Transcript Provider Documentation for Coding and Reimbursement

Basic Diabetes Mellitus Pathology
and Diagnosis Coding
January 23, 2008 1– 3 pm MST
Irene Mueller, EdD, RHIA
Montana Hospital
Association
MT-NC Tele-Video
Spring 2008
http://www.medicinenet.com/diabetes_mellitus/article.htm
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Objective
Assign correct ICD-9-CM codes by
applying knowledge of
• Basic ICD-9-CM coding conventions,
• Basic ICD-9-CM coding process, and
• DM Anatomy, Types, Etiology, Signs and
Symptoms, Diagnosis, Acute and Chronic
Complications (Manifestations), and
Treatments
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1/23/08 Schedule
• 1pm – 1:05
– Introductions/Overview of session
• 1:05 – 1:50 pm
– Diabetes Mellitus Pathology
• 1:50 – 2 pm Break
• 2:00 - 2:45
– DM Coding Process
• 2:45- 3:00 pm
– Questions
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Anatomy of Diabetes
• Diabetes Mellitus
–
–
–
–
1st described in 1552 BC
Mellitus = Honey
Urine smells sweet
Food Metabolism disorder
• Pancreas
• Insulin hormone
– Polydipsia, Polyuria,
– Polyphagia
• 3rd leading cause of
DEATH in US (7th in 1996)
• DM costs $98 BILLION
annually in US
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• Diabetes Insipidus
–
–
–
–
1761 –Scots carried to NA
Insipidus = tasteless
Urine has no odor
Water Metabolism disorder
• Kidney (NDI)
• Pituitary (CDI)
– Polydipsia, Polyuria
– Much rarer
• 3/100,000
Pancreas
• Accessory organ of Digestive System
– compound gland, has endocrine and exocrine functions
• Responds to hormones
– when food enters the duodenum, secretin & pancreozymin
are released into the bloodstream
• Functions3
– the pancreatic cells produce & release large amounts of
water, bicarbonate, and digestive enzymes, which flow into
the intestine (exocrines).
– Islets (or islands) of Langerhans - secrete insulin and
glucagon, which control sugar storage in the body. Insulin
stimulates cells to remove sugar from the bloodstream and
use it. Glucagon releases stored sugar and increases the
blood sugar level, acting as a control mechanism
whenever the body produces too much insulin. They are
both secreted directly into the bloodstream (endocrines).
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Pancreas Anatomy
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Normal glucose control
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Source: http://cascadevalley.org/resources/news/fw04-3.php
DM Definition
• “A group of metabolic diseases
characterized by high blood sugar
(glucose) levels, which result from defects
in insulin secretion, or action, or both.”1
• “A chronic disorder of carbohydrate, fat,
and protein metabolism caused by
inadequate production of insulin by the
pancreas OR faulty utilization of insulin by
the cells”2 of the body.
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Etiology of DM
• When blood glucose rises (after eating)
insulin is released
• Insulin helps the cells take in glucose and
convert it to energy.
• Extra fat tissue can make your body
resistant to the action of insulin, but
exercise helps insulin work well.
• DM occurs when insulin is absent,
insufficient, or not used properly.
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Types of DM
•
•
•
•
•
•
•
Pre-Diabetes
Type 1 (about 10% of patients, 1 million in US)
Type 2 (about 90% of patients)
Gestational DM (GDM)
Neonatal DM
Secondary DM
Wolfram syndrome
– Autosomal recessive
– Type 1 DM, DI, Optic atrophy, Deafness, Ataxia,
Peripheral neuropathy
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Pre-Diabetes
• At least 54 million U.S. adults had prediabetes in 2002.
• Most people with pre-diabetes develop
Type 2 DM within 10 years
– Unless lose 5 to 7 % of body weight—about
10/15 pounds for someone who weighs 200
lbs.
• Pre-diabetes also creates a higher risk of
heart disease.
• Also documented as impaired fasting
glucose (IFG = 100 – 126 mg/dl) or
impaired glucose tolerance (IGT)
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Risk Factors for Pre-Diabetes
• Genes are partly responsible
• Too much fat interferes with muscles'
ability to use insulin.
• Lack of exercise further reduces
muscles' ability to use insulin.
• Metabolic Syndrome (Insulin
Resistance Syndrome, formerly
Syndrome X).
