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CHAPTER II

REVIEW OF RELATED LITERATURE

THE NERVOUS SYSTEM

The nervous system is the master controlling and communicating system of the body.

Every thought, action, and emotion reflects its activity. It is a signaling device, or means of

communicating with body cells, is electrical impulses, which are rapid and specific and cause

almost immediate responses.

The structural classification, which includes all nervous system organs, has two

subdivisions- the central and peripheral nervous system. The central nervous system (CNS),

consists of the brain and spinal cord. They interpret incoming sensory information and issue

instruction based on the past experience and current conditions. The peripheral nervous system

(PNS), the part of the nervous system outside of the central nervous system, consist of mainly

nerves that extend from the brain to the spinal cord. Spinal nerves carry impulses to and from the

spinal cord. Cranial nerves carry impulses to and from the brain. These nerves serve as

communication line. They link all parts of the body by carrying impulses from the sensory

receptors to the central nervous system and from the central nervous system to the appropriate

glands or muscles.

During embryonic development, the central nervous system first appears as a simple tube,

the neural tube, which extends down the dorsal median plane of the developing embryo’s body.

By the fourth week, the anterior end of the neural tube begins to expand, and brain formation

begins. The central canal of the neural tube, which continuous between the brain and the spinal

cord, becomes enlarged in four regions of the brain to form chambers called ventricles.
The adult’s brain’s unimpressive appearance gives few hints of its remarkable abilities. It

is about two good fistfuls of pinkish gray tissue, wrinkled like a walnut, and with the texture of

cold oatmeal. It weighs a little over three pounds. Because the brain is the largest and most

complex mass of nervous tissue in the body, it is commonly discussed in terms of its four major

regions- cerebral hemispheres, diencephalon, brain stem, and cerebellum.

The paired cerebral hemispheres are the most superior part of the brain and together are a

good deal larger that the other three brain regions combined. In fact, the cerebral hemispheres

enclose and obscure most of the brain stem, so many brain stem structures cannot normally be

seen unless sagittal section is made.

The entire surface of the cerebral hemispheres exhibits elevated ridges of tissue called

gyri, separated by shallow grooves called sulci. Less numerous are the deeper grooves called

fissures, which separate large regions of the brain. Many of the fissures and gyri are important

anatomical land marks. The cerebral hemispheres are separated by a single deep fissure, the

longtitudinal fissure. Other fissures or sulci divide each cerebral hemisphere into a number of

lobes, named for the cranial bones that lie over them. S[eech, memory, logical and emotional

response, as well as consciousness, interpretation of sensation, and voluntary movement, are all

functions of cerebral cortex neurons, and many of the functional areas of the cerebral

hemispheres have been identified. The somatic sensory are is located in the parietal lobe

posterior to the central sulcus. Impulses traveling from the body’s sensory receptors (except for

the special senses) are localized and interpreted in this area of the brain. The somatic sensory

area allows you to recognize pain, coldness, or a light touch. The body is represented in an

upside-down manner in the sensory area. Body regions with the most sensory receptors – the lips

and the fingertips- send impulses to neurons that make up a large part of the sensory cortex.
Furthermore, the sensory pathways are crossed pathways- meaning that the left side of the

sensory cortex receives impulses from the right side of the body, and vice versa.

Impulses from the special sense organs are interpreted in other cortical areas. For

example, the visual area is located in the posterior part of the occipital lobe, the auditory area is

in the temporal love bordering the lateral sulcus, and the olfactory area is found deep inside the

temporal lobe.

The primary motor area that allows us to consciously move our skeletal muscles is

anterior to the central sulcus in the frontal lobe. The axons of these motor neurons from the

major voluntary motor tract- the pyramidal, or corticospinal, tract, which descends to the cord.

As in the comatic sensory cortex, the body is represented upside-down and the pathways are

crossed. Most of the neurons in the primary motor area control body areas having the finest

motor control; that is, the face, mouth, and the hands. A specialized area that is very involved in

our ability to speak, Broca’s area, is found at the base of the precentral gyrus. Damage to this are,

which is located in only one cerebral hemisphere (usually left), causes inability to say words

properly. You know what you want to say but you can’t vocalize the words.

Areas involved in higher intellectual reasoning are believed to be in the anterior part of

the frontal lobes. Complex memories appear to be stored in the temporal and frontal lobes. The

speech area is located at the junction of the temporal, parietal, and occipital lobes. The speech

area allows one to sound out words. This area (like Broca’s area) is usually in only one cerebral

hemisphere. The frontal lobes house areas involved with language comprehension (word

meanings).

The cell bodies of neurons involved in the cerebral hemisphere functions named above

are found only in the outermost gray matter of the cerebrum, the cerebral cortex. As noted
earlier, the cortical region is highly ridged and convoluted, providing more room for the

thousands of neurons found there.

Most of the remaining cerebral hemisphere tissue- the deeper cerebral white matter- is

composed of fiber tracts (bundles of nerve fibers) carrying impulses to or from the cortex. One

very large fiber tract, the corpus callosum connects the cerebral hemispheres. The corpus

callosum arches above the structures of the brain stem and allows the cerebral hemispheres to

communicate with one another. This is important because, as already noted, some of the cortical

functional areas are in only one hemisphere. Although most of the gray matter is in the cerebral

cortex, there are several “islands” of gray matter, called basal nuclei, buried deep within the

white matter of the cerebral hemispheres. The basal nuclei help regulate voluntary motor

activities by modifying instructions sent to the skeletal muscles by the primary motor cortex.

The diencephalon, or interbrain, sits atop the brain stem and is enclosed by the cerebral

hemispheres. The major structures of the diencephalon are the thalamus, hypothalamus, and

epithalamus, The thalamus, which encloses the shallow third ventricle of the brain, is a relay

station for sensory impulses passing upward to the sensory cortex. As impulses surge through the

thalamus, we have a crude recognition of whether the sensation we are about to have is pleasure

or unpleasant. The actual localization and interpretation of the sensation is done by neurons of

the sensory cortex.

The hypothalamus makes up the floor of the diencephalon. It is an important autonomic

nervous system center because it plays a role in the regulation of body temperature, water

balance, and metabolism. The hypothalamus is also the center for many drives and emotions, and

as such it is an important part of the so-called limbic system, or “emotional-visceral brain”.


The epithalamus forms the roof of the third ventricle. Important parts of the epithalamus

are the pineal body (part of the endocrine system) and the choroid plexus of the third ventricle.

The choroid plexus, knots of capillaries within each ventricle, from the cerebrospinal fluid.

The brain stem is about the size of a thumb in diameter and approximately 3 inches long.

Its structures are the midbrain, pons, and medulla oblongata.

Midbrain is a relatively small part of the brain stem. It extends from the mammillary

bodies to the pons inferiorly. The cerebral aqueduct is a tiny canal that travels through the

midbrain and connects the third ventricle of the diencephalon to the fourth ventricle below.

Anteriorly, the midbrain is composed primarily of two bulging fober tracts, the cerebral

peduncles (little feet of cerebrum), which convey ascending and descending impulses. Dorsally

located are four rounded protrusions called the corpora quadrigemina.

