RECENT GUIDELINES IN MANAGEMENT OF HYPERGLYCEMIC EMERGENCIES

Abstract

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as nonketotic hyperglycemia) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia and each represents an extreme in the spectrum. DKA is more common in younger patients with type 1 diabetes, though it can occur in type 2 diabetes. HHS occurs less frequently, and is associated with higher mortality, representing underlying comorbidity. For both DKA and HHS, the classic clinical presentation includes a history of polyuria, polydipsia, weight loss, vomiting, abdominal pain (only in DKA), dehydration, weakness, clouded sensorium, and possibly coma DKA and HHS differ clinically according to the presence of ketoacidosis and usually the degree of hyperglycemia. In HHS, there is little or no ketoacid accumulation, the serum glucose concentration frequently exceeds 1000 mg/dL, the plasma osmolality may reach 380 mosmol/kg, and neurologic abnormalities are frequently present (including coma in 25 to 50 % of cases) . Most patients with HHS have an admission pH >7.30, a serum bicarbonate >20 meq/L, a serum glucose >600 mg/dL , and test negative for ketones in serum and urine, although mild ketonemia may be present. DKA is characterized by the triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. Metabolic acidosis is often the major finding. The serum glucose concentration is usually greater than 500 mg/dL and less than 800 mg/dL. However, serum glucose concentrations may exceed 900 mg/dL in patients with DKA who are comatose. A precipitating event can usually be identified in patients with DKA or HHS. The most common are infection (most often pneumonia or urinary tract infection) and discontinuation of or inadequate insulin therapy. The initial evaluation of patients with hyperglycemic crises should include assessment of cardiorespiratory status, volume status, and mental status. Abdominal pain is common in DKA but not in HHS, and requires evaluation if it does not resolve with treatment of the acidosis. Neurologic symptoms, which may include focal findings, are more often seen in HHS and primarily occur when the effective serum osmolality is greater than 320 to 330 mosmol/kg. The presence of stupor or coma in diabetic patients with an effective serum osmolality below 320 mosmol/kg demands immediate consideration of other causes of the mental status change. The initial laboratory evaluation of a patient with suspected DKA or HHS should include determination of: serum glucose, serum electrolytes (with calculation of the anion gap), BUN, plasma creatinine,complete blood count with differential, urinalysis and urine ketones by dipstick, plasma osmolality, serum ketones (if urine ketones are present), arterial blood gas if the serum bicarbonate is substantially reduced and ECG Additional testing, such as cultures of urine, sputum, and blood, serum lipase and amylase, and chest x-ray, should be performed on a case-by-case basis. Therapy for both diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) includes: fluid replacement to correct both hypovolemia and hyperosmolality, insulin administration to correct hyperglycemia and, in DKA, metabolic acidosis, potassium repletion, and, in selected patients with DKA, sodium bicarbonate. Frequent monitoring is essential and underlying precipitating events should be identified and corrected. It is advised to begin with isotonic (0.9 %) saline infused at a rate of 15 to 20 mL/kg per hour, in the absence of cardiac compromise, for the first few hours. This is followed by one half isotonic (0.45 %) saline at 4 to 14 mL/kg per hour if the serum sodium is normal or elevated; isotonic saline is continued if hyponatremia is present. We add dextrose to the saline solution when the serum glucose reaches 200 mg/dL in DKA or 250 to 300 mg/dL in HHS. The insulin regimen is the same in DKA and HHS. If the serum potassium is ≥3.3 meq/L, we give a continuous intravenous infusion of regular insulin at 0.14 U/kg per hour; at this dose, an initial intravenous bolus is not necessary. An alternative option is to administer an IV bolus (0.1 U/kg body weight) of regular insulin, followed by a continuous infusion at a dose of 0.1 U/kg per hour. The dose is doubled if the glucose does not fall by 50 to 70 mg/dL in the first hour. It is recommended that replacement with intravenous potassium chloride be initiated when the serum potassium concentration is ≤5.3 meq/L. Patients with an initial serum potassium below 3.3 meq/L should receive aggressive fluid and potassium replacement prior to treatment with insulin to prevent initial worsening of the hypokalemia. Indications for sodium bicarbonate therapy to help correct the metabolic acidosis are controversial. Suggested treatment with intravenous sodium bicarbonate in patients with an arterial pH less than 6.9 . Cerebral edema is rare in adults, but is associated with high rates of morbidity and mortality. Possible preventive measures in high-risk patients include gradual rather than rapid correction of fluid and sodium deficits (maximum reduction in plasma osmolality of 3 mosmol/kg per hour), and maintenance of a slightly elevated serum glucose until the patient is stable. Hyperglycemic emergencies are usually preventable.Established patients should be educated on how to manage their diabetes during stress or infection; this “sick-day management” includes never omitting insulin, preventing dehydration and hypoglycemia, monitoring blood glucose frequently, testing for ketosis, administering supplemental rapid-acting insulin doses according to prescribed guidelines, treating underlying triggers early and aggressively and having frequent contact with their diabetes health care team to evaluate their acute condition .