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Procedure
Practice 08/15/98 - Coding
Recommendations
Feature
Article 08/15/98:
Diabetes Mellitus
Diabetes is a chronic metabolic disease of
the pancreatic islet cells. The cost to treat diabetes in
the United States in 1995, including hospitalizations, medical
care, and supplies, totaled over $46 billion. Over 16 million
people have this serious, lifelong condition, and over 650,000
people are newly diagnosed with diabetes each year. Although
it occurs most often in older adults, diabetes is also one
of the most common chronic childhood diseases in the United
States. About 127,000 children and teenagers age 19 and younger
have diabetes.
Functions of Insulin
Diabetes mellitus occurs when the pancreatic islet cells
cannot produce sufficient insulin or when cells cannot use
insulin efficiently. Insulin has multiple effects that influence
the metabolism of carbohydrates, proteins, and fats. Insulin
enables glucose, the body’s main fuel source, to move
from blood into cells where it is used for growth and energy.
In muscle and liver cells, insulin promotes storage of glucose
as glycogen. In adipose tissue, insulin promotes the conversion
of glucose into fat (triglyceride) and storage of the newly
formed triglyceride within the fat cells. Insulin also promotes
entry of amino acids into the cells and stimulates protein
synthesis. The main stimulus for insulin release is elevation
of the level of glucose in the blood, which usually occurs
immediately after eating.
Biochemical Disturbances
In diabetes mellitus, glucose is absorbed normally into the
bloodstream. However, because of lack of insulin or insulin
insensitivity, it is not used normally for energy generation
and is not stored normally as glycogen. Consequently, it accumulates
in the bloodstream, resulting in a high level of blood glucose
(hyperglycemia). The excessive glucose spills over
into the urine (glycosuria) and is then excreted. Because
the glucose must be excreted in the urine in solution, the
body loses excessive amounts of water and electrolytes. This
may lead to a disturbance in water balance and acid-base balance.
Protein synthesis is also compromised, and body protein is
broken down into amino acids. The liver converts these amino
acids to glucose, augmenting the hyperglycemia and leading
to additional losses of glucose, water, and electrolytes in
the urine.
The three main types of diabetes are insulin-dependent, also
known as Type I diabetes; noninsulin-dependent, also called
Type II diabetes; and gestational diabetes, which occurs during
pregnancy.
Insulin-Dependent Diabetes
Mellitus (IDDM) or Type I Diabetes
IDDM usually results from damage or destruction of the pancreatic
islets, leading to reduction or absence of insulin secretion.
Diabetes sometimes follows a viral infection, which suggests
that the virus may have induced the disease by injuring or
destroying the islets. Many patients with this type of diabetes
have antibodies directed against their own islet cells, indicating
an abnormal immune response may also play a part in causing
the disease.
IDDM most often develops in children and young adults. For
this reason, IDDM used to be known as "juvenile"
diabetes. IDDM is one of the most common chronic disorders
in American children. Each year, from 11,000 to 12,000 children
are diagnosed with IDDM. Among the more than 7 million people
in the United States who are being treated for diabetes, about
5 to 10 percent have IDDM.
Noninsulin-Dependent Diabetes
Mellitus (NIDDM) or Type II Diabetes
NIDDM is the most common type of diabetes. It accounts for
90 to 95 percent of diagnosed diabetes. NIDDM usually develops
in adults over age 40 and is most common in overweight people.
People with NIDDM usually produce some insulin, but the body
cells cannot use it efficiently because the cells are insulin-resistant.
The end result is hyperglycemia and inability of the body
to use its main source of fuel.
Gestational Diabetes
This diabetes classification refers to abnormal glucose tolerance
test results during pregnancy. It usually ends after delivery,
but women with gestational diabetes may develop NIDDM later
in life. Gestational diabetes results from the body's resistance
to the action of insulin. This resistance is caused by hormones
produced by the placenta. Women with gestational diabetes
require treatment for blood glucose control during pregnancy,
primarily to prevent adverse effects to the fetus, but they
return to normal glucose tolerance after pregnancy. Gestational
diabetes is usually treated with dietary adjustments, although
some women may need insulin. Gestational diabetes cannot be
treated with oral hypoglycemic medications because these medicines
can harm the fetus.
