Angeles University Foundation

Angeles City
Graduate School Program

A Case Study

Presented to:

Annalyn Paano, R.N, M.A.N

Professor
Nursing Concepts III
Advanced Medical-Surgical Nursing

Presented by:

Juan Paulo L. Uy, R.N.

April 11, 2008

I. Introduction
 Diabetes is a disease that affects millions of people across the globe. Diabetes is

classified as a set of related diseases that occur when the body cannot regulate the

amount of sugar, or glucose, in the bloodstream. Diabetes mellitus is the epidemic of the

new millennium. This disorder has increased more than 6-fold during the last 40 years,

and the more than 798,000 new cases diagnosed each year in the United States have

resulted in direct and indirect costs that total more than $100 billion per year.

In the United States, approximately 17 million people, or 6.2% of the population,

are estimated to have diabetes, with a growing incidence. Roughly one third of this

population is estimated to be undiagnosed with type II diabetes. The prevalence of

diabetes is higher in certain racial and ethnic groups, affecting approximately 13% of

African Americans, 10.2% of Hispanics, and 15.1% of Native Americans, primarily with

type II diabetes.

According to the Philippines’ Department of Health, it is estimated that there are

about 3 million Filipinos who are diabetic, 50% are undiagnosed.

Based on the recent estimates of the World Health Organization (WHO), the

Philippines have been included in the top 10 countries with highest diabetes prevalence

by year 2030. In the next 25 years, WHO predicted that the Philippines and Egypt will

replace Italy and the Russian Federation in the top 10 list as diabetes rates in both

countries continue to escalate.

Patients with diabetes are more likely to develop eye problems such as cataracts

and glaucoma, but the disease’s affect on the retina is the main threat to vision. Most

patients develop diabetic changes in the retina after approximately 20 years. The effect

of diabetes on the eye is called diabetic retinopathy.

Diabetic retinopathy is the most common microvascular complication of diabetes,

affecting approximately 49% of those with diabetes. Of the 209 million Americans over
the age of 18 years, diabetic retinopathy affects more than 5.3 million, or a little more

than 2.5% of the entire adult US population.

According to the World Health Organization, diabetic retinopathy is the leading

cause of blindness in working age adults and a leading cause of vision loss in diabetics.

The American Diabetes Association reports that there are approximately 18 million

diabetics in the U.S. and approximately 1.3 million newly diagnosed cases of diabetes in

the U.S. each year. Prevent Blindness America and the National Eye Institute estimate

that in the U.S. there are over 5.3 million people aged 18 or older with diabetic

retinopathy, including approximately 500,000 with DME. The CDC estimates that there

are approximately 75,000 new cases of DME in the U.S. each year.

Incidence (annual) of Diabetic Retinopathy presented by the Research to Prevent

Blindness is 65,000 diabetics develop proliferative retinopathy, the most sight-

threatening stage in the US, while the incidence rate is approximately 1 in 4,184 or

0.02% or 65,000 people in USA. Incidence extrapolations for USA for Diabetic

Retinopathy: 65,000 per year, 5,416 per month, 1,250 per week, 178 per day, 7 per

hour, 0 per minute, 0 per second.

Objectives:

1. To better understand the how diabetic retinopathy occurs.

2. To identify signs and symptoms of the disease

3. To know what are the types of diagnostic procedures to confirm existence of the

disease.

4. To enumerate treatment regimen and surgical procedures done in treating the

disease.

5. To identify nursing responsibilities in the treatment of the disease.

 Reasons for Choosing the Disease:

I choose this disease because I find it interesting. I am not familiar with the condition

that is why this case study will help me understand fully the disease condition. Though

the disease is uncommon, it is the number one cause of blindness in diabetic patients. I

believe that vision is one of the most important senses that we have, so we should take

care of our eyes.

II. Nursing Process

A. Personal Data

The patient is Mrs. Chubby, a 57 year old female, who is a natural born Filipino

residing in Pugad baboy Village, who was diagnosed of having Diabetic Retinopathy OU, with

Retinal Detachment OS.

She was born on March 20, 1950 in Bataan, where she is presently residing with the

family of her second child. Mrs. Chubby is an active member of the Christian community, attending

bible studies and other charismatic studies. Her faith in God, according to the patient, is the one thing

that keeps her living in spite and despite of her present condition. She further explains that God has a

purpose or plan for her why she had acquired her present condition, and that no resentment can be

found on Mrs. Chubby.

According to Mrs. Chubby their family is fund with eating foods high in cholesterol like

chicharon, lechon and sisig. Her husband cooks well that’s why all of them enjoys eating a lot. Her

height is 5’5” and she weights 240 lbs, she is overweight.

