Complications: Acute and Chronic
TERMS
QUICK LOOK AT THE CHAPTER AHEAD
This chapter reviews complications of diabetes mellitus (DM), both acute and chronic. Acute complications of DM include hypoglycemia, ketonuria, ketonemia, diabetic ketoacidosis (DKA), and hyperglycemic hypersomolar nonketotic syndrome (HHNKS). Chronic complications of DM include macrovascular disease, microvascular disease, nephropathy, retinopathy, and neuropathy.
ACUTE COMPLICATIONSHypoglycemia
When blood glucose falls below 60 mg/dL (below 70 mg/dL in preschool children) the child experiences hypoglycemia (insulin reaction). Causes of hypoglycemia include taking too much insulin, delaying or omitting meals, and high-energy activities such as playing hard or exercising vigorously without eating extra carbohydrates (exercise moves glucose into muscle cells). Hypoglycemia develops quickly, and the child presents with adrenergic signs such as hunger, weakness, shakiness, sweating, drowsiness, pallor, clammy skin, and headache and central nervous system signs such as irritability, tearfulness, euphoria, or temper tantrum-like behavior. A young child may tell the parent or caregiver that they feel “funny.”
Giving the conscious child simple sugar, such as 4 ounces of juice, regular (not sugarfree) soda, or milk, reverses hypoglycemia. After 10 minutes the blood glucose should be rechecked. If it is still below 60 mg/dL, the juice, soda, or milk is repeated. If the serum glucose is above 60 mg/dL, solid food is given. If the child is unconscious, subcutaneous or intramuscular glucagon or intravenous glucose is administered. Left untreated, loss of consciousness, seizures, and brain damage occur.
Hypoglycemia develops quickly, and the child presents with adrenergic signs such as hunger, weakness, shakiness, sweating, drowsiness, pallor, clammy skin, and headache and central nervous system signs such as irritability, tearfulness, euphoria, or temper tantrum-like behavior.Ketonuria, Ketonemia, and Diabetic Ketoacidosis (DKA)
If the child has an illness, even if it appears to be mild, or if they have a fasting glucose level above 240 mg/dL, the urine and/or serum ketone level(s) should be monitored. Blood ketone levels can be assessed by using the Precision Xtra© meter. If moderate or significant ketones in the urine are detected (ketonuria), if the serum ketone level is above 1.0 mmol/L (ketonemia), or if deep rapid respirations (Kussmaul respirations) are noted, the health care provider must be notified at once.
Diabetic ketoacidosis (DKA) (also known as metabolic acidosis), which has a 3-10% mortality rate, is indicated by a blood pH below 7.30, hyperglycemia (above 250 mg/dL), low serum bicarbonate (below 15 mEq/L), ketonemia, and ketonuria. It develops when there is a lack of insulin, resulting in the inability to use glucose for energy. DKA can result from a severe infection, stress, surgery, and an empty insulin pump or lack of subcutaneous insulin.
Serum glucose levels rise and counter-regulatory hormones are activated. Cortisol, glucagon, and catecholamines stimulate the liver to produce glucose, reduce the utilization of glucose by cells, and initiate lipolysis. Ketone byproducts of lipolysis build up in the bloodstream and are excreted by the kidneys, along with sodium bicarbonate.
Compensatory measures for combating metabolic acidosis include Kussmaul respirations. This type of respiratory pattern allows a large amount of carbon dioxide to be exhaled in an attempt to lower the amount of carbonic acid produced. When water in the blood combines with carbon dioxide carbonic acid is produced, adding to the already high acid load. By lowering the amount of carbon dioxide in the blood, less carbonic acid is produced. As acetone produced by ketosis is released from the bloodstream via respirations, the child’s breath adopts the characteristic fruity odor of DKA. Severe hyperglycemia leads to polyuria, hypovolemia, and hypoperfusion and eventually causes lactic acidosis.