Hypoglycemia
Very low blood sugar is called hypoglycemia and is sometimes
referred to as an "insulin reaction." This condition
can be caused by too much insulin, too little or delayed food,
exercise, alcohol, or any combination of these factors. The
normal pancreas continuously monitors blood glucose and adjusts
insulin output to maintain a normal blood sugar range of 70-110
mg/dl. The patient with IDDM must constantly adjust the insulin
dose to match exercise and eating patterns. If there is too
much insulin, blood sugar drops and hypoglycemia results.
The adrenal glands respond to the hypoglycemia by releasing
epinephrine. The epinephrine causes conversion of stored glycogen
to glucose and the blood sugar goes up. Epinephrine also causes
other body responses: sweating, hyperactive reflexes, rapid
heart rate, elevated blood pressure, anxiety, and tremors.
Because the nervous system requires glucose to function properly,
neurologic symptoms occur if the blood sugar continues to
fall. The patient becomes confused, may lose consciousness
or have convulsions, and if left untreated, will lapse into
a coma.
Diabetic Ketoacidosis
This condition occurs only in people with IDDM. In addition
to causing hyperglycemia, lack of insulin causes the body
to break down stored fats in an effort to provide cells with
alternative fuel sources. Organic acids called ketone bodies
are a waste byproduct of the fat-to-energy conversion. Ketones
accumulate in the blood and spill over into the urine as the
body attempts to excrete them. This condition is called ketosis.
The circulatory system has a natural bicarbonate buffer system
to neutralize the acid from the ketones, but in severe diabetes,
this buffer system cannot maintain a normal pH and diabetic
ketoacidosis (DKA) results. Symptoms of ketoacidosis include
abdominal pain, vomiting, rapid breathing, and extreme fatigue.
A "fruity odor" is often detected on the breath
of a patient in diabetic ketoacidosis. This odor is due to
the respiratory system’s efforts to rid the body of acetone,
another waste product of ketosis. Acetone is a central nervous
system anesthetic. Although the exact cause of DKA coma has
not been clearly established, excess acetone is considered
a contributing factor.
Nonketotic Hyperglycemic
Hyperosmolar Coma (NKHHC)
NKHHC is an acute complication caused by the hyperglycemia
that occurs in NIDDM. Much less insulin is needed to prevent
conversion of stored fat to energy than is needed to move
glucose from the bloodstream into cells. Although the cells
of people with NIDDM are resistant to insulin, the cells’
response to insulin is adequate to prevent ketosis, but inadequate
to prevent hyperglycemia. Consequently, as blood sugars rise,
water moves by osmosis from the cells into the more concentrated,
glucose-laden extracellular solution. The cells become dehydrated,
neuron function is impaired, and coma results.
Diabetes is associated with long-term complications that
affect almost every major part of the body. It contributes
to blindness, heart disease, strokes, kidney failure, amputations,
and nerve damage. Uncontrolled diabetes can complicate pregnancy
and cause birth defects in babies born to women with diabetes.
Diabetic Nephropathy
Diabetic Nephopathy (kidney disease) is a life-threatening
complication of IDDM in about 40 percent of people who have
had diabetes for 20 or more years. Degenerative changes occur
within the glomerular arterioles and capillaries within the
kidneys. These changes impair renal function and may result
in renal failure or end-stage renal disease (ESRD). Patients
with ESRD require regular dialysis.
Diabetic Eye Disease
Diabetes may lead to several types of eye damage:
- Diabetic retinopathy is
the leading cause of blindness in American adults. It is
caused by damage to the capillaries that supply the retina
with blood. Over time, the blood vessels may rupture or
leak. In patients with high blood sugars, retinopathy becomes
more severe and new blood vessels may grow on the retina.
These vessels may bleed into the vitreous (the clear gel
that fills the eye) or detach the retina from its normal
position because of bleeding or scar formation.
- Cataracts are degenerative
opacities of the lens of the eye accompanied by painless,
progressive loss of vision. Diabetics are more susceptible
to senile cataracts and develop them at an earlier age than
nondiabetics. People with IDDM may also have a true diabetic
cataract, known as a snowflake cataract.
- Glaucoma is an increase
in fluid pressure inside the eye that leads to optic nerve
damage and loss of vision.
Diabetic Neuropathy
This condition can develop at any time. The etiology of diabetic
neuropathy is uncertain, but several factors are likely to
contribute to the disorder. Hyperglycemia causes chemical
changes in nerves that impair their ability to transmit signals.