Mrs. Chubby is a mother of two boys and one girl. Her eldest is working and residing

in the United States while the second and youngest children live with her. Mr and Mrs. Chubby’s

source of income is the husband’s pension and the monthly allowance that their child who works in

abroad gives them. These have become the means of sustaining their basic needs, including her

medical regimen. According to her, health is wealth, and thus, having a healthy body is important in

their family. That is why she never failed to consult medical advice regarding her disease condition
from the time she was diagnosed of having Diabetes Mellitus Type 2. She strictly complies with her

medical regimen at present, as evidence of regular check-ups made every month and effective drug

maintenance.

B. Pertinent Family History

Genogram:

Father Side Mother Side

(+)DM (+) DM

F(+)DM (+)DM (+)DM M(+)DM

*(+)DM

Legend:

= male

= = female

F = father

M = mother

* = Mrs. Chubby

Narrative:

Mrs. Chubby stated that from the paternal side, three members of the family suffered

from Diabetes Mellitus, that was her grandfather, her father and youngest uncle. She doesn’t
remember anymore if DM was the primary cause of their death. As to her maternal side, she recalled

that her grandmother had the disease, the eldest sister of her mother and just recently, they have

found out that her mother has also acquired the disease. It is believed by the patient that she has

inherited the said disease condition from both parent side.

C. History of Past lIlness

Mrs. Chubby had history of any disease except from occasional colds, fever and cough. She had

chicken pox when she was just a maiden. When she was 25 years old she was hospitalized

because of UTI.

D. History of Present Illness

Mrs. Chubby was diagnosed of having Diabetes Mellitus Type 2 when she was 35 years

old. She relates that she was experiencing the so-called 3P’s of the disease when she decided to

consult her physician. Her fasting blood sugar on the time of her diagnosis was 240 mg/dl. With this,

she was given medications and was advised on proper disease management. Glucophage 500 mg/tab 3

times a day and Diamicron 80 mg/tab. ½ tab 2 times a day are the medications prescribed to her.

The condition started on June 2006 that Mrs. Chubby experienced blurring of vision in

her both eyes. This made her to consult an ophthalmologist. According to the ophthalmologist she

consulted, abnormal blood vessels were found in both of her eyes, and that she needs to undergo the

Laser Therapy in order to stop the growth of these blood vessels. She willingly subjected herself in

that treatment on July 2006 due to her fear of being blind. The therapy was done three times on both

eyes during that time. After three months following the treatment, blurring of vision on her left eye

was observed. Again, this condition opted her to seek medical treatment. As for the findings on her

condition, it was found out that her left eye’s blood vessels bleed and laser therapy is needed to be
done right away. The patient followed the doctor’s advice and had undergone laser therapy on her left

eye on October 2006. After a month following the therapy, her ophthalmologist suggested another

laser therapy for both eyes as bleeding vessels were inspected again. And this happened on November

2006. After this, she experienced an improvement on her vision for both eyes.

On December 2006, Mrs. Chubby consulted another ophthalmologist so as to have the

so-called second opinion. It was from this doctor that the patient learned much of her disease Diabetic

Retinopathy. The patient had undergone another laser therapy on this month in order to save her

vision.

On 2007, Mrs. Chubby suddenly experienced elevated blood pressure during her

check-up. With this, she was confined in a private hospital and undergone treatment in lowering her

blood pressure. Mrs. Chubby then had blurring of vision on both eyes. Her doctor explained to her

that she needs to have another operation for her eyes, which is in order to prevent further impairment.

The operation is called “Vitrectomy”.

It was on April 2007, according to the patient, that she undergone on the said

procedure. She mentioned that her doctor placed silicone oil in her left eye as a part of the procedure.

After the operation, the patient experienced improvement on her vision. Mrs. Chubby then did not

experience any further visual disturbances until August 2007, she then again consulted her doctor due

to blurring of vision on her right eye. And with this, the doctor advised the patient to have Vitrectomy

on the right eye. And so, it was on the following month that the patient had the said operation. Mrs.

Chubby further explained that her doctor presented to her the consequences of the said operation for

both eyes. According to her doctor, with Vitrectomy, the chance of improving the left eye’s vision is

on a 50-50 probability scale, it may have 50% chance of improving or it may also have 50% chance

of losing her vision. And as for the right eye’s vision with Vitrectomy, it will really improve a lot,

which is it will no longer have blurred vision and may even have clearer sight as compared to what

the patient have experienced before. The patient had her regular check ups following the said

operation.
 March 15, 2008, the patient had another eye complaint this time on her left eye. She

stated that she sees black color in the corner of her eye. She then consulted her doctor, and she was

diagnosed of having Retinal Detachment. Due to this complaint, she was advised to be admitted and

the operation recommended to her by her physician was Scleral Buckling. The consequence of the

procedure was explained by her physician and Mrs. Chubby will undergo on the said procedure on

March 17, 2008. Unfortunately, the procedure was not performed due to unstable blood sugar level

and high BP. The operation was rescheduled on March 20, 2008.