Pons is the round structure that protrudes just below the midbrain. Pons means “bridge”,

and this area of the brain stem is mostly fiber tracts. However, it does have important nuclei

involved in the control of breathing.

Medulla oblongata is the most inferior part of the brain stem. It merges into the spinal

cord below without any obvious change in structure. Like the pons, the medulla is an important

fiber tract area. The medulla also contains many nuclei that regulate vital visceral activities. It

contains centers that control heart rate, blood pressure, breathing, swallowing, and vomiting,

among others. The fourth ventricle lies posterior to the pons and medulla and anterior to the

cerebellum.

Cerebellum, the large cauliflowerlike projects dorsally from under the occipital lobe of

the cerebrum. Like the cerebrum it has two hemispheres and a convoluted surface. The

cerebellum also has an outer cortex made up of gray matter and an inner region of white matter.
The cerebellum provides the precise timing for skeletal muscle activity and controls our balance

and equilibrium. Fibers reach the cerebellum from the equilibrium apparatus of the inner ear, the

eye, the proprioceptors of the skeletal muscles and tendons, and many other areas. The

cerebellum can be compared to an automatic pilot, continuously comparing the brain’s

“intentions” with actual body performance by monitoring body position and amount of tension in

various body parts.

Nervous tissue is very soft and delicate, and the irreplaceable neurons are injured by even

slightest pressure. Nature has tried to protect the brain and spinal cord by enclosing them within

bone, membranes, and watery cushion. Protection from harmful substances on the blood is

provided by the so-called blood-brain barrier.

The three connective tissue membranes covering and protecting the central nervous

system structures are meninges. The outermost layer the leathery durame mater, meaning “tough

or hard mother,” is a double-layered membrane where it surrounds the brain. One of its layers is

attached to the inner surface of the skull, forming the periosteum. The other called the meningeal

layer, forms the outermost covering of the brain and continues as dura mater of the spinal cord.

The dural layers are fused together except in three areas where they separate to enclose dural

sinuses that collect venous blood. In several places, the inner dural membrane extends inward to

form a fold that attaches the brain to the cranial cavity.

The middle meningeal layer is the weblike arachnoid mater. Its threadlike extensions

span the subarachnoid space to attach it to the innermost membrane, the pia mater. The delicate

pia mater clings tightly to the surface of the brain and spinal cord, following every fold. The

subarachnoid space is filled with cerebrospinal fluid. Specialized projections of the arachnoid
membrane, arachnoud villi, protrude through the dura mater. The cerebrospinal fluid is absorbed

into the venous blood in the dural sinuses through the arachnoid villi.

Cerebrospinal fluid (CSF), is a watery “broth: similar in its make up to blood plasma,

from which it forms. However, it contains less protein, more vitamin C, and its ion composition

is different. It continually formed from blood by choroid plexus. Choroid plexus are clusters of

capillaries hanging from the “roof” in each of the brain ventricles. The cerebrospinal fluid in and

around the brain and cord forms a watery cushion that protects the fragile nervous tissue from

blows and other trauma.

The cerebrospinal fluid is continually moving. It circulates from the two lateral ventricles

( in the cerebral hemispheres) into the third ventricle (in the diencephalon), and then through the

cerebral aqueduct of the midbrain into the fourth ventricle dorsal to the pons and medulla

oblongata. Some of the fluid reaching the fourth ventricle continues down the central canal of the

spinal cord, but most of it circulates into the subarachnoid space through three openings in the

walls of the fourth ventricle. The fluid returns to the blood in the dural sinuses through the

arachnoid villi. Ordinarily, cerebrospinal fluid forms and drains at a constant rate so that its

normal pressure and volume (150ml) are maintained. Any significant changes in cerebrospinal

fluid composition = nay be a sign of meningitis or certain brain pathologies.

Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco,

Calif.: Benjamin Cummings


Neurology

The brain and the rest of the nervous system are composed of many different types of cells, but

the primary functional unit is a cell called the neuron. All sensations, movements, thoughts,

memories, and feelings are the result of signals that pass through neurons.

Neurons consist of three parts.

The cell body contains the nucleus, where most of the molecules that the neuron needs to survive

and function are manufactured. Dendrites extend out from the cell body like the branches of a

tree and receive messages from other nerve cells. Signals then pass from the dendrites through

the cell body and may travel away from the cell body down an axon to another neuron, a muscle

cell, or cells in some other organ.

The neuron is usually surrounded by many support cells. Some types of cells wrap around the

axon to form an insulating sheath. This sheath can include a fatty molecule called myelin, which

provides insulation for the axon and helps nerve signals travel faster and farther. Axons may be

very short, such as those that carry signals from one cell in the cortex to another cell less than a

hair's width away. Or axons may be very long, such as those that carry messages from the brain

all the way down the spinal cord. Scientists have learned a great deal about neurons by studying

the synapse, the place where a signal passes from the neuron to another cell. When the signal

reaches the end of the axon it stimulates tiny sacs. These sacs release chemicals known as

neurotransmitters into the synapse. The neurotransmitters cross the synapse and attach to

receptors on the neighboring cell. These receptors can change the properties of the receiving cell.

If the receiving cell is also a neuron, the signal can continue the transmission to the next cell.
Some Key Neurotransmitters at Work

Acetylcholine is called an excitatory neurotransmitter because it generally makes cells more

excitable. It governs muscle contractions and causes glands to secrete hormones. Alzheimer's

disease, which initially affects memory formation, is associated with a shortage of acetylcholine.

GABA (gamma-aminobutyric acid) is called an inhibitory neurotransmitter because it tends to

make cells less excitable. It helps control muscle activity and is an important part of the visual

system. Drugs that increase GABA levels in the brain are used to treat epileptic seizures and

tremors in patients with Huntington's disease.

Serotonin is an inhibitory neurotransmitter that constricts blood vessels and brings on sleep. It is

also involved in temperature regulation. Dopamine is an inhibitory neurotransmitter involved in

mood and the control of complex movements. The loss of dopamine activity in some portions of

the brain leads to the muscular rigidity of Parkinson's disease. Many medications used to treat

behavioral disorders work by modifying the action of dopamine in the brain.

Neurological Disorders

When the brain is healthy it functions quickly and automatically. But when problems occur, the

results can be devastating. Some 50 million people in this country - one in five - suffer from

damage to the nervous system. The NINDS supports research on more than 600 neurological

diseases. Some of the major types of disorders include: neurogenetic diseases (such as

Huntington's disease and muscular dystrophy), developmental disorders (such as cerebral palsy),

degenerative diseases of adult life (such as Parkinson's disease and Alzheimer's disease),
metabolic diseases (such as Gaucher's disease), cerebrovascular diseases (such as stroke and

vascular dementia), trauma (such as spinal cord and head injury), convulsive disorders (such as

epilepsy), infectious diseases (such as AIDS dementia), and brain tumors.

