HHS vs DKA Flashcards
Preventing Hyperglycemic-Hyperosmolar State.
Hyperglycemic-hyperosmolar state (HHS) is a hyperosmolar (increased blood osmolarity) state caused by hyperglycemia. The processes of HHS are outlined in Fig. 64-10. Both HHS and diabetic ketoacidosis (DKA) are caused by hyperglycemia and dehydration. HHS differs from DKA in that ketone levels are absent or low and blood glucose levels are much higher. Blood glucose levels may exceed 600 mg/dL (33.3 mmol/L), and blood osmolarity may exceed 320 mOsm/L. Table 64-13 lists the differences between DKA and HHS.
HHS results from a sustained osmotic diuresis. Kidney impairment in HHS allows for extremely high blood
glucose levels. As blood concentrations of glucose exceed the renal threshold, the kidney’s capacity to reabsorb glucose is exceeded.
Decreased blood volume, caused by osmotic diuresis, or underlying kidney disease, common in many older patients with diabetes, results in further deterioration of kidney function. The decreased volume further reduces glomerular filtration rate, causing the glucose level to increase. Decreased kidney perfusion from hypovolemia further impairs kidney function.
HHS occurs most often in older patients with type 2 diabetes mellitus, many of whom did not know that they had diabetes. Mortality rates in older patients are as high as 40% to 70%. The onset of HHS is slow and may not be recognized. The older patient often seeks medical attention later and is sicker than the younger patient. HHS does not occur in adequately hydrated patients. Older patients are at greater risk for dehydration and HHS because of age-related changes in thirst perception, poor urine-concentrating abilities, and use of diuretics. Stress to all older adults, especially those who have diabetes, the importance of maintaining hydration.
Myocardial infarction, sepsis, pancreatitis, stroke, and some drugs (glucocorticoids, diuretics, phenytoin [Dilantin], beta blockers, and calcium channel blockers) also may cause HHS. Central nervous system (CNS) changes range from confusion to complete coma. Unlike DKA, patients with HHS may have seizures and reversible paralysis. The degree of neurologic impairment is related to serum osmolarity, with coma occurring once serum osmolarity is greater than 350 mOsm/L (350 mmol/L).
The development of HHS rather than DKA is related to residual insulin secretion. In HHS, the patient secretes just enough insulin to prevent ketosis but not enough to prevent hyperglycemia. The hyperglycemia of HHS is more severe than that of DKA, greatly increasing blood osmolarity, leading to extreme diuresis with severe dehydration and electrolyte loss.
Considerations for Older Adults
Diabetic ketoacidosis (DKA) is characterized by uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones. This condition results from the combination of insulin deficiency and an increase in hormone release that leads to increased liver and kidney glucose production and decreased glucose use in peripheral tissues (Fig. 64-9). Laboratory diagnosis of DKA is shown in Table 64-13. All of these changes increase ketoacid production with resultant ketonemia and metabolic acidosis.
DKA occurs most often in patients with type 1 DM but also can occur in those with type 2 DM who are under severe stress (e.g., trauma, surgery, infection). Some people with type 2 diabetes have a syndrome known as ketosis-prone diabetes or KPD (Palmer & Jessup, 2012). This problem is not yet fully characterized, and it is important to remember that regardless of whether the patient with DKA has type 1 or type 2 diabetes, management of the acute episode is the same. The most common precipitating factor for DKA is infection. Death occurs in up to 10% of these cases even with appropriate treatment.
Hyperglycemia leads to osmotic diuresis with dehydration and electrolyte loss. Classic manifestations of DKA include polyuria, polydipsia, polyphagia, vomiting, abdominal pain, dehydration, weakness, confusion, shock, and coma. Mental status can vary from total alertness to profound coma. As ketone levels rise, the pH of the blood decreases and acidosis occurs. Kussmaul respirations (very deep and rapid respirations) cause respiratory alkalosis in an attempt to correct metabolic acidosis by exhaling carbon dioxide. Initial serum sodium levels may be low or normal. Initial potassium levels depend on how long DKA existed before treatment. After therapy starts, serum potassium levels drop quickly.
Preventing Diabetic Ketoacidosis.