A. Physical Examination – March 15, 2008

 Vital Signs: BP-140/90 mmHg, T-37, PR-86, RR-20

 Head

Round shape, no tenderness, swelling or lesions noted upon

palpation, no abnormal configuration noted

 Hair and Scalp

Hair evenly distributed, thick, black, dry and wavy up to shoulder

length hair, no lice or dandruff noted upon inspection, no lesions or

masses

 Face and Skull

Symmetrical facial movements

Smooth skull contour, no nodules / depressions

 Skin

Brown complexion, slightly dry skin

 Skin warm to touch

Skin turgor - skin brings back to previous state after pinching

No edema/lesions noted, no pigmentation

 Eyes

Eyebrows symmetrically aligned with equal movements

Eyebrows and eyelashes are evenly distributed

Transparent bulbar conjunctive, with white sclera

OD - clear cornea, pupil react to light and accommodation, can

read newspaper print, bold and small font at a distance of 12

inches away from the tip of the nose

OS - hazy cornea, pupil not reactive to light and accommodation,

cannot read newspaper print

 Ears

Symmetrical in shape not tender, recoils after it is folded

No lesions, symmetrical with the outer cantus of the eye

 Nose

No discharge, no lesions, no tenderness

Air moves freely through the nares as she breathes

 Lips

No blister / cracks noted, pink, able to do purse lips, symmetric

contour

Moist, smooth, glistening

 

 Teeth and gums

Pink gums, not swollen

Slightly yellow teeth

 Tongue

Centered tongue, no lesions, smooth movement

 Neck

Equal in size, head centered with muscles (trapezius and sternocleidomastoid)

equal in size

No unusual mass noted upon palpation

No enlargement of lymph nodes

Trachea is in midline position

No distention of veins

No enlargement of thyroid glands

Cricoid cartilage elevates when swallowing

 Thorax and lungs

Spine is vertically aligned, no tenderness, pain, or unusual mass

upon palpation

Tactile fremitus present

Clear breath sounds

 Heart

Has a regular rate and rhythm

 Breast

Rounded, slightly unequal in size

 Skin uniform in color, smooth

No tenderness, masses, lesions noted

 Abdomen

Uniform in color, no swelling or lump noted

Tympanic sound heard upon auscultation

 Extremities

No edema, deformities, tenderness noted

Have symmetrical lower and upper extremities

Clean fingernails and toenails

Blanch test (color return < 3 seconds)

III. The Anatomy and Physiology

 The Pancreas

The pancreas is a small organ, approximately six inches long, located in the upper

abdomen, and adjacent to the small intestine. It lies toward your back. Because it is so deep within

your body, doctors have difficulty diagnosing disease in the pancreas.

 Completes the job of breaking down protein, carbohydrates, and fats using digestive juices of

pancreas combined with juices from the intestines.

 Secretes hormones that affect the level of sugar in the blood.

 Produces chemicals that neutralize stomach acids that pass from the stomach into the small

intestine by using substances in pancreatic juice.

 Contains Islets of Langerhans, which are tiny groups of specialized cells that are scattered

throughout the organ.

These cells secrete:

 Glucagon—raises the level of glucose (sugar) in the blood

 Insulin—stimulates cells to use glucose

 Somatostatin—may regulate the secretion of glucagons and insulin.

   The human pancreas is an amazing organ with two main functions: [1] to produce

pancreatic endocrine hormones (e.g., insulin & glucagon) which help regulate many aspects of our

metabolism and [2], to produce pancreatic digestive enzymes.  The hormone function of the pancreas

is the emphasis of this portion of Endocrine Web ~ this is referred to as the Endocrine Pancreas. 

Pancreatic production of insulin, somatostatin, gastrin, and glucagon plays an important role in

maintaining sugar and salt balance in our bodies and therefore any problem in the production or

regulation of these hormones will manifest itself with problems with blood sugar and fluid / salt

imbalances.

The digestive portion of the pancreas makes up more than 90 percent of its total cell

mass.  The digestive (or exocrine) pancreas is responsible for making digestive enzymes which are

secreted into the intestines to help digest (break down) the food we eat.  These enzymes digest

proteins, fats, and carbohydrates into much smaller molecules so our intestines can absorb them.   The

picture above is an accurate representation of the pancreas which lies next to the duodenum (the first

part of the small intestine right after the stomach). The actual size of the pancreas is similar to a

banana which has been stepped on...it has a slight curve to it, and its about the same length, width,

and thickness.  The yellow "tube" running through the middle of the pancreas is called the pancreatic

duct.  It drains all the digestive enzymes from the pancreatic cells where they are made into the

duodenum where they mix with food as it comes out of the stomach.