Researchers have discovered that high glucose levels cause
an accumulation of a sugar called sorbitol and depletion of
a substance called myoinositol. However, studies have not
shown conclusively that these changes are the direct cause
of nerve damage. More recently, researchers have focused on
the effects of excessive glucose metabolism on the amount
of nitric oxide in nerves. Nitric oxide dilates blood vessels.
In diabetics, low levels of nitric oxide may cause constriction
of blood vessels supplying the nerves, contributing to nerve
damage. Ongoing research focuses on how these changes occur,
how they are connected, how they cause nerve damage, and how
to prevent and treat damage.
Significant neuropathy often occurs within the first 10 years
after diagnosis of diabetes, and the risk of developing neuropathy
increases the longer a person has diabetes. Symptoms depend
upon which nerves are affected. Neuropathy may be diffuse,
affecting many parts of the body, or focal, affecting
a single nerve or body part.
- Diffuse Neuropathy
The two categories of diffuse neuropathy are peripheral
neuropathy affecting the feet and hands and autonomic
neuropathy affecting the internal organs.
Peripheral neuropathy most commonly damages the
nerves of the limbs, especially the feet. Nerves on both
sides of the body are affected. Common symptoms of this
kind of neuropathy are numbness or insensitivity to pain
or temperature; tingling, burning, or prickling; sharp pains
or cramps; extreme sensitivity to touch; or loss of balance
and coordination.
The damage to nerves often results in loss of reflexes and
muscle weakness. The foot often becomes wider and shorter,
the gait changes, and foot ulcers occur as pressure is put
on parts of the foot that are less protected. Because of
the loss of sensation, injuries may go unnoticed and often
become infected. If ulcers or foot injuries are not treated,
the infection may involve the bone (osteomyelitis)
and require amputation.
Autonomic Neuropathy (Visceral Neuropathy) affects
the nerves that serve the heart and internal organs and
produces changes in many processes and systems:
- Urination and sexual response. Autonomic neuropathy
most often affects the organs that control urination and
sexual function. Nerve damage can prevent the bladder
from emptying completely, so bacteria grow more easily
in the urinary tract. When the nerves of the bladder are
damaged, a person may have difficulty knowing when the
bladder is full, resulting in urinary incontinence. The
nerve damage and circulatory problems of diabetes can
also lead to a gradual loss of sexual response in both
men and women.
- Digestion. Digestion is affected when nerve damage
causes the stomach to empty too slowly, a disorder called
gastric stasis. When the condition is severe (gastroparesis),
it is accompanied by persistent nausea and vomiting, bloating,
and loss of appetite. Blood glucose levels tend to fluctuate
greatly with this condition. If nerves in the esophagus
are involved, swallowing may be difficult. Nerve damage
to the bowels can cause constipation or frequent diarrhea.
- Cardiovascular system. Damage to the cardiovascular
system interferes with the nerve impulses from various
parts of the body that signal the need for blood, regulate
blood pressure, and control heart rate. As a result, blood
pressure may drop sharply after sitting or standing (orthostatic
hypotension), causing light-headedness or syncope.
Cardiovascular neuropathy may also affect the perception
of pain from heart disease. People may not experience
angina, or they may suffer painless heart attacks.
- Perspiration. Autonomic neuropathy may affect
the nerves that control sweat glands, making it difficult
for the body to regulate its temperature. The nerve damage
may cause profuse perspiration (hyperhidrosis)
or a marked decrease in perspiration (hypohidrosis
or hyphidrosis).
- Focal Neuropathy (Multiplex Neuropathy)
Occasionally, diabetic neuropathy appears suddenly and affects
specific nerves in the trunk, legs, or head. Focal neuropathy
is unpredictable and occurs most often in older people who
have mild diabetes. Although painful, it is usually a self-limiting
problem that improves after a period of weeks or months
without causing long-term damage. Pain may occur in the
front of the leg or thigh; in the pelvis and low back; in
one side of the face, causing facial paralysis (Bell’s
palsy); behind the eye; or in the chest or abdomen.
Focal neuropathy may also cause double vision (diplopia),
inability to focus the eye, and hearing problems.
