When to seek care. The bottom line. Read this next. Diabetes Risk Factors. Medically reviewed by Maria Prelipcean, M. Medically reviewed by Tyler Walker, MD. Medically reviewed by Kelly Wood, MD. Hyperglycemia vs. Medically reviewed by Harshil Matta, DO. Medically reviewed by Jenneh Rishe, RN. Griffith, MD. How Do Insulin Pumps Work? Medically reviewed by Stella Bard, MD. HHS is manifested by marked elevation of blood glucose, hyperosmolality and little or no ketosis.
Precipitating causes of HHS are infection, undiagnosed diabetes and substance abuse. Insulin has five main actions: 1 to drive glucose into cells; 2 to drive potassium into cells; 3 to create an anabolic environment; 4 to inhibit breakdown of fat; and 5 to block the breakdown of proteins. Table 1. Diabetic ketoacidosis typically develops in patients who lack significant endogenous insulin; this insufficiency of circulating insulin causes hyperglycemia and hyperkalemia, the creation of a catabolic state with high levels of both ketone bodies and free-fatty acids due to the breakdown of proteins and fats.
In contrast, HHS occurs in patients who produce a sufficient amount of insulin to drive potassium into cells and to inhibit the breakdown of proteins and fats; as such these patients are not ketoacidotic.
Hospitalizations for diabetes and DKA are rising, possibly because of increased diabetes prevalence and higher insulin costs. HHS is associated with high mortality risks, which is particularly worrisome during the COVID pandemic, when healthcare resources have been stretched thin.
To help ensure early identification and treatment of these conditions, this article provides an overview of both. See Diabetes physiology review. This side-by-side comparison highlights the differences and similarities between diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS. Insulin also prevents fatty acids and amino acids from converting into keto acids and glucose gluconeogenesis. When insulin production is inhibited, Type 1 or Type 2 diabetes may result.
DKA typically occurs in patients with Type 1 diabetes, although prevalence in those with Type 2 diabetes is rising accounting for an estimated 1 in 5 cases. To diagnose DKA, these three elements must be present: diabetes hyperglycemia , ketones serum , and anion-gap acidosis. In addition, DKA must be distinguished from alcoholic ketoacidosis which typically occurs without hyperglycemia , starvation ketosis which occurs with prolonged starvation or removal of carbohydrates from the diet , and other causes of anion-gap metabolic acidosis such as lactic acidosis, advanced kidney disease, or excessive ingestion of aspirin, acetaminophen, or methanol.
In some patients, DKA may be the initial indication of diabetes. In those with longstanding diabetes, DKA may be the result of missed insulin doses or a relative lack of insulin for example, taking usual insulin doses during times of stress such as illness, infection, steroid use, or new myocardial infarction or stroke.
DKA also can occur because of an insulin pump malfunction such as a tubing kink or inserting into a site with poor insulin absorption.
Patients with eating disorders may withhold insulin doses to create a catabolic state that leads to weight loss taking insulin typically causes weight gain , leading to DKA. In addition, the oral diabetes medications sodium glucose-cotransporter 2 inhibitors SGLT-2 inhibitors have been associated with increased risk for DKA, especially in patients who also are taking insulin.
The cause may be a combination of an increased loss of glucose through the kidneys, decreased insulin needs, and increased insulin resistance from underlying stress or illness. DKA typically evolves rapidly with initial signs and symptoms of polyuria, polydipsia, fatigue, abdominal pain, nausea, and vomiting. Over time, mental status changes may arise, leading to coma.
During a physical exam, a person with DKA typically shows signs of dehydration, including tachycardia and hypotension, with deep, rapid Kussmaul breathing and a fruity smelling acetone odor on the breath. If the patient is dehydrated, blood urea nitrogen and creatinine will be elevated. Serum potassium typically is elevated, with hyperkalemia occurring as potassium ions shift outside the cells as a result of acidosis. A total potassium deficit usually occurs in DKA because of acidosis, GI losses, and osmotic diuresis.
When potassium is low, the patient should be monitored closely, as hypokalemia can lead to life-threatening arrhythmias. Sodium also may be low, resulting from losses caused by increased urine output and vomiting, although hyperglycemia itself can lead to pseudohyponatremia.
However, because high blood glucose levels may cause a falsely low sodium level many electronic health records systems have a calculator to determine the actual sodium level based on blood glucose level , the sodium level may need to be corrected.
Hyperventilation may cause low pH 6. DKA treatment goals include restoring volume status and peripheral perfusion, improving glycemic control, and correcting electrolyte imbalances and ketosis. This is done by administering I. In addition, underlying causes must be identified and treated. As acidosis resolves, blood glucose levels will decline more quickly. Standardized I. However, protocols specific to DKA are recommended because those used to correct hyperglycemia in Type 2 diabetes may be too aggressive.
Because DKA is a state of dehydration, with estimated deficits of 4 to 6 liters, I. The addition of dextrose counterbalances the insulin infusion, which needs to continue until acidosis is corrected, as indicated by normalization of bicarbonate and anion gap. In addition, the dextrose infusion reduces the risk of cerebral edema, which can occur when blood glucose is corrected too rapidly. In most cases, the initial electrolyte imbalances should resolve on their own with I. Treatment with sodium bicarbonate is controversial.
It may lead to hypokalemia and impaired tissue oxygenation if it corrects acidosis too rapidly or to cerebral acidosis when cerebrospinal fluid pH is lowered. No significant difference was shown to exist between the I. These studies typically excluded pregnant patients and those with hypotension or underlying cardiac, hepatic, or renal disease. Those patients would be more safely treated in an ICU setting with I.
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