The Endocrine Pancreas

The emphasis of the remainder of these pages within Endocrine Web is on the Endocrine

Pancreas.  Approximately 5 percent of the total pancreatic mass is comprised of endocrine cells. 

These endocrine cells are clustered in groups within the pancreas which look like little islands of cells

when examined under a microscope.  This appearance led to these groups of pancreatic endocrine

cells being called "Pancreatic Islets".  Within pancreatic islets are cells which make specific
pancreatic endocrine hormones, of which there are only a few (the most famous of course being

insulin).  These cells within the islets are called "Pancreatic Islet Cells".

Pancreatic islets are scattered throughout the pancreas.  Like all endocrine glands, they

secrete their hormones into the bloodstream and not into tubes or ducts like the digestive pancreas.  

Because of this need to secrete their hormones into the blood stream, pancreatic islets are surrounded

by small blood vessels.  This relationship is shown in the picture of a pancreatic islet where islet cells

are secreting their hormones into nearby blood vessels.  Remember, the purpose of endocrine cells is

to make hormones which are secreted into the blood stream where they gain access to other cells very

far away with the goal of making those cells respond in a specific fashion.

 Pancreatic Endocrine Hormones and Their Purpose

1. Insulin

- Regulate blood glucose (sugar) in the normal range

- Forces many cells of the body to absorb and use glucose thereby

decreasing blood sugar levels

2. Glucagon

- Assist insulin in regulating blood glucose (sugar) in the normal range

(actions are opposite of insulin)

- Forces many cells of the body to release/produce glucose (increasing

blood sugar)

The Human Eye

 The human eye is the organ which gives us the sense of sight, allowing us to learn more

about the surrounding world than we do with any of the other four senses.  We use our eyes in almost

every activity we perform, whether reading, working, watching television, writing a letter, driving a

car, and in countless other ways.  Most people probably would agree that sight is the sense they value

more than all the rest.

The eye allows us to see and interpret the shapes, colors, and dimensions of objects in the

world by processing the light they reflect or emit.  The eye is able to see in bright light or in dim light,

but it cannot see an object when light is absent.

Parts of the Eye

The conjunctiva is a mucous membrane that lines the inner surfaces of the eyelids and folds back

to cover the front surface of the eyeball, except for the central clear portion of the outer eye (the

cornea).  The entire conjuntiva is transparent.

The conjunctiva is composed of 3 sections:

1. palpebral conjunctiva (covers the posterior surface of the eyelids)

2. bulbar conjunctiva (coats the anterior portion of the eyeball)

3. fornix (the transition portion forming the junction between the posterior eyelid and the eyeball)

The iris, visible through the clear cornea as the colored disc inside the eye, is a thin

diaphragm composed mostly of connective tissue and smooth muscle fibers.  It lies between the

cornea and the crystalline lens.  The iris divides the anterior compartment, the space separating the

cornea and the lens, into the anterior chamber (between the cornea and the iris) and the posterior

chamber (between the iris and the lens).The iris is composed of 3 layers, from the front to the back:

endothelium, stroma and epithelium. The color of the iris, which is established genetically, is

determined by the amount of pigment present in this eye structure.  No pigment at all (in the case of

an albino) results in a pink iris.  Some pigment causes the iris to appear blue.  Increasing amounts of

iris pigment produce green, hazel, and brown irises (or irides). 

The pupil—the (normally) circular hole in the middle of the iris, comparable to the

apperture of a camera—regulates the amount of light passing through to the retina at the back of the

eye. As the amount of light entering the eye diminishes (such as in the dark or at night), the iris dilator

muscle (which runs radially through the iris like spokes on a wheel) pulls away from the center,

causing the pupil to “dilate” and allowing more light to reach the retina.  When too much light is

entering the eye, the iris sphincter muscle (which encircles the pupil) pulls toward the center, causing

the pupil to “constrict” and allowing less light to reach the retina.

Constriction of the pupil also occurs when the crystalline lens accommodates (changes

focus) to a near distance; this reaction is known as the “near reflex.”  A representation of

parasympathic pathways in the pupillary light reflex can be seen here: parasympathic response. 

Sometimes the pupil does not react properly, due to cranial nerve or muscle problems.