Source: Antonios N., Silliman S., 2005, Diabetes Mellitus and Stroke, from

http://www.dcmsonline.org/jax-medicine/2005journals/Diabetes/diab05g-stroke.pdf

CARDIOVASCULAR SYSTEM

The cardiovascular system can be thought of as the transport system of the body. This

system has three main components: the heart, the blood vessel and the blood itself. The heart is

the system's pump and the blood vessels are like the delivery routes. Blood can be thought of as a

fluid which contains the oxygen and nutrients the body needs and carries the wastes which need

to be removed. The following information describes the structure and function of the heart and

the cardiovascular system as a whole.

The heart's job is to pump blood around the body. The heart is located in between the two

lungs. It lies left of the middle of the chest. It is a muscle about the size of a fist, and is roughly

cone-shaped. It is about 12cm long, 9cm across the broadest point and about 6cm thick.

The pericardium is a fibrous covering which wraps around the whole heart. It holds the heart in

place but allows it to move as it beats. The wall of the heart itself is made up of a special type of

muscle called cardiac muscle.


Chambers of the Heart

The heart has two sides, the right side and the left side. The heart has four chambers. The left and

right side each have two chambers, a top chamber and a bottom chamber. The two top chambers

are known as the left and right atria(singular: atrium). The atria receive blood from different

sources. The left atrium receives blood from the lungs and the right atrium receives blood from

the rest of the body. The bottom two chambers are known as the left and right ventricles.

The ventricles pump blood out to different parts of the body. The right ventricle pumps blood to

the lungs while the left ventricle pumps out blood to the rest of the body. The ventricles have

much thicker walls than the atria which allows them to perform more work by pumping out

blood to the whole body.

Blood Vessels

Blood Vessels are tubes which carry blood. Veins are blood vessels which carry blood from the

body back to the heart.Arteries are blood vessels which carry blood from the heart to the body.

There are also microscopic blood vessels which connect arteries and veins together

called capillaries. There are a few main blood vessels which connect to different chambers of the

heart. The aorta is the largest artery in our body. The left ventricle pumps blood into the aorta

which then carries it to the rest of the body through smaller arteries. The pulmonary trunk is the

large artery which the right ventricle pumps into. It splits into pulmonary arteries which take the

blood to the lungs. The pulmonary veins take blood from the lungs to the left atrium. All the

other veins in our body drain into the inferior vena cava (IVC) or thesuperior vena cava (SVC).

These two large veins then take the blood from the rest of the body into the right atrium.
Valves

Valves are fibrous flaps of tissue found between the heart chambers and in the blood vessels.

They are rather like gates which prevent blood from flowing in the wrong direction. They are

found in a number of places. Valves between the atria and ventricles are known as the right and

left atrioventricular valves, otherwise known as the tricuspid and mitral valves respectively.

Valves between the ventricles and the great arteries are known as the semilunar valves. Theaortic

valve is found at the base of the aorta, while the pulmonary valve is found the base of the

pulmonary trunk. There are also many valves found in veins throughout the body. However,

there are no valves found in any of the other arteries besides the aorta and pulmonary trunk.

Cardiovascular System

The cardiovascular system refers to the heart, blood vessels and the blood. Blood contains

oxygen and other nutrients which your body needs to survive. The body takes these essential

nutrients from the blood. At the same time, the body dumps waste products like carbon dioxide,

back into the blood, so they can be removed. The main function of the cardiovascular system is

therefore to maintain blood flow to all parts of the body, to allow it to survive. Veins deliver used

blood from the body back to the heart. Blood in the veins is low in oxygen (as it has been taken

out by the body) and high in carbon dioxide (as the body has unloaded it back into the blood).

All the veins drain into the superior and inferior vena cava which then drain into the right atrium.

The right atrium pumps blood into the right ventricle. Then the right ventricle pumps blood to

the pulmonary trunk, through the pulmonary arteries and into the lungs. In the lungs the blood

picks up oxygen that we breathe in and gets rid of carbon dioxide, which we breathe out. The

blood is becomes rich in oxygen which the body can use. From the lungs, blood drains into the
left atrium and is then pumped into the left ventricle. The left ventricle then pumps this oxygen-

rich blood out into the aorta which then distributes it to the rest of the body through other

arteries. The main arteries which branch off the aorta and take blood to specific parts of the body

are:

• Carotid arteries, which take blood to the neck and head

• Coronary arteries, which provide blood supply to the heart itself

• Hepatic artery, which takes blood to the liver with branches going to the stomach

• Mesenteric artery, which takes blood to the intestines

• Renal arteries, which takes blood to the kidneys

• Femoral arteries, which take blood to the legs

The body is then able to use the oxygen in the blood to carry out its normal functions. This blood

will again return back to the heart through the veins and the cycle continues.

Cardiac Cycle

The cardiac cycle is the sequence of events that occurs in one complete beat of the heart. The

pumping phase of the cycle, also known as systole, occurs when heart muscle contracts. The

filling phase, which is known as diastole, occurs when heart muscle relaxes. At the beginning of

the cardiac cycle, both atria and ventricles are in diastole. During this time, all the chambers of

the heart are relaxed and receive blood. The atrioventricular valves are open. Atrial

systolefollows this phase. During atrial systole, the left and right atria contract at the same time

and push blood into the left and right ventricles, respectively. The next phase is ventricular

systole. During ventricular systole, the left and right ventricles contract at the same time and

pump blood into the aorta and pulmonary trunk, respectively. In ventricular systole, the atria are
relaxed and receive blood. The atrioventricular valves close immediately after ventricular systole

begins to stop blood going back into the atria. However, the semilunar valves are open during

this phase to allow the blood to flow into the aorta and pulmonary trunk. Following this

phase, the ventricles relax that is ventricular diastoleoccurs. The semilunar valves close to stop

the blood from flowing back into the ventricles from the aorta and pulmonary trunk. The atria

and ventricles once again are in diastole together and the cycle begins again.

Components of the Heartbeat

The adult heart beats around 70 to 80 times a minute at rest. When you listen to your heart with a

stethoscope you can hear your heart beat. The sound is usually described as "lubb-dupp". The

"lubb" also known as the first heart sound, is caused by the closure of the atrioventricular valves.

The "dupp" sound is due to the closure of the semilunar valves when the ventricles relax (at the

beginning of ventricular diastole). Abnormal heart sounds are known as murmurs. Murmurs may

indicate a problem with the heart valves, but many types of murmur are no cause for concern.

The Electrocardiogram

The heart has an inbuilt rhythm of contraction and relaxation. A small group of heart muscle

cells called the pacemaker help achieve this. The pacemaker generates an electrical impulse

which spreads over the atria, making them contract. This impulse then spreads to the ventricles,

causing them to contract. The electrical changes that spread through the heart can be detected at

the surface of the body by an instrument called the electrocardiograph. Electrodes are placed in a

number of positions over the chest and the electrical changes are recorded on moving graph

paper as an electrocardiogram (ECG).


Effects of Aging on the Heart in Men and Women

As a part of the normal aging process a number of changes occur to the cardiovascular

system.

• Our heart rate slows down because the time between heartbeats increases as we age. This

is one of the main reasons why the heart is unable to pump out more blood during exercise when

we become old.

• The amount of blood the heart pumps each minute can change as we age. It decreases

slightly in older women. However, it does not change in healthy older men who have no heart

disease. The reason for the difference between the sexes is not fully understood.