Cardiovascular and Circulatory
Disease
Diabetics have increased risk of arteriosclerosis and associated
vascular complications such as stroke, heart attack, and gangrene
of the extremities due to ischemia. Diabetic vascular problems
are believed to result from both abnormalities in fat metabolism
and elevated blood lipids. People with diabetes are at greater
risk for stroke and other forms of large blood vessel disease.
Blockage of blood vessels in the extremities is called peripheral
vascular disease (PVD). PVD causes poor circulation and
contributes to foot and leg ulcers.
Periodontal (Gum) Disease
Periodontal disease is the inflammation of the tissues that
surround and support the teeth: gingiva, alveolar bone, periodontal
ligament, and cementum. Periodontal disease starts as gingivitis,
which causes sore, bleeding gums. Without treatment, teeth
may loosen and fall out.
Diabetics with poor sugar control are especially susceptible
to gingivitis.
Diabetes causes increased risks of obstetric complications
such as infection, diabetic ketoacidosis, preterm labor, and
pregnancy-induced hypertension. Type I or II diabetic pregnancies
also involve increased risk of neonatal mortality due to congenital
malformation. Prenatal screenings of high risk diabetic mothers
with serum alpha-fetoprotein testing, ultrasound imaging,
nonstress testing, and fetal echocardiography, increase the
chances for a healthy pregnancy and delivery. Infants of diabetic
mothers are often large for gestational age (LGA).
They are generally heavy with poor muscle tone, and they are
at increased risk for hyperbilirubinemia.
Illness and stress raise blood glucose levels. Hospitalized
patients with NIDDM sometimes need a brief period of insulin
therapy during an acute phase of illness or injury. Coders
may mistakenly conclude that because the chart documents insulin
therapy, the patient has IDDM. Any questions about the nature
of the patient’s diabetes should be brought to the attending
physician.
Before the discovery of insulin in 1921, all people with
IDDM died within a few years after the appearance of the disease.
Although insulin injections do not cure diabetes, its discovery
was the first major breakthrough in diabetes treatment. Today,
daily injections of insulin are the basic therapy for IDDM.
Injections must be balanced with meals and daily activities,
and glucose levels must be closely monitored through frequent
blood sugar testing. Diet, exercise, and blood testing for
glucose are also the basis for management of NIDDM. In addition,
some people with NIDDM take oral hypoglycemic drugs or insulin
to lower their blood glucose levels.
In recent years, advances in diabetes research have led to
better ways to manage diabetes and treat its complications.
Major advances include:
- Genetically engineered insulin that reduces allergic
and other adverse reactions;
- Self-monitoring of blood glucose to enable closer diabetic
control;
- Hemoglobin A1c testing to monitor average blood glucoses
over a 2-3 month period;
- External and implantable insulin pumps that deliver
insulin in a more natural way, simulating normal pancreatic
function;
- Laser treatment for diabetic eye disease, reducing the
risk of blindness;
- New oral agents to treat NIDDM;
- Use of antihypertensive ACE-inhibitors to prevent or
delay kidney failure in diabetics; and
- Pancreas and islet cell transplantation
Other improvements in diabetes management being developed
include insulin in the form of nasal sprays, patches, or pills
and devices to test blood sugar levels without having to prick
a finger to get a blood sample.
Researchers are working to develop less harmful drugs and
better methods of transplanting pancreatic tissue to prevent
rejection by the body, such as encapsulating the islet cells
in a semi-permeable membrane that offers protection from immune
attack, implanting the cells in the thymus gland to induce
tolerance by the immune system, and using bioengineering techniques
to create artificial islet cells that secrete insulin in response
to increased sugar levels in the blood.
Test Your Coding Skills!
Because of the complexities involved in selecting
and sequencing the correct diagnosis codes for diabetes and
its complications, this month’s procedure
practice uses a real discharge
summary instead of our usual operative report. Read the summary
carefully and then assign and sequence all diagnoses and procedures.
Use both ICD-9-CM and CPT-4 procedure codes when applicable
for procedure coding. Compare your answers with our
coding recommendations.
Good luck!
Back to:
Top
- Basic
Biochemistry - Types
of Diabetes - Acute
Complications - Late
Complications
Complications
of Pregnancy - Illness
and Stress - Treatment
- Current
Research
If you have comments or suggestions about our code selections
or about any topic on our Coding Edge® pages, please e-mail
us at codingedge@lagunamedsys.com.
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