The iris is the most anterior portion of the uvea or uveal tract (also known as the tunica

vasculosa or vascular tunic).  Anatomical structures posterior to the iris, which also are part of the

uvea, are the ciliary body (within which is the ciliary muscle which controls the shape of the

crystalline lens) and the choroid (located underneath the retina and which contains the retina’s blood

supply
 The transparent crystalline lens of the eye is located immediately behind the iris.  It is

composed of fibers that come from epithelial (hormone-producing) cells.  In fact, the cytoplasm of

these cells makes up the transparent substance of the lens. The crystalline lens is composed of 4

layers, from the surface to the center: capsule, subcapsular epithelium, cortex, nucleus

The lens capsule is a clear, membrane-like structure that is quite elastic, a quality that

keeps it under constant tension.  As a result, the lens naturally tends towards a rounder or more

globular configuration, a shape it must assume for the eye to focus at a near distance.  Slender but

very strong suspensory ligaments (also known as zonules), which attach at one end to the lens capsule

and at the other end to the ciliary processes of the circular ciliary body around the inside of the eye,

hold the lens in place.

The aqueous is the thin, watery fluid that fills the space between the cornea and the iris

(anterior chamber).  It is continually produced by the ciliary body, the part of the eye that lies just

behind the iris.  This fluid nourishes the cornea and the lens and gives the front of the eye its form and

shape. Along its circumference, the cornea is continuous with the sclera: the white, opaque portion of

the eye.  The sclera makes up the back five-sixths of the eye’s outer layer.  It provides protection and

serves as an attachment for the extraocular muscles which move the eye. Coating the outer surface of

the cornea is a “pre-corneal tear film.”  People normally blink the eyelids of their eyes about every six

seconds to replenish the tear film.  Tears have four main functions on the eye:

 wetting the corneal epithelium, thereby preventing it from being damaged due to dryness

 creating a smooth optical surface on the front of the microscopically irregular corneal surface

 acting as the main supplier of oxygen and other nutrients to the cornea

 containing an enzyme called “lysozyme” which destroys bacteria and prevents the growth of

microcysts on the cornea.

The most external layer of the tear film is the lipid or oil layer.  This layer prevents the

lacrimal layer beneath it from evaporating, as well as preventing the tears from flowing over the edge

of the lower eyelid (“epiphora”).  The lipid component of the tear film is produced by sebaceous
glands known as “Meibomian” glands (located in the tarsal plates along the eyelid margins) and the

glands of “Zeis” (which open into the hair follicles of the eyelashes).  An enlargement of a Meibonian

gland is known as a “chalazion,” while an infection of a Zeis gland is known as a “hordeolum” or

“sty(e).”

Below the lipid layer is located the lacrimal or aqueous layer of the tear film.   This

middle layer is the thickest of the three tear layers, and it is formed primarily by the glands of

“Krause” and “Wolfring” and secondarily by the “lacrimal” gland, all of which are located in the

eyelids.  (The lacrimal gland is the major producer of tears when one is crying or due to foreign body

irritation.)  The lacrimal fluid, containing salts, proteins, and lysozyme, has several functions: taking

the main nutrients (such as oxygen) to the cornea, carrying waste products away from the cornea,

helping to prevent corneal infection, and maintaining the tonicity of the tear film.

The optic nerve (also known as cranial nerve II) is a continuation of the axons of the

ganglion cells in the retina.  There are approximately 1.1 million nerve cells in each optic nerve.  The

optic nerve, which acts like a cable connecting the eye with the brain, actually is more like brain

tissue than it is nerve tissue.

Diabetic retinopathy is an eye disease caused by complications of diabetes. Diabetes

causes damages to the blood vessels that nourish the retina, the seeing part of the eye.
IV. The Client and Her Illness

A.1 Schematic Diagram (Book-based)

Non-modifiable Factors Modifiable Factors

> Older age > Glucose control
> Family history of DM > Duration of the disease
> Diet (high CHO)
> Sedentary lifestyle

endothelial damage sluggish circulation focal capillary

occlusion

Endothelial damage Focal capillary occlusion

Weakened retinal capillaries retinal capillary closure

Outpouching of the retinal ischemia

capillary walls

abnormal growth of new

microaneurysms blood vessels

ruptured microaneurysms traction retinal detachment

retinal hemorrhage breakdown of the blood-retina

barrier allowing leakage of the
serum CHON and lipids

retinal thickening & exudates

 retinal capillaries necrosis

scar formation

macular edema

damage to cones

blurring of vision

continuous damage

Loss of vision
 A.2 Schematic Diagram (Client-centered)