• As we age, our blood pressure falls much more on standing from the sitting

position compared to when we are younger. This phenomenon is known as postural hypotension.

This explains why elderly people are more likely to feel dizzy or to fall when they stand up

quickly from a resting position.

Source: Virtual medical centers.com, Created: 26/6/2006, Modified: 11/5/2010, from

http://www.virtualmedicalcentre.com/anatomy.asp?sid=16#C1

BLOOD FLOW

When the ventricles contract, they force blood into large, thick-walled elastic arteries that

expand as the blood is pushed into them. The high pressure in these arteries forces blood to
continually move into areas where the pressure is lower. The pressure is highest in the large

arteries and continues to drop throughout the pathway, reaching zero or negative pressure at the

venae cavae.

Peripheral resistance is the amount of friction encountered by the blood as it flows

through the blood vessels. It is increased by many factors, but probably the most important is the

constriction, or narrowing of blood vessels, especially arterioles, as a result of sympathetic

nervous system activity or atherosclerosis. Increased blood volume or blood viscosity (thickness)

also raise peripheral resistance. Any factor that increases either the cardiac output or peripheral

resistance causes an almost immediate reflex rise in blood pressure. Many factors can alter blood

pressure, such as: age, weight, time of day of, exercise, body position, emotional state and

various drugs, to name a few.

Neural factors: the autonomic nervous system. The parasympathetic division of

autonomic nervous system has little or no effect on blood pressure, but sympathetic division is

important and is responsive to many different factors. The major action of sympathetic nerves on

the vascular system is to cause vasoconstriction, or narrowing of the blood vessels, which

increases blood pressure. The sympathetic center on the medulla of the brain is activated to cause

vasoconstriction in many different circumstances. When we stand up suddenly after lying down,

the effect of gravity causes the blood to pull in the vessels of the legs and feet and the blood

pressure drops. This activates pressoreceptors (called baroreceptors) in the large arteries of the

neck and chest. They send of warning signs that result in reflexive vasoconstriction, which

increases blood pressure back to homeostatic levels. When blood volume suddenly decreases, as
in hemorrhage, blood pressure drops, and the heart begins to beat more rapidly ( as it tries to

compensate). However, because venous return is reduced by blood loss. The heart also beats

weakly and inefficiently. In such cases, the sympathetic nervous system causes vasoconstriction

to increase the blood pressure so that venous return increase and circulation can continue.

The final example concerns sympathetic nervous system activity when we exercise vigorously or

are frightened and have to make a hasty escape. Under these conditions, there is a generalized

vasoconstriction except in the skeletal muscles to dilate to increase blood flow to the working

muscles. (It should be noted that the sympathetic nerves never cause vasoconstriction of blood

vessels of the heart or brain)

Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco, Calif.:

Benjamin Cummings

ENDOCRINE SYSTEM

Endocrine glands: Endocrine organs, called glands, secrete hormones into the bloodstream.

Hormones affect the activity of target sites that are often located far from the site of release.

Exocrine organs direct the function of their target sites by releasing their active.

Human endocrine system: The major endocrine organs include the hypothalamus and the

hypophysis, or pituitary gland. Other endocrine glands within the body include: thyroid,

parathyroids, adrenals, pancreas, ovaries, and testes.


• The hypothalamus: The hypothalamus is located in the forebrain, directly above the

pituitary gland. The hypothalamus receives input from other parts of the brain and from

peripheral nerves. This input affects neurosecretory cells within the hypothalamus.

• The pituitary gland: The anterior pituitary synthesizes its own hormones. Capillaries

within the anterior pituitary receive signals from the hypothalamus that tell the anterior

pituitary whether or not to release certain hormones.

• The thyroid gland: The thyroid gland is a bilobed structure found at the trachea. It

synthesizes and secretes three hormones:

1. thyroxine (T4),

2. triiodothyronine (T3), and

3. calcitonin.

The parathyroids are four small glands embedded in the thyroid. They produce and

secrete parathyroid hormone (PTH).

• The adrenal gland: The adrenal glands are located on top of the kidneys. Each gland is

subdivided into an outer adrenal cortex and an inner adrenal medulla.

• The pancreas: The pancreas is both an endocrine organ and an exocrine organ. The

exocrine portion of the pancreas secretes digestive enzymes into the pancreatic duct. The

endocrine portion of the pancreas secretes hormones, including insulin and glucagon.

• The testes: The testes are responsible for the synthesis and secretion of androgens, such

as testosterone. Interstitial cells, located between the seminiferous tubules of the testes,

produce androgens.
• The ovaries: The ovaries produce and secrete steroid hormones known as estrogens and

progesterone.

Source: Rapid Learning Center, The Endocrine System, Updated 2011,

http://www.rapidlearningcenter.com/biology/anatomy-physiology/15-The-Endocrine-

System.html

ISCHEMIC INFARCT/ STROKE

Cerebral infarction is focal brain necrosis due to complete and prolonged ischemia that

affects all tissue elements, neurons, glia, and vessels.

The basic mechanisms of cell and tissue injury that were discussed under HIE apply also to

infarcts. One additional concept, the ischemic penumbra, is worth stressing. In every infarct,

there is a central core of total ischemia and necrosis which is irreversible. This area is surrounded

by a zone of borderline ischemic tissue, the ischemic penumbra. Ischemia, in the penumbra,

causes dysfunction due to ionic and metabolic dysfunction but is not severe enough to result in

structural damage. Prompt restoration of perfusion in the penumbra by injection of thrombolytic

agents may prevent structural damage in this area, thus limiting the neurological deficit.

Ischemic stroke is an emergency. The window of opportunity for salvaging the penumbra is very

short. If adequate blood supply is not restored within 3 hours, necrosis extends to the penumbra.

According to some authors, embolism is the most frequent cause of ischemic infarction.

Most emboli are fragments of blood clots that originate in the heart or major vessels. Conditions
causing cardiac emboli include myocardial infarcts, atrial fibrillation and other arrhythmias,

rheumatic heart disease, bacterial and non-bacterial endocarditis, prosthetic valves, mitral valve

prolapse, atrial myxoma, calcified mitral annulus, and cardiomyopathy. An embolus cannot be

distinguished grossly or microscopically from a locally formed thrombus. An infarct is assumed

to be embolic if it is hemorrhagic, there is a source of emboli, there are multiple infarcts of the

brain and other organs (kidney, spleen), and there is no atherosclerosis or other vascular disease.

Some emboli consist of atheromatous material that is detached from ulcerated atheromas of the

aorta or carotid arteries. Vascular manipulation (angiography, carotid endarterectomy) may cause

atheromatous embolism. Rarer causes of embolism are fat, air, and tumor emboli. Unlike

atherothrombotic infarcts, which may evolve within hours or days, embolic infarcts have

an abrupt onset.

Because the risk factors for these types of brain infarction are identical to the risks for coronary

artery disease and other blood vessel diseases, patients most at risk for ischemic stroke are often

the same patients who have heart disease or other peripheral vascular disease. Other causes of

ischemic stroke are less common. Blood clots from aneurysms, from heart conditions (such as

atrial fibrillation, septal defects or valve disease) and other sources are less common but do occur

in some patients.

