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. Hypo glycemia, 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 store. 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 fluid, 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 is 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. The microvascular disease may also
impair skin healing, so that even minor breaks in the skin can develop into a major
infection and deep ulcer, especially in the lower extremities. Control of blood
glucose can prevent or delay many of these complications, but may not reverse
them once established. Macrovascular complications involve atherosclerosis of
large blood vessels, such as those supplying the heart, brain, and extremities.
This can lead to angina, myocardial infarction, transient ischemic attacks,
strokes, and peripheral arterial disease.
Cardiovascular disease is 2 to 4
times more prevalent in diabetic patients and is responsible for approximately
75% of diabetes-related deaths. Diabetic foot syndrome is common among
diabetics due to the atherosclerosis of the blood vessels to the extremities.
It results from 3 factors: neuropathy, ischemia, and sepsis. Loss of sensory
nerves in the feet leads to painless trauma and potential ulcer formation. The
lack of blood supply (ischemia) results in slower healing and possible sepsis.
These events can result in gangrene and ultimately amputation.
Blood sugar
control is so important, as well as IV antibiotics to limit the spread of
infection. Foot care is an important aspect of diabetic teaching, with proper
toenail trimming and the use of orthotic shoes to prevent ongoing trauma
associated with a diabetic foot. Immune dysfunction is another major
complication, developing from the direct effects of hyperglycemia on cellular
immunity. Therefore, diabetic patients are especially susceptible to bacterial
and fungal infections. In order to prevent and avoid the complications associated
with diabetes, achieving and maintaining adequate control of blood sugar, diet,
exercise, medications, monitoring, and education is a must.
Let’s go over a couple of questions for review: A patient presents with a blood glucose of 425,
positive ketones in their urine sample, weakness, vomiting, and fruity-smelling
breath.
What complications of diabetes are they exhibiting?
A. Hypoglycemia
B.
Nephropathy
C. Diabetic ketoacidosis
D. Hyperosmolar Hyperglycemic State
If you
chose C, diabetic ketoacidosis, you’re right!
Those are all signs and symptoms
of the acute complication of DKA.
Here’s another one - Microvascular chronic complications
include which of the following?
A. Diabetic
retinopathy and peripheral vascular disease
B. Diabetic nephropathy and diabetic neuropathy
C. Cerebrovascular disease and coronary artery disease
D. All of the above
If you chose B, diabetic nephropathy, and diabetic neuropathy,
you’re correct! Microvascular complications affect the smaller blood vessels
leading to neuropathy, nephropathy, and retinopathy.
Thank you for reading this
article about the complications of diabetes!
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