Non-modifiable Factors Modifiable Factors

> age (57years old) > Glucose control
>family history of DM > Duration of the disease
> Diet (high CHO)
> Diagnosed with DM
>overweight

endothelial damage sluggish circulation focal capillary

occlusion

Endothelial damage Focal capillary occlusion

Weakened retinal capillaries retinal capillary closure

Outpouching of the retinal ischemia

capillary walls

abnormal growth of new

microaneurysms blood vessels

ruptured microaneurysms new vessels cannot replace the

necessary nutrients

retinal hemorrhage
traction retinal detachment

breakdown of the blood-retina

barrier allowing leakage of the
serum CHON and lipids

retinal thickening & exudates

retinal capillaries necrosis

scar formation

macular edema

damage to cones
 blurring of vision

continuous damage

loss of vision

Diabetic Retinopathy with

Retinal Detachment

B. Synthesis of the Disease

 Type 2 diabetes is also known as insulin-resistant diabetes, non-insulin dependent

diabetes, and adult-onset diabetes. Diabetes is a disease in which blood glucose levels are above

normal. Most of the food we eat is turned into glucose, or sugar, for our bodies to use for energy. The

pancreas, an organ that lies near the stomach, makes a hormone called insulin to help glucose get into

the cells of our bodies. When you have diabetes, your body either doesn't make enough insulin or

can't use its own insulin as well as it should. This causes sugar to build up in your blood.

Diabetic Mellitus Type 2 is one of the two major types of diabetes, the type in which the

beta cells of the pancreas produce insulin but the body is unable to use it effectively because the cells

of the body are resistant to the action of insulin. Although this type of diabetes may not carry the

same risk of death from ketoacidosis, it otherwise involves many of the same risks of complications

as does type 1 diabetes (in which there is a lack of insulin).

The pathogenesis of type 2 diabetes mellitus differs significantly from that of type 1. A

limited beta cell response to hyperglycemia appears to be a major factor in its development. Beta cells

chronically exposed to high blood levels become progressively less efficient when responding to

further glucose elevations. This phenomenon is called, desensitization, is reversible by normalizing

glucose levels. The ratio of proinsulin (a precursor of insulin) to insulin secreted also increases.

A second pathophysiologic process in type 2 diabetes mellitus resistance to the biologic

activity of insulin in both the liver and the peripheral tissues. This state is known as insulin resistance.

People with type 2 diabetes have a decreased sensitivity to glucose levels, which result to continued

hepatic glucose production, even with high plasma glucose levels. This is coupled with an inability of

muscle and fat tissues to increase glucose uptake. The mechanism causing peripheral insulin

resistance is not clear; however, it appears to occur after insulin binds to a receptor on the cell surface.

Insulin is a building (anabolic) hormone. Without insulin, three major metabolic

problems occur: a) decreased glucose utilization, b) increased fat mobilization, and c) increased

protein utilization.

A. Decreased Glucose Utilization

 In diabetes, cells that require insulin as a carrier for glucose can take only in about 25%

of the glucose they require for fuel. Nerve tissues, erythrocyte, and the cells of the intestines, liver,

and kidney tubules do not require insulin for glucose transport. Skeletal and cardiac muscles do.

Without adequate amounts of insulin, much of the ingested glucose cannot be used.

With inadequate amounts of insulin, blood glucose levels rise. This elevation continues

because the liver cannot store glucose as glycogen without sufficient insulin levels. In an attempt to

restore balance and return blood glucose levels to normal, the kidneys excrete the excess glucose.

Glucose excreted in the urine acts as an osmotic diuretic and causes excretion of increased amounts of

water, resulting in fluid volume deficit.

B. Increased Fat Mobilization

This occurs occasionally with severe stress in type 2 diabetes, the body turns to fat stores

for energy production when glucose in unavailable. Fat metabolism causes breakdown products called

ketones to form. Ketones accumulate in the blood and are excreted through the kidneys and lungs.

Ketone levels can be measures in the blood and the urine; high levels can serve as an indicator of

uncontrolled diabetes.

C. Increased Protein Utilization

Lack of insulin leads to protein wasting. In healthy people, proteins are constantly being

broken down and rebuilt. Amino acids are converted to glucose in the liver, further elevating glucose

levels.

Predisposing Factors/ Precipitating Factors:

Diabetes Mellitus Type is a disorder involving both genetic and environmental factors. It

is not associated with HLA tissue types, and circulating ICA’s are rarely present. Heredity plays a

major role in the expression of type 2 Diabetes. It is more common in the identical twins (58-75 %

incidence) than in the general population. Obesity is also a major risk factor, 85% of all people with

Type 2 diabetes are obese. It is unclear whether impaired tissue (liver and muscle) sensitivity to

insulin or impaired insulin secretion is the primary defect in this type of diabetes. In addition, the
prevalence of coronary artery disease in people with type 2 diabetes is twice that in the non-diabetic

population, and cardiovascular and total mortality rates are two-fold to three-fold greater than in non-

diabetic people.

Risk factors for type 2 diabetes include older age, obesity, family history of diabetes, and prior

history of gestational diabetes, impaired glucose tolerance, physical inactivity, and race/ethnicity.