Source: Agmanolis, D. , 2005, Cerebral Ischemia and Stroke, Retrieved June, 2010, from

http://www.neuropathologyweb.org/chapter2/chapter2bCerebralinfarcts.html

Essentials of Diagnosis

• Sudden onset of characteristic neurologic deficit.


• Patient often has history of hypertension, diabetes mellitus, valvular heart disease, or

atherosclerosis.

• Distinctive neurologic signs reflect the region of the brain involved.

General Considerations

In the USA, stroke remains the third leading cause of death, despite a general decline in the

incidence of stroke in the last 30 years. The precise reasons for this decline are uncertain, but

increased awareness of risk factors (hypertension, diabetes, hyperlipidemia, cigarette smoking,

cardiac disease, AIDS, recreational drug abuse, heavy alcohol consumption, family history of

stroke) and improved prophylactic measures and surveillance of those at increased risk have

been contributory. A previous stroke makes individual patients more susceptible to further

strokes.

For years, strokes have been subdivided pathologically into infarcts (thrombotic or embolic)

and hemorrhages, and clinical criteria for distinguishing between these possibilities have been

emphasized. However, it is often difficult to determine on clinical grounds the pathological basis

for stroke.

1. LACUNAR INFARCTION

Lacunar infarcts are small lesions (usually < 5 mm in diameter) that occur in the

distribution of short penetrating arterioles in the basal ganglia, pons, cerebellum, anterior

limb of the internal capsule, and less commonly, the deep cerebral white matter. Lacunar

infarcts are associated with poorly controlled hypertension or diabetes and have been

found in several clinical syndromes, including contralateral pure motor or pure sensory
deficit, ipsilateral ataxia with crucal paresis, and dysathria with clumsiness of the hand.

The neurological deficit may progress over 24-36 hours before stabilizing.

Lacunar infarcts are sometimes visible on CT scans as small, punched-out, hypodense

areas, but in other patients no abnormality is seen. In some instances, patients with a

clinical syndrome suggestive of lacunar infarction are found on CT scanning to have a

severe hemispheric infarct.

The prognosis for recovery from the deficit produced by a lacunar infarct is usually

good, with partial or complete resolution occurring over the following 4-6 weeks in many

instances.

2. CEREBRAL INFARCTION

Thrombotic of embolic occlusion of a major vessel leads to cerebral infarction.

Causes include the disorders predisposing to transient ischemic attacks (see above) and

atherosclerosis of cerebral arteries. The resulting deficit depends upon the particular

vessel involved and the extent of any collateral circulation. Cerebral ischemia leads to

release of excitatory and other neurons, thereby leading to cell death and increasing the

neurologic deficit.
Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis

& treatment (45th ed.). New York: Lange Medical Books/Mcgraw-Hill.

ISCHEMIC STROKE PATHOPHYSIOLOGY

In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a

blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic

events referred to as the ischemic cascade.

The ischemic cascade begins when cerebral blood flow decreases less that 25 mL per 100 100g

of blood per minute. At this point, neurons are no longer able to maintain aerobic respiration.

The mitochondria must then switch to the anaerobic respiration, which generates large amounts

of lactic acid, causing a change in pH. This switch to the less efficient anaerobic respiration also

renders the neuron incapable of producing sufficient quatities of adenosine triphosphate (ATP)

to fuel the depolarization processes. The membrane pumps that maintain electrolyte balances

bagin to fail, and the cells cease to function.

Early in the cascade, an area of low cerebral blood flow, referred to as the penumbra region,

exists around the area of infarction. The penumbra region is ischemic brain tissue that may be

slavaged with timely intervention. The ischemic cascade threatens cells in the penumbra

because memebrane depolarization of the cell wall leads to an increase in intracellular calcium

and the release of glutamate. The influx of calcium and the release of glutamate, if continued,

activate a number of damaging pathways that result in the destruction of the cell membrane, the

release of more calcium and glutamate, vasoconstriction, and the generation of free radicals.
These processes enlarge the area of infarction into the penumbra, extending the stroke. A person

experiencing a stroke typically loses 1.9 million neurons each minute that a stroke is not treated,

and the ischemic brain ages 3.6 years each hour without treatment.

Each steps in the ischemic cascade represents an opportunity for intervention to limit the extent

of secondary brain damage caused by stroke. The penumbra area may be revitalized by

administration of tissue plasminogen activator. Medications that protect the brain form

secondary injury are called neuroprotectants. A number of ongoing clinical trials focus on

neuroprotective medications and strategies to improve stroke recovery and survivial

Source: Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-

surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &

Wilkins.

Pathophysiology of Middle Cerbral Artery Infarct

Two approaches are used to describe middle cerebral artery (MCA) anatomy. The

functional branching approach follows the MCA trunk from the source to the end branches. The

segmental approach analyzes branches of the MCA in relation to brain landmarks, dividing the

artery into 4 main segments. In the segmental approach, M1 is the portion most proximal to the

origin of the vessel, and M4 includes the terminal MCA branches at the brain surface. (Normal

intracerebral vascular anatomy is shown in the images below.)

The segmental approach is applied most often for angiographic purposes and relates

segments of the MCA to specific cerebral landmarks. The first of 4 segments, M1, describes the
artery from its origin to the limen insulae, most of which is the portion from which the

lenticulostriate arteries arise. The second portion of M1 describes the 3 branches that result from

the bifurcation of the MCA and enter the sylvian sulcus. M2 is the segment that runs along the

insula, and M3 follows the operculum superior to the insula. Finally, M4 describes branches of

the MCA that perfuse nearly the entire convex surface of the cerebral hemispheres, aside from

the frontal pole and posterior rim.

Using the functional branching approach to anatomy, the MCA generally arises as a

single trunk 18-26 mm long with a diameter of approximately 3 mm. The first branches consist

of 15-17 small lenticulostriate arteries that supply the putamen and pallidum or the lentiform

nucleus, internal capsule, and caudate nucleus of the basal ganglia. Occasionally, a few of the

smaller lenticulostriate arteries arise from the internal carotid arteries. After the lenticulostriate

branches, the MCA generally bifurcates, forming superior and inferior divisions. The superior

branch supplies the prefrontal and orbitofrontal cortex, and the inferior branch supplies the

anterior, middle, and polar temporal regions.

Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from

http://emedicine.medscape.com/article/323120-overview

MANIFESTATIONS OF PATIENT WITH ISCHEMIC INFARCT


Ischemic infactions usually are not demonstrated on gross examination for 6-12 hrs. The

initial change of the affected area is a slight discoloration and softening with the gray matter

taking on a muddy color and the white matter losing is normal fine-grained appearance.

After 24-48 hours, infarction, necrosis, circumlesional swelling and mushy disintegration

of the affected area are evident.

Chipps, E. M., Clanin, N. J., & Campbell, V. G. (1992). Neurologic disorders . St. Louis: Mosby

Year Book.

A. Symptoms and Signs: Onset is usually abrupt, and there may then be very little

progression except that due to brain swelling. Clinical evaluation always includes

examination of the heart and auscultation over the subclavian and carotid vessels to

determine whether there are any bruits.

