Diabetes Complications | NCLEX RN Review
Diabetes is a group of metabolic diseases characterized by hyperglycemia (high blood sugar) that results from defects in insulin secretion, insulin action, or both, and affects multiple systems of the body. Uncontrolled diabetes can cause metabolic imbalance leading to acute complications, requiring immediate medical attention.
Ongoing hyperglycemia will then develop into chronic complications. Let’s start by looking at the acute complications that require immediate medical intervention. Hypoglycemia, or a blood glucose level of less than 60 mg/dL, is a potential complication of insulin therapy or oral hypoglycemic agents.
It can also be caused by skipping a meal, inconsistent carbohydrate intake, over-exercising, or alcohol consumption. Common signs and symptoms of hypoglycemia may be adrenergic (caused by activation of the sympathetic nervous system) or neuroglycopenic(which is caused by depression of central nervous system acts as the brain receives an insufficient supply of glucose).
Adrenergic symptoms usually result from a rapid drop in glucose and occur first, including being pale, sweaty, having tachycardia, palpitations, nervousness, irritability, feeling cold, weak, trembling, and hungry. The particular signs and symptoms vary depending on the blood glucose level, how fast the glucose level dropped, and the duration of hypoglycemia.
When hypoglycemia is slow-developing, as with long-acting insulin or with oral hypoglycemic agents, the central nervous system signs and symptoms predominate. Those signs include headache, mental confusion, numbness around the mouth, incoherent speech, double vision, fatigue, emotional lability, convulsions, and coma.
If a rapid drop in blood sugar occurs and is allowed to persist, both the sympathetic and central nervous system signs usually occur. The diabetic patient should be educated about recognizing signs of hypoglycemia and how to treat it.
As long as the patient is conscious, they should self-treat with 15 g of quick-acting carbohydrates, such as 4 oz of juice (no added sugar), 3-4 glucose tablets, or 3 hard candies. Recheck the fingerstick blood glucose in 15minutes and if it remains below 60, the patient should self-treat again.
In an unconscious patient, never try to give oral glucose. In the hospital setting, one ampule of 50%dextrose is given IV push. In the outpatient setting a friend or family member can inject 1mg of glucagon subcutaneously, which causes the liver to release its glycogen stores.
The patient will usually regain consciousness within 10-20 minutes, and should then eat a snack of 45g carbohydrates to aid in replacing glycogen stores. Patients are often nauseated after receiving glucagon and may vomit.
When hypoglycemia is severe, seizures may also occur. Diabetic ketoacidosis (DKA) is another serious acute complication when excess blood acids, called ketones, build up in the body. Ketones are formed when the body burns fat for fuel instead of glucose.
This can occur when there is not enough insulin in the body to process sugars. DKA is triggered by illness or not taking insulin. The progressive hyperglycemia causes glucose to spill out into the urine, resulting in water and electrolyte losses, causing dehydration and an increase in thirst. The lack of insulin and the corresponding elevation of glucagon leads to increased release of glucose by the liver as well as ketone bodies, which are acidic and must be cleared from the circulation.
DKA can occur in patients with type 1 or type2 diabetes, but it’s rare with type 2. The risk for DKA is increased with type 1 diabetes, under age 19, stress, physical or emotional trauma, high fever, heart attack, stroke, smoking, or drugs/alcohol.
Signs and symptoms of DKA include high blood sugar levels, high levels of ketones in urine, fruity-smelling breath, flushed face, nausea and vomiting, abdominal pain, rapid deep gasping breaths, frequent urination, extreme thirst, dry mouth and skin, weakness, confusion, and loss of consciousness.
If left untreated, DKA can lead to coma or death. Treatment involves rehydration with IV fluids, insulin therapy, and electrolyte replacement. Hyperglycemic Hyperosmolar Nonketotic Syndrome(HHNS) has some similarities to DKA but is an acute complication of type 2 diabetes.
The differences include profound dehydration, with the fluid deficit as high as 8-9 liters. Blood sugar levels are higher, with serum glucose levels in the range of 600 to 2000.
Ketosis is absent because patients with type2 diabetes have insulin secretion to prevent ketosis. The kidneys try to get rid of the extra blood sugar by putting more glucose into the urine, which increases urination and loss of body fluids, causing dehydration.
Dehydration makes the blood thicker and the blood sugar level is too high for the kidneys to be able to fix. This also causes an imbalance of minerals in the blood, especially sodium and potassium.
This imbalance of fluids, glucose, and minerals in the body can lead to severe problems, such as brain swelling, abnormal heart rhythms, seizures, coma, or organ failure. Without rapid treatment, HHNS can cause death.
Primary treatment involves IV rehydration, which resolves the hyperglycemia, so IV insulin is usually not needed. Ok, now let’s look at the chronic complications of diabetes, that develop from ongoing hyperglycemia.
They are classified as microvascular or macrovascular. These complications are a result of the length and degree of hyperglycemia.
Microvascular complications affect the smaller blood vessels, such as the eyes (leading to diabetic retinopathy), kidneys (leading to diabetic nephropathy), and nerves (leading to neuropathy).
The effects of high blood glucose, as well as high blood pressure, can damage eye blood vessels, causing retinopathy, cataracts, and glaucoma.
Diabetic retinopathy is the leading cause of new blindness among adults 20 to 74 years old in the United States. High blood pressure also accelerates the development and progression of retinopathy.
Diabetic nephropathy is the leading cause of end-stage renal disease in the US, with 20% of all diabetic patients having nephropathy. Excess blood glucose overworks the kidneys and high blood pressure damages the small blood vessels.
Microscopic amounts of albumin in the urine the earliest lab abnormality, which may then progress to albuminuria (clinical proteinuria). Aggressive blood pressure control lessens the albuminuria, decreases the rate of deterioration of the kidneys, and improves survival.
Diabetic neuropathy affects 60-70% of diabetic patients and involves damage to nerves in the peripheral nervous system. The most common symptoms involve numbness in the legs or feet; but depending on the nerves affected, it can also cause shooting pains; problems with the digestive system, urinary tract, blood vessels, and the heart.