African Americans, Hispanic/Latino Americans, American Indians, and some Asian Americans and

Pacific Islanders are at particularly high risk for type 2 diabetes.

Signs and Symptoms with Rationale:

 Hyperglycemia(fasting blood glucose above 125 mg/dl)- elevated blood glucose level due to

inadequate amounts of insulin

 Polyuria- increased frequency of urination because kidneys excrete the excess glucose. Glucose

excreted in the urine acts as an osmotic diuretic and causes excretion of increased amounts of

water.

 Polydipsia- increased thirst and fluid intake due to increased amounts of water loss.

 Polyphagia- increased hunger and food intake, that is due to inadequate amount of insulin needed

to transport glucose into the cell to carry its metabolic processes

 Weight Loss- due to depletion of water, glycogen, triglycerides stores

 Weakness and fatigue, dizziness- decreased plasma volume leads to postural hypotension;

potassium loss and protein catabolism contribute to weakness

Patients with diabetes are more likely to develop eye problems such as cataracts and

glaucoma, but the disease’s affect on the retina is the main threat to vision. Most patients develop

diabetic changes in the retina after approximately 20 years. The effect of diabetes on the eye is called

diabetic retinopathy.

Diabetic retinopathy is a complication of diabetes and a leading cause of blindness. It

occurs when diabetes damages the tiny blood vessels inside the retina, the light-sensitive tissue at the

back of the eye. A healthy retina is necessary for good vision. If you have diabetic retinopathy, at first
you may notice no changes to your vision. But over time, diabetic retinopathy can get worse and

cause vision loss. Diabetic retinopathy usually affects both eyes.

Signs and Symptoms with Rationale

In the early, most treatable stages of diabetic retinopathy, you usually experience no

visual symptoms or pain. The disease can even progress to an advanced stage without any noticeable

change in your vision.

The affect of diabetic retinopathy on vision varies widely, depending on the stage of the

disease. Some common symptoms of diabetic retinopathy are listed below, however, diabetes may

cause other eye symptoms.

 Blurred vision (this is often linked to blood sugar levels)- delicate vessels hemorrhage easily

 Floaters and flashes, "Spiders," "cobwebs" or tiny specks floating in your vision - Blood may

leak into the retina and vitreous

 Sudden loss of vision- the arteries in the retina become weakened and leak, forming small, dot-

like hemorrhages; continued abnormal vessel growth and scar tissue.

 Fluctuating visual acuity- unstable blood sugar

 Swelling within the crystalline lens results in large sudden shifts in refraction as well as

premature cataract formation. Changes in visual acuity will depend upon the severity and stage of

the disease.

 Intraretinal dot and blot hemorrhages, exudates, intraretinal microvascular abnormalities (IRMA)

microaneurysms, edema and cotton wool infarcts- weakening of the arterioles and capillaries in

the retina.

 Microaneurysms
 Earliest clinical sign of diabetic retinopathy

 Secondary to capillary wall outpouching due to pericyte loss

 Appear as small red dots in the superficial retinal layers

 Fibrin and RBC accumulation in the microaneurysm lumen

 Rupture produces blot/flame hemorrhages

 May appear yellowish in time as endothelial cells proliferate and produce basement membrane

 Dot and blot hemorrhages

o Occur as microaneurysms rupture in the deeper layers of the retina such as the inner

nuclear and outer plexiform layers

o Appear similar to microaneurysms if they are small; fluorescein angiography may be

needed to distinguish between the two

 Flame-shaped hemorrhages - Splinter hemorrhages that occur in the more superficial nerve

fiber layer

 Retinal edema and hard exudates - Caused by the breakdown of the blood-retina barrier

allowing leakage of serum proteins, lipids, and protein from the vessels

 Cotton-wool spots

 Nerve fiber layer infarction from occlusion of precapillary arterioles

 Fluorescein angiography - No capillary perfusion

 Frequently bordered by microaneurysms and vascular hyperpermeability

 Venous loops, venous beading

o Frequently adjacent to areas of nonperfusion

o Reflects increasing retinal ischemia

o Most significant predictor of progression to PDR

 Intraretinal microvascular abnormalities

 Remodeled capillary beds without proliferative changes

 Collateral vessels that do not leak on fluorescein angiography

 Usually can be found on the borders of the nonperfused retina

 Macular edema

This condition is the leading cause of visual impairment in patients with diabetes. It has

been reported that 75,000 new cases of macular edema are diagnosed annually.