1. Obstruction of carotid circulation- Occlusion of the anterior cerebral artery distal to

its junction with the anterior communicating artery causes weaknesses of the arm,

especially proximally. There may be a contralateral grasp reflex, paratonic rigidity,

and abulia (lack of initiative) or frank confusion. Urinary incontinence is not

uncommon, particularly if behavioral disturbances are conspicuous. Bilateral anterior

cerebral infarction is especially likely to cause marked behavioral changes and

memory disturbances. Unilateral anterior cerebral artery occlusion proximal to the

junction with the anterior communicating artery is generally well tolerated because of

the collateral supply from the other side.


Middle cerebral artery occlusion leads to contralateral hemiplegia, hemisensory

loss, and homonymous hemianopia (ie, bilaterally symmetric loss of vision in half of

the visual fields), with the eyes deviated to the side of the lesion. If the dominant

hemisphere is involved, global aphasia is also present. It may impossible to

distinguish this clinically from occlusion of the internal carotid artery. With occlusion

of either of these arteries, there may also be considerable swelling of the hemisphere,

leading to drowsiness, stupor, and coma in extreme cases. Occlusions of different

branches of the middle cerebral artery cause more limited findings. For example,

involvement of the anterior main division leads to a predominantly expressive

dysphasia and to contralateral paralysis and loss of sensations in the arm, the face,

and to a lesser extent, the leg. Posterior branch occlusion produces a receptive

(Wernicke’s) aphasia and a homonymous visual field defect. With involvement of the

nondominant hemisphere, speech and comprehension are preserved, but there may be

a confusional state, dressing apraxia, and constructional and spatial deficits.

2. Obstruction of vertebrobasilar circulation-Occlusion of the posterior cerebral

artery may lead to a thalamic syndrome in which contralateral hemisensory

disturbance occurs, followed by the development of spontaneous pain and

hyperpathia. There is often a macular-sparing homonymous hemianopia and

sometimes a mild, usually temporary, hemiparesis. Depending on the site of the

lesion and the collateral circulation, the severity of these deficits may also occur,

including involuntary movements and alexia. Occlusion of the main artery beyond the

origin of its penetrating branches may lead solely to a macular-sparing hemianopia.


Vertebral artery occlusion distally, below the origin of the anterior spinal and

posterior inferior cerebellar arteries, may be clinically silent because the circulation is

maintained by the other vertebral artery. If the remaining vertebral artery is

congenitally small or severely atherosclerotic, however, a deficit similar to that of

basilar artery occlusion is seen unless there is good collateral circulation from the

anterior circulation through the cycle of Willis.

When the small paramedian arteries arising from the vertebral artery are occluded,

contralateral hemiplegia and sensory deficit occur in association with ipsilateral

cranial nerve palsy at the level of the lesion. An obstruction of the posterior inferior

cerebellar artery or an obstruction of the vertebral artery just before it branches to this

vessel leads ipsilaterally to spinothalamic sensory loss involving the face, ninth and

tenth cranial nerve lesions, limb ataxia and numbness, and Horner’s syndrome,

combined with contralateral spinothalamic sensory loss involving the limbs.

Occlusions of both vertebral arteries and the basilar artery lead to a coma with

pinpoint pupils, flaccid quadriplegia and sensory loss, and variable cranial nerve

abnormalities. With partial basilar artery occlusion, there may be diplopia, visual loss,

vertigo, dysarthria, ataxia, weakness or sensory disturbances in some or all of the

limbs, and discrete cranial nerve palsies. In patients with hemiplegia of pontine

origin, the eyes are often deviated to the paralyzed side, whereas in patients with a

hemispheric lesion, the eyes commonly deviate from the hemiplegic side.

Occlusion of any of the major cerebellar arteries produces vertigo, nausea,

vomiting, nystagmus, ipsilateral limb ataxia, and contralateral spinothalamic sensory


loss in the limbs. If the superior cerebellar artery is involved, the contralateral

spinothalamic loss also involves the face; with occlusion of the anterior inferior

cerebellar artery, there is ipsilateral spinothalamic sensory loss involving the face,

usually in conjunction with ipsilateral facial weakness and deafness. Massive

cerebellar infarction may lead to coma, tonsillar herniation, and death.

3. Coma-Infarction in either the carotid or vertebrobasilar territory may lead to loss of

consciousness. For example, an infarct involving one cerebral hemisphere may lead

to such swelling that the function of the other hemisphere or the rostral brain stem is

disturbed and coma results. Similarly, coma occurs with bilateral brain stem

infarction when this involves the reticular formation, and it occurs with brain stem

compression after cerebellar infarction.

B. Imaging: Radiography of the chest may reveal cardiomegaly or valvular calcification;

the presence of a neoplasm would suggest that the neurologic deficit is due to metastasis

rather than stroke. A CT scan of the head (without contrast) is important in excluding

cerebral infarct and tumor. CT scanning is preferable to MRI in the acute stage because it

is quicker and because intracranial hemorrhage is not easily detected by MRI within the

first 48 hours after a bleeding episode.

C. Laboratory and Other Studies: Investigations should include a complete blood count,

sedimentation rate, blood glucose determination, and serologic tests for syphilis.

Antiphospholipid antibodies (lupus anticoagulants and anticardiolipin antibodies)

promote thrombosis and are associated with an increased incidence of stroke. Similarly,

elevated serum cholesterol and lipids may indicate an increased risk of thrombotic stroke.
Electrocardiography will help exclude a cardiac arrhythmia or recent myocardial

infarction that might be serving as a source of embolization. Blood cultures should be

performed if endocarditis is suspected, echocardiography if heart disease is suspected,

and Holter monitoring if paroxysmal cardiac arrhythmia requires exclusion. Examination

of the cerebrospinal fluid is not always necessary but may be helpful if there is diagnostic

uncertainty; it should be delayed until after CT scanning.

Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis &

treatment (45th ed.). New York: Lange Medical Books/Mcgraw-Hill.

Patients with middle cerebral artery stroke syndrome (MCA stroke syndrome) may have some

basic physical findings, as follows:

Main trunk occlusion of either side yields contralateral hemiplegia, eye deviation toward the side

of the MCA infarct, contralateral hemianopia, and contralateral hemianesthesia. Eye and head

deviation toward the side of the lesion is probably due to damage of the lateral gaze center

(Brodmann area 8), or it can represent classic neglect, particularly when the right MCA is

involved.

Trunk occlusion involving the dominant hemisphere causes global aphasia, whereas involvement

of the nondominant hemisphere causes impaired perception of deficits (anosognosia) resulting

from the stroke and more qualitative deficits of speech. Superior division infarcts lead to

contralateral deficits with significant involvement of the upper extremity and face and partial

sparing of the contralateral leg and foot.


Inferior division infarcts of the dominant hemisphere lead to Wernicke's aphasia. Such infarcts

on either side yield a superior quadrantanopsia or homonymous hemianopia, depending on the

extent of infarction. Right inferior branch infarcts also may lead to a left visual neglect. Finally,

resultant temporal lobe damage can lead to an agitated and confused state.