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Metabolic Syndrome
• Insulin Resistance Syndrome, (formerly
Syndrome X). Any 3 of the following
– excess weight around the waist (central
obesity – apple vs pear) (40+ inches - males,
35+ inches –females),
– low HDL (good) cholesterol levels, (<40 mg/dL
– males, <50 – females)
– high levels of triglycerides (150 mg/dL +)
– high blood pressure (130/85),
– high fasting blood glucose (110mg/dL +)
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Type 1 DM
• Previously IDDM, juvenile onset, ketone-prone
• Autoimmune disease
– Immune system attacks beta cells in pancreas, which
can’t make insulin
• Causes include
– Genetic (white, northern European heritage)
– Viral infections (mumps, Coxsackie)
– Environmental toxins? (cow’s milk/wheat in early diet?)
rat poison (pyriminil)
• Insulin tx required for survival
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Type 1 DM
• Usually occurs in young (<30), lean people
• Older patients can get Type 1
– LADA – Latent Autoimmune Diabetes in Adults
– Slow, progressive form of Type 1 DM
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Type 2 DM
• Previously - NIDDM, adult-onset DM (AODM),
maturity onset, ketosis resistant, non-ketosis
prone
• Patients produce inadequate insulin, even if
more than normal amounts, because of
• Insulin resistance
– Cells of body are insensitive to insulin
– Especially muscle and fat cells
• Steady Decline in insulin production
• Glucogenesis by liver continues even though
glucose is elevated
• Recent studies show 15 to 45 % of all children
with DM have Type 2 DM.
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Risk Factors for Type 2 DM
• Obesity in adults and children
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– Chance of DM doubles with every
20% increase over desirable body
weight.
– The CDC predicts if the current rate
of obesity continues, one-third of the
children born in 2000 will develop
DM.
– up to 85% of children with Type 2 DM
are obese.
– Obese diabetics are also insulin
resistant.
Risk Factors for Type 2 DM
• Obesity and insulin resistance
– Research indicates
– Fat cells produce fatty acids and secrete
proteins that interfere with secretion and
action of insulin
• Obesity is most important controllable risk
factor
• High saturated fats, refined carbs,
sedentary lifestyle
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Other Risk Factors for Type 2 DM
• Genetics - 45%-80% of diabetics have at least one
parent with DM or a hx of DM over several
generations.
• Race - more common among African-Americans,
Mexican-Americans, and American Indians.
• Sex - Girls are nearly twice as likely as boys to
develop type 2 DM. This is due to a greater insulin
resistance.
• Puberty - Most cases of DM in children are
diagnosed between the ages of 12-16. During puberty
there is increased resistance to insulin action,
resulting in hyperinsulinemia. Growth hormone, which
increases slightly in puberty, also has anti-insulin
effects.
• Age – prevalence increases with years of age
• Prior gestational diabetes
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Gestational DM
• Pregnancy-related hormone changes can
elevate glucose in genetically-predisposed
• Usually resolves after birth
• 25-50% of GDM women will get Type 2 DM
– Require insulin during pregnancy
– Remain overweight after birth
• Risk factors
– Family hx of DM, Obesity, 25+ yo
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Neonatal DM
• Rare metabolic disorder (1 of every
300,000-400,000 newborns)
– Autosomal dominant genetic disorder
– Within first 3 -6 months of life
– Hyperglycemia combined with low insulin
levels
– Two groups
• Transient NDM (50-60% of cases)
• Permanent NDM
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Secondary DM
• Caused by another medical condition
– Pancreas affected
• Chronic pancreatitis (alcohol, other toxins)
• Trauma
• Surgical removal results in DM Type 1
– Hormonal disturbances
• Acromegaly (excessive growth hormone)
• Cushing syndrome (excessive cortisol)
– Medications may cause DM/worsen control
• Corticosteroids, diuretics, beta blockers, some antipsychotics (schizophrenia)
• Tx of HIV/AIDS (Pentam)
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Tx of cancer - Asparaginase (Elspar)
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Signs and Symptoms of DM
• Hyperglycemia
• Cells deprived of fuel
– Metabolize fats & protein
– Ketone bodies as waste in
blood (ketosis)
• Ketonuria
• Acidosis
• Dehydration
• N&V
• Fruity breath odor
• Yeast infections
• Bladder & Skin infections
• Coma
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•
•
•
•
•
•
•
Polyuria
Polyphagia
Polydipsia
Weight loss
Fatigue
Pruritis (genital area)
Blurred vision
• GDM – may be
symptomless!