 Possibly due to functional damage and necrosis of retinal capillaries

 Clinically significant macular edema (CSME) is defined as any of the following:

o Retinal thickening located 500 mm or less from the center of the foveal

avascular zone (FAZ)

o Hard exudates with retinal thickening 500 mm or less from the center of the

FAZ

o Retinal thickening 1 disc area or larger in size located within 1 disc diameter

of the FAZ

Proliferative diabetic retinopathy is the result of severe vascular compromise and is

visible as neovascularization of the disc (NVD), neovascularization elsewhere (NVE) and

neovascularization of the iris (NVI, or rubeosis irides). Neurological complications include palsies of

the third, fourth and sixth cranial nerves as well as diabetic papillitis and facial nerve paralysis.

VI. Summary of Findings

Upon the completion of the case study, I was able to convey an in-depth and reliable

knowledge and advanced understanding of all the clinically relevant facets of diabetic retinopathy,

have demonstrated a clear , advanced understanding of the epidemiology, pathogenesis, and

pathophysiology of diabetic retinopathy, have an advanced understanding of the indications for

treatment of diabetic retinopathy by laser and retinal surgery and a clear working knowledge of the

associated side-effects, and have an advanced knowledge of the therapies to prevent diabetic

retinopathy and its progress as well as vascular disease risk factor modification.

As for the patient-centered, the patient have identified the different risk factors

associated with the progressive development of Diabetic Retinopathy, demonstrated proper ways on

the care of the eyes, especially on preventing further loss of vision, apprehended new methods

currently used in treating the said disease ,understood the disease process itself, achieving full

awareness and self-control and has modified behavior in coping up with Diabetic Retinopathy, thus

having an effective and improve management of the disease itself.

VII. Conclusion

Diabetic Retinopathy is a major complication of Diabetes Mellitus that is said to be

alarming. From its development 20 years after the onset of the disease, its effect cannot be really seen

until the damage it has caused is severe in nature. And that this disease can be a complication of both

types of Diabetes Mellitus. And that no one is secured and safe of not acquiring the disease once DM

is diagnosed.

It can also be concluded that there are different treatments used in managing the disease

such as Laser therapy, Cryoretinopexy, Vitrectomy and Scleral Buckling, each having its benefits to

the patient’s condition. And that these operations are interrelated with each other. Over all, all of these

improve the condition of the patient though certain risks are considered.

As a whole, Diabetic Retinopathy is a progressive disease that can be minimized by

proper medical consultation and appropriate management especially if done earlier.

VIII. Recommendations

The nurse recommends that strict compliance of the patient to the medical advises must

be implemented. Regular monitoring of the patient’s condition must be of top priority. Although the

patient has accepted her present condition, she must still considers the different benefits that she can
get from subjecting herself with the specific treatments mentioned. Another thing is the patient must

always stick with her treatment regimen including strict drug compliance. This is in order to avoid

further loss of vision on the improved right eye. The use of different sources as the patient copes up

with her disease is also a major factor to consider.

IX. Learning Derived

From this case study, I have learned that Diabetic Retinopathy is a serious complication

of Diabetes Mellitus that needs to be really given enough focus and attention. It doesn’t only affect

the physiological nature of a person but the over all aspect thereof. As what I have seen with my

patient, her outlook in life is really different from that of a normal healthy person. This is true

especially when it comes to faith in God. In her case, her faith in God becomes stronger as she

continuously battle with her disease.

On the knowledge part, I have learned basically on how the disease can cause loss of

vision within a short duration of time. Just what I have observed form my patient. But although this is

the scenario, hope still lights up due to the different ways of managing the said complication. And it is

nice to know that there are on-going studies that really focus on preventing the occurrence of Diabetic

Retinopathy.

X. Bibliography

A. Book References:

1. Pharmacology. A Nursing Process Approach. 2nd edition. Evelyn R. Hayes, W.B.

Saunders Company.

2. Nurses’s Pocket Guide. 8th edition. Marilynn E. Doenges et.al., FA Davis

Company
 3. Essentials of Anatomy and Physiology. 5th edition. Seeley, Stephens, Tate

4. Medical-Surgical Nursing. 7th edition. Joyce Black

5. Medical-Surgical Nursing: Concepts and Clinical Application. 1 st edition.

Marietta Udan

B. Internet Sources:

http://www.webmd.com/hw/health_guide_atoz/hw187645.asp

http://www.stlukeseye.com/Conditions/DiabeticRetinopathy.asp

http://www.eyemdlink.com/Condition.asp?ConditionID=3

http://www.medscape.com/viewarticle/444561

http://www.sciencedaily.com/releases/2006/02/060227184647.htm

http://medweb.bham.ac.uk/easdec/diabetic_retinopathy_mech.html

http://medweb.bham.ac.uk/easdec/Information_for_patients.html#e

http://www.visionchannel.net/anatomy.shtml

http://www.medscape.com/medline/abstract/12494366

http://www.eyemdlink.com/EyeProcedure.asp?EyeProcedureID=19