Specific neurologic sequelae

• Loss of consciousness - Initially this is rare after MCA stroke, but it occurs slightly more

often than in vertebrobasilar strokes (8.4% vs 5.7%). Loss of consciousness most often is

attributable to seizures, but it may result from secondary edema and subsequent

brainstem herniation.

• Hemiparesis and hemiplegia

o Surprisingly, assigning clear-cut syndromes of weakness to specific territories of

MCA infarct has posed a significant challenge. The prognosis of such motor

deficit also has not completely been elucidated, with case reports of remarkable

recovery from dense limb involvement.

o Partial hemiparesis patterns have been mapped more readily to certain MCA

territory infarcts. The National Institute of Neurological and Communicative

Disorders and Stroke (NINCDS) data bank project gathered pilot data from 488

patients with unilateral hemisphere strokes. The following conclusions arose

from the analysis of the project data:

 Equivalent weakness of the hip, foot, shoulder, and hand was the most

common finding among the patients in the NINCDS project, accounting

for 71.2% of cases.


 Hemiparesis with distal predominance describes another 23.5% of cases,

with weakness of the lower face, lower legs, toes, fingers, and forearm and

sparing of the forehead and proximal muscles of the upper and lower

extremities. The resultant deficit is believed to be due to the large

representation of the affected muscles in the homunculus.

 Faciobrachial paresis describes weakness of the lower face, jaw, tongue,

oropharynx, and ipsilateral upper extremity. The weakness of the upper

extremity is often more pronounced in the distal musculature of the hand

and forearm. These deficits result from ischemic insult of the insula and

operculum.

o Although uncommon, movement disorders such as athetosis, chorea, and dystonia

have been described as sequelae of MCA territory stroke.

• Visual deficits

o Hemianopia has long been known to accompany the syndrome following a large

MCA infarct; yet, only the superior portion of the optic radiation is supplied by

the MCA. The resultant hemianopia is probably due to a massive infarct with

subsequent edema affecting adjacent structures.

o Quadrantanopsia can be attributed to a parietal infarct affecting the deep fibers of

the upper optic radiation; however, this condition is rare.

• Neglect

o Neglect in classic form has been attributed to parietal insult, but data from

positron emission tomography (PET) scanning reveal that frontal lesions can

cause similar but more transient sequelae.


o At times, visual neglect is difficult to distinguish from hemianopia. Subtle signs

(eg, a patient who responds to a stimulus from the left by turning right and also

fails to blink upon threatening stimuli to the affected side) can aid in diagnosing

neglect. Patients with visual neglect often have difficulty naming objects

presented on the affected side.

o Motor neglect with underuse of the side contralateral to the cerebral insult appears

much like a hemiparesis. Special efforts must be made by the examiner to

encourage the patient to demonstrate strength and dexterity. Typically, the patient

has delayed withdrawal to noxious stimuli, fails to place the affected hand in the

lap when seated, and falls heavily to the affected side with no apparent effort to

minimize impact.

• Autonomic dysfunction

o Autonomic disturbance after MCA stroke often can be evidenced by contralateral

edema of the hand and foot arising within hours of the infarct and lasting up to 2

weeks. This edema is in contrast to the dependent edema that develops subacutely

in the distal aspect of a plegic extremity.

o Excessive sweating contralateral to the territory of an MCA stroke can be

indicative of a larger lesion, affecting deep and superficial branches.

Left-hemisphere (dominant) infarction - The left cerebral hemisphere is dominant for speech and

language in more than 95% of right-handed individuals. Defining cerebral dominance for left-

handed individuals is more difficult, but most left-handed patients also appear to have a

dominant left hemisphere. One study analyzing left-handed patients with aphasia showed that
60% had lesions confined to the left hemisphere. Other studies reveal bilateral speech

representation in as many as 15% of left-handed patients.

• Aphasia

o Ischemic injury to the sylvian fissure of the dominant hemisphere is the lesion

most likely to lead to dysphasia. Describing deficits in speech may be easier if

pathologies are categorized as fluent versus nonfluent. In this context, fluent does

not describe correct use of language or grammar but simply the ability to produce

sounds readily. Nonfluent dysphasia describes a deficit in which a difficulty in

producing words or sounds is appreciated.

o Surprisingly, studies have revealed patients with only mild speech deficits, despite

localized infarcts in cerebral areas thought to be essential for speech and

language. Such studies suggest a major role of deeper structures, particularly the

thalamus, in this function.

o Broca's aphasia, also termed expressive or motor aphasia, describes the ability to

comprehend written and spoken language, with nonfluent or impaired expression

of either spoken or written language.

 The infarct responsible for Broca's aphasia encompasses the insula and

frontoparietal operculum.

 Global aphasia can be assumed wrongly in these patients if the examiner

does not use comprehension testing with simple questions. Initially, the

patient's profound impairment is difficult to differentiate from a global

aphasia, and only later does a speech disturbance arise that is isolated to

writing (agraphia) and speech production.


 Dyspraxia describes the impaired cooperation of the oropharyngeal and

respiratory elements necessary for speech. Individuals with dyspraxia have

a hesitant and somewhat telegraphic verbal response.

 Agrammatism describes the shortened speech patients use to

communicate. These individuals sometimes utter only individual words to

communicate an idea.

o Wernicke's aphasia, also termed receptive or sensory aphasia, is caused most

often by occlusion of the lower division of the MCA bifurcation or one of its

branches. Patients with Wernicke's aphasia vocalize smoothly and with

expression, but they demonstrate paraphasias or speech with distorted phonetic

structure, word substitution, and additional prefixes and suffixes. The speech is

fluent but can be without understandable words.

 The infarct responsible for a classic Wernicke's aphasia includes the

dominant posterior temporal, inferior parietal, and lateral temporo-

occipital regions.

 Contrary to the manifestation of motor aphasia, speech is rich in words but

is missing key words and ideas and may be perseverative. The patients

demonstrate pure-word deafness, with the inability to repeat words, along

with alexia, the inability to recognize or comprehend written language.

o The classic cause of conductive aphasia is thought to be a disruption of neural

pathways or of the arcuate fasciculus connecting the motor and sensory areas

concerned with speech. The clinical features of conductive aphasia are not
explained completely by this theory. Distinguishing a conductive aphasia is an

especially difficult challenge for the clinician.

 Patients with conductive aphasia have significant difficulty repeating

unfamiliar phrases and words and demonstrate much better auditory and

written comprehension than do individuals with Wernicke's aphasia;

however, patients with conductive aphasia are more likely to recognize the

deficit and to make an effort to self-correct.

 Anatomically, insult to the isolated arcuate fasciculus is believed to be

responsible for the symptoms; however, scant case reports actually

document such a correlation. In fact, patients with the described syndrome

more frequently have more superficial infarcts involving 1 or 2 recently

discovered tracts.