Diagnosis of DM
• Patient Hx
• 2 + tests on different days
– Fasting Glucose
• Presence in urine
• Glucose
– Acetone
• Insulin level in blood
• Eye exam to check for diabetic retinopathy
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Glucose Testing
• GTT (Glucose
Tolerance Test)
• Urine tests should be
negative for presence
of glucose
• 2 hour postprandial
– Usually after lunch
– 65-139 mg/dl
• Random – 200+ = DM
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GTT Results
Time
Normal
Fasting*
70-100
(preferred) mg/dl
30 minutes 100-140
1 hour
120-170
2 hours
70-120
3 hours
70-120
* Fasting = 8 hours minimum
Complications vs Manifestations
• Complication – “a secondary disease or
condition that develops in the course of a
primary disease or condition and arises
either as a result of it or from independent
causes”
• Manifestation – “a perceptible, outward, or
visible expression (as of a disease or
abnormal condition)”
• Source: MedlinePlus dictionary
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Acute Manifestations
• Diabetic ketoacidosis (DKA)
– usually Type 1 DM
• Hyperosmolarity
– usually Type 2
• Hypoglycemia
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Diabetic Ketoacidosis
– Ketones in blood turn blood acidic
– S&S/Finding
• – N&V, abdominal pain
• Glycourea, hyperglycemia, acidosis, low plasma
bicarbonate
– Progresses rapidly to shock, coma, death
– Also caused by infection, stress, trauma,
meds (corticosteroids)
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Hyperosmolarity
• Hyperosmolarity – the blood has a high concentration of
sodium, glucose, and other molecules that normally
attract water into the bloodstream.
• When kidneys are conserving water (dehydration),
glucose can’t leave body in urine, causing higher glucose
in blood, which increases need for fluids, etc.
• Causes include: infection, meds that lower glucose
tolerance or increase fluid loss, inability to control
glucose, stress (AMI, stroke, etc).
• S&S: weakness, thirst, nausea, lethargy, confusion,
convulsions, speech impairment, dysfunctional
movement, loss of feeling, coma
• Coma (higher risk of death than DKA)
– NKHHC Nonketontic hyperglycemic hyperosmolar coma
– HONK - hyperosmolar non-ketontic coma
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Hypoglycemia
• Abnormally low blood glucose
– Too much meds/insulin (Insulin reaction)
– Missed meal
– Excessive exercise
– CNS S&S – dizzy, confused, weak, tremors
– Blood glucose = < 65 mg/dl
– Can progress to coma, seizures, brain death
• <40 mg/dl
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Chronic Manifestations
• Caused by blood vessel disease
– Microvascular
• Eyes, Kidneys, Nerves
– Macrovascular
• Heart
• DM accelerates arterio/atherosclerosis
• ASCVD can result in (angina, MI), stroke,
claudication, BUT are NOT direct DM complications
• Periodontal disease
– untreated also makes control of DM more difficult
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Eye Complications
•
•
•
•
•
•
•
Diabetic Retinopathy
Clinically significant macula edema
Vitreous hemorrhage
Retinal detachment
Proliferative vitreoretinopthy
Neovascular glaucoma
Diabetic cataract
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Eye complications
•
•
•
•
Diabetic Retinopathy
DM for at least 5 years
Small blood vessels leak protein/blood
Also causes microaneurysms/neovasularization
(brittle)
• Progresses to retinal scarring and detachment
(impaired vision, blindness)
• 50% of patients have this after 10 years
• 80% of patients have this after 15 years
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Diabetic Retinopathy
• Nonproliferative (Background)
– Microaneurysms and intraretinal hemorrhages
• Proliferative
– More extensive hemorrhages
– Neovascularization
• Disease progresses from mild to moderate to
severe diabetic nonproliferative, then to
proliferative
• Diabetic macular edema can occur at any stage
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Eye
• Cataracts and Glaucoma more common in
Diabetics
• When glucose varies, lens of eye shrinks
and swells, causing blurry vision
• Blood glucose should be controlled before
new eye prescription
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Kidney Complications
• Diabetic nephropathy
• 1st, small blood vessel disease causes
leakage of protein in urine
• 2nd, kidneys lose ability to clean/filter blood
• 3rd, need for dialysis / transplant
• Progression slows significantly with control
of HBP and high blood glucose
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Renal manifestations
• Diabetic renal failure
• Diabetic uremia
• Diabetic glomerulonephrosis
with renal failure
• Diabetic nephropathy
with chronic renal failure
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Nerve complications
• Diabetic neuropathy
• Caused by ischemia
• Symptoms
– Numbness, burning, aching of feet/lower ext.