High serum levels of lipids, cholesterol, triglycerides, and free fatty acids are present because the body breaks down fat for an energy source when insulin is not available to move glucose into cells. Electrolyte imbalances also occur during DKA. Potassium shifts from inside the cell to outside the cell in response to metabolic acidosis, resulting in hyperkalemia. Low serum sodium (hyponatremia) occurs because water is pulled into the bloodstream in response to a high glucose load (high serum osmolarity). This increased water load in the bloodstream dilutes serum sodium levels (hemodilution). Serum sodium levels also drop because diuresis associated with severe hyperglycemia flushes sodium out of the body. In addition to a serum pH below 7.3, polyuria, dehydration, and thirst, a child with DKA also presents with nausea, vomiting, abdominal or chest pain, postural hypotension, tachycardia, and central nervous system depression. Chloride, phosphate, and magnesium levels will also be depleted.
Treatment for DKA includes intravenous insulin, fluid, salt and potassium replacement, correction of acidosis, and return to glucose, not fat, utilization for energy. As the hyperglycemia is corrected, potassium
moves back into the cells, so intravenous potassium is given to prevent severe hypokalemia and dysrhythmias. Intracellular osmolality in the brain also increases in response to the severe hyperglycemia; therefore, to prevent cerebral edema and brain herniation from water rapidly infusing brain cells, fluid and glucose correction must be done gradually.
moves back into the cells, so intravenous potassium is given to prevent severe hypokalemia and dysrhythmias. Intracellular osmolality in the brain also increases in response to the severe hyperglycemia; therefore, to prevent cerebral edema and brain herniation from water rapidly infusing brain cells, fluid and glucose correction must be done gradually.
Hyperglycemic Hypersomolar Nonketotic Syndrome (HHNKS)
The mortality rate for hyperglycemic hypersomolar nonketotic syndrome (HHNKS) is 10-20%. This syndrome, which is caused by dehydration, is characterized by a high serum glucose level (800-2,400 mg/dL [hyperglycemic]), a high serum osmolality (340 mOsm/L [hyperosmolar]), and the absence of ketosis (nonketotic). Because children and adolescents with type 2 diabetes mellitus (DM) continue to have an endogenous supply of insulin, lipolysis is suppressed; however, dehydration and electrolyte imbalance are often severe in HHNKS.
Neurological signs such as hemiparesis, seizure, and aphasia are often mistaken for a brain attack (stroke). The child will complain of extreme thirst. Events that may lead to HHNKS include infection.
The treatment for HHNKS is similar to the treatment for DKA, and as in DKA fluid replacement cannot be rapid or cerebral edema results. It may take weeks before potassium stores are returned to normal.
Neurological signs such as hemiparesis, seizure, and aphasia are often mistaken for a brain attack (stroke).
CHRONIC COMPLICATIONSMacrovascular Disease
Under treated or untreated type 2 DM is considered an independent risk factor for coronary artery disease, cerebrovascular disease, and peripheral vascular disease. Because children and adolescents are developing type 2 DM at an alarming rate, they are at risk for developing these chronic complications of DM as adults.
The risk of macrovascular complications is not gender specific, with both men and women at risk for developing coronary artery disease,
myocardial infarction (either silent or with typical presenting signs), angina, brain attack (cerebrovascular accident or stroke), peripheral vascular disease, and sudden death (Table 28-1). It has been estimated that up to 75% of people with type 2 DM will die because of macrovascular disease. The mortality rate after a myocardial infarction is higher in people with diabetes than in the general population.
myocardial infarction (either silent or with typical presenting signs), angina, brain attack (cerebrovascular accident or stroke), peripheral vascular disease, and sudden death (Table 28-1). It has been estimated that up to 75% of people with type 2 DM will die because of macrovascular disease. The mortality rate after a myocardial infarction is higher in people with diabetes than in the general population.
It has been estimated that up to 75% of people with type 2 DM will die because of macrovascular disease.Microvascular Disease
Microvascular disease (nephropathy, retinopathy, and neuropathies) is thought to be caused by capillary vessel occlusion from protein deposits on vessel walls. Microcirculation is compromised by the narrow vessel walls.
Microvascular disease is thought to be caused by capillary vessel occlusion from protein deposits on vessel walls.Table 28-1 Macrovascular Disease Development Theory | ||||||||
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