Diabetic ketoacidosis(DKA) & Hyperosmolar hyperglycemic hyperglycemic state(HHS)
Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar status (HHS) are typical complications of diabetes mellitus. These are commonly characterized by insulin deficiency, volume depletion, and acid-base abnormalities. Generally, DKA has ketoacidosis associated with hyperglycemia and is known to occur mainly in diabetes mellitus (DM) type 1, but it also occurs in DM type 2 patients who do not show immunological characteristics of DM type 1. On the other hand, HHS is mainly found in DM type 2. DKA occurs well in younger patients under 65 years, whereas HHS tends to occur mainly in patients over 65 years of age
Symptoms
DKA generally has an acute tendency to develop for 24 hours. In some cases, DM type 1 is found through the diagnosis of DKA, but it is common in DM type 1 patients who are undergoing blood glucose control after diagnosis. Patients with DKA show nausea / vomiting and also thirst / polyuria due to hyperglycemia. In addition, increased osmolarity, dehydration, hypotension, cerebral edema, tachycardia, shortness of breath, Kussmaul respirations, and abdominal pain may be associated with metabolic acidosis through ketogenesis.
The precipitating factors that can cause DKA include insulin deficiency, infection, infarction, and pregnancy.
Pathogenesis
Both DKA and HHS begin with the development of extracellular glucose concentration due to insulin deficiency. The insulin deficiency causes increased glucose release in the liver via glycogenolysis and gluconeogenesis, leading to osmotic diuresis and dehydration as symptoms of glycosuria.
In addition, lipolysis increases FFA release to increase ketone body and cause ketone body to cause metabolic acidosis.
In order to correct metabolic acidosis, the bicarbonate buffering system occurs and causes hyperventilation, resulting in symptoms of kussmaul respiration.
Diagnosis
To distinguish between DKA and HHS, the laboratory findings should be compared based on pathophysiology. First, HHS is a hyperglycemia characterized by simple hypovolemia. Therefore, glucose is mostly higher than 600 and effective serum osmolality is more than 320mOsm / kg.
On the other hand, ketones are found in urine and serum due to ketoacidosis of DKA. Because of this, the arterial pH is decreased to 7.3 or less and the loss of bicarbonate is often observed, which is often measured as 15mEq / l. In addition, anion gap is often widespread.
On the other hand, HHS occurs frequently in older DM type 2. Because DKA and HHS have some common mechanisms of pathophysiologic development, clinical features are similar. Commonly, they represent polydipsia, polyuria, weakness, hypothermia, tachycardia, tachypnea, altered sensorium, and the like. As we will see later, DKA, unlike HHS, shows metabolic acidosis through ketogenesis, which does not significantly increase blood sugar. Therefore, nausea, vomiting, abdominal pain, ileus, Kussmaul breathing, and acetone breath are characteristic. On the other hand, HHS shows characteristic features of hyperglycemia and thus poor appetite, symptoms of accompanying illness, and mental status changes [1]
Symptoms
DKA generally has an acute tendency to develop for 24 hours. In some cases, DM type 1 is found through the diagnosis of DKA, but it is common in DM type 1 patients who are undergoing blood glucose control after diagnosis. Patients with DKA show nausea / vomiting and also thirst / polyuria due to hyperglycemia. In addition, increased osmolarity, dehydration, hypotension, cerebral edema, tachycardia, shortness of breath, Kussmaul respirations, and abdominal pain may be associated with metabolic acidosis through ketogenesis.
The precipitating factors that can cause DKA include insulin deficiency, infection, infarction, and pregnancy.
Pathogenesis
Both DKA and HHS begin with the development of extracellular glucose concentration due to insulin deficiency. The insulin deficiency causes increased glucose release in the liver via glycogenolysis and gluconeogenesis, leading to osmotic diuresis and dehydration as symptoms of glycosuria.
In addition, lipolysis increases FFA release to increase ketone body and cause ketone body to cause metabolic acidosis.
In order to correct metabolic acidosis, the bicarbonate buffering system occurs and causes hyperventilation, resulting in symptoms of kussmaul respiration.
Diagnosis
To distinguish between DKA and HHS, the laboratory findings should be compared based on pathophysiology. First, HHS is a hyperglycemia characterized by simple hypovolemia. Therefore, glucose is mostly higher than 600 and effective serum osmolality is more than 320mOsm / kg.
On the other hand, ketones are found in urine and serum due to ketoacidosis of DKA. Because of this, the arterial pH is decreased to 7.3 or less and the loss of bicarbonate is often observed, which is often measured as 15mEq / l. In addition, anion gap is often widespread.
On the other hand, HHS occurs frequently in older DM type 2. Because DKA and HHS have some common mechanisms of pathophysiologic development, clinical features are similar. Commonly, they represent polydipsia, polyuria, weakness, hypothermia, tachycardia, tachypnea, altered sensorium, and the like. As we will see later, DKA, unlike HHS, shows metabolic acidosis through ketogenesis, which does not significantly increase blood sugar. Therefore, nausea, vomiting, abdominal pain, ileus, Kussmaul breathing, and acetone breath are characteristic. On the other hand, HHS shows characteristic features of hyperglycemia and thus poor appetite, symptoms of accompanying illness, and mental status changes [1]