– Lack of awareness of injuries
– Combined with poor blood flow, can lead to
serious infections, ulcers, gangrene
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Nerve Complications
• Erectile Dysfunction
– Also caused by poor blood flow due to DM
• Gastroparesis – Stomach and intestines
nerves affected
– ineffective contractions, delayed emptying of
stomach
– Nausea
– Weight loss
– Diarrhea
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Prevention of Type 2 DM
• Diabetes Prevention Program (DPP)
• 3,234 Americans
– IGT
• Diet and Exercise
– Lost 5-7% of weight
– Exercised 30 minutes/day
• Reduced risk of DM Type 2 by 58%
• Metformin (Glucophage) reduced risk by
31%
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Tx of DM
• Intense control of blood glucose (not too low)
– Decreases complications
• Nephropathy
• Neuropathy
• Retinopathy
• Macrovascular conditions
– FG – 70-120 mg/dl
– <160 after meals
– A1c level near normal
• Decrease insulin demand (diet, exercise, drugs)
• Increase insulin supply (insulin, other meds)
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Monitoring Glucose Levels
• Patient self-testing
• Hemoglobin A1c
– Indicates how much glucose sticks to a red
blood cell over its life of 3 months
– Gives an overview of pt’s glucose control
– Normal = 4 – 5.9%, <5%
– Well controlled DM patients = < 6.5 – 7%
• Mean blood glucose = 145 -170
– Poorly controlled DM patients = 8%+
• Mean blood glucose = 205 +
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A1c
• 10% decrease of microvascular disease
for every 1% reduction of A1c
– 37% decrease for Type 2 DM
• 24% decrease of macrovascular disease
for every 1% reduction of A1c
• 14% decrease of MI for every 1%
decrease of A1c in Type 2 DM
• 21% decrease of Death for every 1%
decrease ofA1c in Type 2 DM
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Medications for type 1 DM
• Insulin
– 1977 human insulin gene cloned – Inhaled insulin
Exubera
– Human insulin now used
Why can’t
• Insulin administration insulin be • Smokers can’t use
• Not sold anymore
taken
in
– Pre-filled pens
(not accepted by
pill form?
– Insulin pumps
pts/drs
• Reservoir, pump, computer
– Intranasal,
• About size of pager
Transderm
• Continuous delivery
• Disappointing results
• Used w/ implantable glucose
– Pancreas
sensors
transplants
• Newest sensors communicate
• Whole pancreas
directly w/insulin pump
(1995 – 8,000)
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• Islet cells
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Medications for type 2 DM
• Meds designed to
– Increase insulin output of pancreas
• Sulfonyureas
• Meglitinides (Prandin, Starlix)
– Decrease glucose release by liver
• Biguanides (metformin (Glucophage)
– Increase target cells’ sensitivity to insulin
• Thiazolidinediones (Rezulin – off market now)
– (Actos, Avandia)
– Decrease absorption of carbs (intestines)
• Enzyme inhibitor (alpha glucosidase inhibitor
(Precose))
– Slow emptying of stomach
• Byetta
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Meds for type 2 DM
• New meds that affect glycemic control
–
–
–
–
Pramlintide (Symlin)
Used with insulin in Type 1 and 2 diabetics
Exenatide (Byetta) – incretin mimetic
These are injected
• DPP-IV inhibitors
– DPP IV is an enzyme that breaks down GLP-1
– Januvia (pill)
• Combination meds
– Glucovance (glyburide/metformin
– Avandmet (rosiglitazone/metformin)
– Metaglip (glipizide/metformin)
– Pioglitazone/metformin (Actosplusmet
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Tx of DM Complications
• Nerve damage pain
– Gabapentin (Neurontin)
– Phenytoin (Dilantin)
– Carbamazepine (Tegretol)
– Despramine (Norpraminine)
– Amitriptyline (Elavil)
– Capsaicin applied topically
– Pregabalin (Lyrica)
– Duloxetine (Cymbalta)
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Break Time
Fluid Exchanges
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Coding DM Diagnoses
• Basic Conventions
– Paired etiology/manifestation convention (dual
coding)
– Multiple codes
– Sequencing
– Index – slanted brackets
– Tabular List - “with”, italics,
• Official Guidelines
– Section I.C.3.A.1-5
– Section I.C.11.F, G
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– Section
I.C.18.D.3
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RHIA
Pre-Diabetes
• Code 790.29
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DM codes
• 250 4th digit
– Presence of any associated manifestation
• 250 5th digit
– Type of DM
– Whether or not “uncontrolled”
• Assign as many 250 codes as needed to
identify all complications/manifestations
• Lists of manifestations under 250.x are
NOT ONLY choices, give examples
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DM documentation
• Dx of diabetes w/o qualification is
interpreted as DM
• Physician must clearly id the DM as cause
of complication or manifestation in order to
use DM codes (250.xx)
• Pt use of insulin does NOT indicate Type 1
• If type not specified, used Type 2, even
when pt is using insulin
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Adjectives in Documentation
• Out of control, brittle, uncontrolled
– Blood sugar is not kept within acceptable
limits by tx
– Indicates that DM has complications
– Specified complication – code complication
with 4th and 5th digit and paired code
– Unspecified complication – use 4th digit .9
• Diabetic, due to DM, etc.
