterial pH is more than 7.3.
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Urine or serum β-hydroxybutyrate is less than 3 mmol/L.
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Effective serum osmolality is more than 320 mOsm/kg (milliosmoles per kilogram).
How to Manage the Hyperglycemic Condition?
Managing hyperglycemic conditions should involve correcting high blood sugar levels, hyperosmolality (high concentrations of sodium, salt, and other substances), dehydration, increased ketonemia, and electrolyte imbalance. In addition, the cause should be identified and treated.
The management includes:
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Monitor the vital signs, insulin dosage, rate of fluid administration, and urine output.
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Repeat laboratory tests every two hours, such as pH, glucose and electrolyte levels, anion gap, and bicarbonate levels.
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Intravenous (IV) fluids are administered 0.9 percent NaCl (sodium chloride) at a rate of 500 to 1000 mL/hour (milliliters per hour) over a starting period of two to four hours. This restores renal perfusion (overall kidney function), expands intravascular volume, and decreases insulin resistance. After the correction of intravascular volume, the saline is administered at a rate of 250 mL/hour, or the saline concentration is changed to 0.45 percent. When the blood sugar levels have reached below 200 mg/dl, five to 10 percent of dextrose is given.
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If serum potassium levels are less than 3.3 mEq/L, insulin should be on hold, and 20 to 30 mEq (milliequivalent) of potassium per liter of fluids should be administered. Low doses are recommended in cases of chronic renal (kidney) failure. If serum potassium levels are above 5.2 mEq/L, potassium is not administered but should be monitored every two hours.
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If the pH is more than 6.9, there is no need for bicarbonate therapy. If the pH is less than 6.9 (severe acidosis), sodium bicarbonate of 50 to 100 mmol in 400 mL of water is given and is repeated every two hours until the pH becomes more than 6.9.
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Insulin should be administered because it lowers serum glucose levels and inhibits ketogenesis (production of ketones), lipolysis (lipid breakdown), and glucagon secretion. Therefore, all these lead to decreased ketoacidosis. Insulin should be continuously given via an IV (intravenous or into the vein) route. 0.1 u/kg (unit per kilogram) of body weight is given, followed by an infusion of insulin at the rate of 0.1 u/kg/hr (unit per kilogram per hour) till the glucose levels reach 200 mg/dl. Then, the insulin is infused at 0.05 u/kg/hr with five percent dextrose to maintain the glucose levels between 150 and 200 mg/dl. This is continued until ketoacidosis is reduced.
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Subcutaneous administration is an alternative to IV infusion of rapid insulin every two hours. 0.2 u/kg body of subcutaneous bolus is given, followed by a subcutaneous infusion of insulin at the rate of 0.2 u/kg/hr till the glucose levels reach 250 mg/dl. Then, the insulin is infused at 0.05 u/kg/hr to maintain glucose levels below 200 mg/dl. This is continued until ketoacidosis is reduced.
Conclusion
The complications of hyperglycemic conditions are mainly diabetic ketoacidosis and hyperglycemic hyperosmolar state, which are severe conditions, and the patient may also go into a coma (prolonged unconscious state). These required immediate evaluations by signs and symptoms, along with laboratory tests. Management includes fluid, bicarbonate, insulin, and potassium therapy.