– Establishes cause and effect
– Code book sometimes assumes (Index) HOW?
– If not clearly documented, query physician
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Modified Documentation
• “poorly controlled” or “poor control” are
NOT same as “out of control”
• Need to query Dr or code not stated as
uncontrolled
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Acute Complications of DM
• Ketoacidosis (DKA)
• Hyperosmolarity
• Other coma
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Ketoacidosis
• Also occurs in alcoholism
• So documentation must connect DM with
ketoacidosis
• 250.1x is only code required
• Can occur in Type 2 DM, but 97% of time in
Type 1 (so code type 1, unless Dr states 2)
• Claims with 250.12 may be queried
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Hyperosmolarity w or w/o Coma
• 250.2x
• Causes include: infection, meds that lower
glucose tolerance or increase fluid loss,
inability to control glucose, stress (AMI,
stroke, etc).
• S&S: weakness, thirst, nausea, lethargy,
confusion, convulsions, speech
impairment, dysfunctional movement, loss
of feeling, coma
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Other coma
• Pts with ketoacidosis who have
progressed to a comatose state
• Hypoglycemic coma in a diabetic pt
• Insulin coma, NOS
• 250.3x
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Chronic complications
• DUAL coding is required
• DM code sequenced 1st unless directed
otherwise by Codebook
• Onset can be early/late, can be in either
type 1 or 2.
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Vision Complications
• Diabetic Retinopathy
• Diabetic macular edema
• Cataracts
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Diabetic Retinopathy
• Code for diabetic macular edema MUST
BE USED with a code for diabetic
retinopathy
• Examples
– Progress note. AODM with diabetic macular
edema and nonproliferative diabetic
retinopathy Codes?
– Progress note. Uncontrolled adult diabetes
with background diabetic retinopathy Codes?
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Cataracts
• Snowflake cataracts occur in DM pts, but
are rare
• Mature senile cataracts also occur in DM,
but NOT caused by DM
• Example: Snowflake cataract/diabetic
cataract
– 250.5x
– 366.41
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Renal Complications
• Nephropathy
– 250.4x
– 583.81
• Nephritis
• Nephrosis
– 250.4x
– 581.81
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• Ch Renal Failure
(new, preferred term
is Ch Kidney Failure)
– 585
• Ch glomerulonephritis
– 250.4s, 582.8x
Renal Failure
• 2 codes required (250.4x and 585)
• Can code intervening condition if
documented and there is room for code
– Shows stage of disease process
• Example: CRF due to diabetic nephrotic
syndrome
– 250.4x
– 581.81
– 585
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HTN and Diabetic Renal failure
• Pts w/ both DM and HTN may develop renal
failure
• Only 2 codes needed, 250.4x and combination
code from 403 or 404
– 5th digit indicates presence of renal failure
• Example: Progressive diabetic nephropathy with
hypertensive renal disease and renal failure
– 250.4x
– 583.81
– 403.91
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Neural Complications
• When specific neurological complication is
documented, assign that specific code
• Neuropathy, Peripheral
– Common DM complication
– 250.6x, 357.2
• Neuropathy, Autonomic
– Must be specifically state by Dr to code
– 250.6x, 337.1
• Neuropathy, Cranial
– 250.6x, 378.51
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Diabetic Vascular Disease
• Peripheral vascular disease
– Frequent complication
– 250.7x, 443.81
• CAD, cardiomyopathy, cerebrovasular
disease are NOT DM complications
– Code separately, UNLESS Dr documents
causal relationship.
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Other DM manifestations
• Ulcers of lower extremities
– Common DM complications
– Result from diabetic neuropathy OR
peripheral vascular disease
– 250.6x OR 250.7x, 707.1x,
– add 785.4 when gangrene present
• *NOT all ulcers in DM pts are diabetic
ulcers
– Query Dr if relationship unclear in
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Other manifestations
• Organic impotence
– Results from diabetic peripheral neuropathy
OR peripheral vascular disease
– 250.6x OR 250.7x, 607.84
• When documentation of these two
conditions does NOT indicate neuro or
vascular causation, then code
– 250.8x
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DM and Pregnancy*
*DM ALWAYS complicates pregnancy
• Gestational DM
• DM mother
• Late pregnancy (24 28 wks)
• Do NOT use 648.8x
for mother dx with DM
BEFORE the
pregnancy
• 648.8x
• NO 250.xx code
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• 648.0x, 250.xx
Neonatal conditions associated
with maternal DM
• 775.0 or 775.1
• 775.1 may require a course of insulin
• Assign ONLY when maternal condition has
actually affected baby
• Normal infant of DM mother
• V30.00, V18.0
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Hypoglycemic Reactions
Can occur in diabetic OR non-diabetic patients
• Diabetic pt
– Occur when imbalance
between patterns of
eating/exercise and
drug doses
– New dx of type 1 DM,
initial phase of tx
– 250.3x with mention of
coma
– 250.8x w/o mention of
coma
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• Non-Diabetic Pt
– 251.0 hypoglycemic
coma
– 251.1 specified
hypoglycemia w/o
coma
– 251.2 hypoglycemia,
NOS
Hypoglycemia
Adverse Effect or Poisoning
• Due to drug used as prescribed
– E code responsible drug
• Hypoglycemic coma or shock
– Incorrect use of anti-diabetic agent
– 962.3, E858.0
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2ndary Diabetes
• 250.xx codes NOT assigned
• 251.3 Postsurgical hypoinsulinemia
• Example: steroid-induced DM
– 251.8, E932.0
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Insulin use
• V58.67 Long-term [current] use of insulin
–
–
–
–
Usually secondary code
Pt’s continuous use of a prescribed drug
NOT used for drug addictions
NOT used for temporary use of insulin to get glucose
under control during an encounter
• Pt routinely takes insulin (Type 1 OR 2 DM)
• Pt taking insulin for gestational DM
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Insulin Pump complications
• 996.57 – used for failure or malfunction of
pump that results in under/over dosing
• 962.3 – used as additional code when
mechanical complication results in
OVERDOSE
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Outpatient Settings
• Code chronic DM conditions ONLY if
relevant to service provided during visit
• Example: Pt with high cholesterol, but no
current medications for it. He comes in for
tx of a closed fx of one rib. Dr. tx fx w/out
manipulation.
• Code(s)?
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DM Example
• Type 2 DM patient presents with acute
extrinsic asthma attack. DM may put pt at
risk for increased risk of infection and
affects the Doctor’s choice of steroids for
use as anti-inflammatory.
• Codes?
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Resources5
• AHA Coding Clinic
– 2005, 1st Q, p. 44, 45
– 2004, 1st Q, p. 14-15
– 2002, 2nd Q, p. 13
– 1997, 4th Q, p. 33
– 1997, 2nd Q, p. 14
– 1993, 4th Q, p. 19
– 1991, 3rd Q, p. 8
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Resources
• Brown, Faye. 2005. ICD-9-CM Coding Handbook, with
Answers. 2006 Rev. Ed. Chicago: AHA Press.
• Green, Michelle A. 2007. 3-2-1Code It! New York:
Thomson Delmar Learning.
• MedlinePlus; a service of the US National Library of
Medicine and the National Institutes of Health.
http://www.nlm.nih.gov/medlineplus/
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References
1Mathur,
R. Diabetes Mellitus. Medicinenet. http://www.medicinenet.com/
Accessed: 1/6/08
2Frazier
and Drzymkowski, Essentials of Human Diseases and
Conditions, 3rd ed. 2004, St. Louis, Elsevier Saunders, p. 168.
3Pancreas. ( 2008). In Encyclopædia Britannica. Retrieved 1/6/08, from
Encyclopædia Britannica Online:
http://www.britannica.com/eb/article-9058232
4Gerbarg, Z. Diabetic Retinopathy: Documentation and Coding.
MDQuickFax. 2006. Retrieved 1/6/08, from
5Howard, A. Coding for Diabetes Mellitus. For the Record, v17, no. 20,
p. 45. (2005)
6Mathur, R. Diabetes Treatment. Medicinenet. hhtp://www.medicinenet.com
Accessed 1/14/08
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[email protected]
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