• Apraxia

o Apraxia refers to the inability to perform a previously learned task despite

preserved strength, vision, and coordination. The condition is due to an insult to

the dominant hemisphere.

o When referring to apraxia, Mohr states, "Motor engrams (programs) that guide

skilled acts have either been lost or cannot be accessed." Generally, the ability is

impaired rather than eliminated; thus, the term dyspraxia is more appropriate.

o The most common form of apraxia is ideomotor apraxia, in which a disconnection

is thought to exist between the cortex containing plans for movement and the

cortex responsible for execution. On verbal command, the patient is

uncoordinated in or is unable to perform simple tasks, such as imitating the use of


a hammer and nail. Often, the patient performs the actual task with much greater

precision. Aphasia and apraxia occur independently, and the cortex responsible

for motor planning is thought to be in the superior parietal lobe.

o Ideational apraxia describes an impaired ability to complete more complex

multistep tasks, such as obtaining a glass of water. Not all experts agree that

ideational and ideomotor apraxias are distinct entities.

o Callosal apraxia is similar to ideomotor apraxia but only involves the

nondominant arm.

o Limb-kinetic apraxia refers to an impaired clumsy manipulation of objects in such

tasks as combing one's hair. Limb-kinetic apraxia can be accompanied by ataxia,

choreoathetosis, spasticity, and weakness. Even after repeated efforts,

performance only slightly improves.

o Oral-buccal-lingual apraxia describes an impaired ability to perform complex

movements of the tongue and face upon command. Often these movements are

performed spontaneously. This condition coexists with Broca's aphasia in 90% of

patients; however, the 2 disorders often exist independently.

Right-hemisphere (nondominant) infarction - Motor deficits following infarction of the

nondominant hemisphere parallel those described previously for dominant-hemisphere lesions.

Additionally, lesions of the nondominant hemisphere can lead to a variety of behavioral

abnormalities. These behavioral deficits correlate much less to location and extent of the

infarction than do deficits following infarcts of the dominant hemisphere, and some are

predictive of an unfavorable long-term outcome after rehabilitation. Insults of the nondominant

hemisphere can affect attention, leading to impersistence and neglect.


• Extinction - This describes inattention to one stimulus when 2 stimuli are presented

simultaneously. Generally, the ignored stimulus is on the left side.

• Neglect - According to Schwartz and colleagues, neglect is "a lack of responsivity to

stimuli on one side of the body, in the absence of any sensory or motor deficit severe

enough to account for the imperception."Such unilateral neglect occurred in 29% of

patients with right-sided brain damage versus 12% of patients with left-sided brain

damage among a stroke population studied by Battersby and coauthors. In severe cases,

the patient often ignores tactile, visual, and auditory stimuli on the left side and is turned

chronically to the right side. When asked to bisect lines, the patient often does this far to

the right of center. Unilateral spatial neglect is a subtler deficit, in which the patient may

fail to read words or recognize figures to the left of midline.More sizable infarcts lead to

anosognosia or imperception of field neglect and imply a much less favorable prognosis.

• Impersistence - This term is used to describe an inability to persist in performing motor

tasks; it is often accompanied with visuomotor and visuospatial deficits. This impairment

places the patient at risk for an unfavorable rehabilitation outcome.

• Dressing apraxia - This finding is much more common in cases of right-hemisphere

infarcts and is attributable to difficulty distinguishing right from left and up from down.

The patient is unable to dress without assistance despite having no apparent hemiplegia

that would prevent the performance of this function.

• Topographic memory deficit - This term is used when individuals become lost in familiar

surroundings. The finding often follows right-hemisphere insults.

• General confusion and delirium - These findings often are more commonly appreciated in

patients with damage to the nondominant hemisphere. The central role the right
hemisphere plays in attention, vigilance, and distinguishing stimuli is probably

responsible for this common presentation.

• Confabulation or unintentional fabrication of information - This is largely due to an

inability to recognize errors, disinhibition, and memory deficits. These deficits all are

common with damage to the nondominant hemisphere and to the frontal lobe.

• Constructional apraxia - This defines a difficulty in manipulating objects in space. This

type of apraxia can be appreciated by having affected patients copy designs or build 3-

dimensional models. This tendency is more common with right-sided lesions than with

left-sided lesions, as is evident in a population of 67 patients with constructional apraxia

studied by Piercy and colleagues. In this group, 25 had left-sided damage and 42 had

damage to the right hemisphere. The apraxia of the patients with a dominant-hemisphere

infarct often is described as decreased attention to detail. The apraxia with right-sides

damage is consistent with neglect, in which features to the left of midline are ignored.

• Allesthesia - This term describes sensory referral. For example, a patient touched on the

left side feels the touch on the right.

• Aprosody, lack of intonation in speech, and affective agnosia - These terms refer to the

inability to perceive or comprehend emotional intonation of speech. The 2 deficits often

coexist and correlate with lesions in the right temporoparietal region.

Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from

http://emedicine.medscape.com/article/323120-overview
Infarction or ischemia affecting the carotid artery may cause a papillary abnormality

ptosis (eyelid drooping), visual deficit, pallor and petechiae of the conjunctiva.

The affected art of the brain is the right hemisphere in which cranial nerve III

(occulomotor nerve) lies. Due to the paralysis of the nerve, sinking of eyeballs, ptosis of the

upper eyelid, slight elevation of lower eyelid, papillary constriction and lack of tearing in the eye

(Horner’s syndrome) is manifested by the patient. The patient may lose her ability to blink.

Without a blink reflex, the cornea will dry and become abraded.

Black, J., & Hawks,J.(2009).Medical Surgical Nursing:Clinical Management for Positive

Outcomes.St. Louis, Missouri: Saunders Elsevier

Causes

The main causes of stroke include ischemia, cardioembolism, hypercoagulable states,

hemorrhage, hypertension, and amyloid or arteriovenous malformation. Thrombotic occlusion of

small and large vessels is still widely accepted as the primary etiology of strokes in general,

causing approximately 51% of all strokes in the anterior, middle, and posterior cerebral

vasculature combined; however, it is a relatively rare cause of middle cerebral artery strokes

(MCA strokes). Estimates suggest that 15-30% of all strokes are thought to be of embolic

etiology. The remaining cases have either an undetermined or a combined etiology or else are

caused by dissection.

• Embolism
o Most of the sources in the literature support embolism as the primary etiology of

MCA strokes. Specifically, cardioembolism accounted for approximately 50% of

total MCA strokes, 34% of deep MCA strokes, and 41% of cortical strokes in a

study by Moulin and coauthors. This same study, with a relatively large cohort,

suggests that cardioembolism may be greatly underdiagnosed and may play a

more common role in posterior and anterior cerebral strokes than previously

thought. The study also revealed paroxysmal atrial fibrillation in 65% of all stroke

patients studied. This cardiac abnormality may be a common poststroke sequela,

but its frequent occurrence certainly supports the need for cardiac monitoring and

a high index of suspicion for cardioembolism in formulating a complete

differential diagnosis.

o Additionally, embolic strokes can occur through the atheromatous plaques of

carotid disease. All of these data support widely accepted diagnostic studies,

including carotid Doppler studies, transesophageal echocardiography studies, and

telemetry to elucidate and treat pathology and prevent future embolic events.

o The location of MCA stroke depends largely on the size of the embolic mass.

Occlusion at the stem is rare and requires embolic matter of at least 3-5 mm.

Emboli can arise because of intravascular, rigid foreign matter (eg, shotgun

pellets, catheter tips, large thrombi combined with bacteria) or as a result of large

calcific plaques formed through direct internal carotid trauma or puncture. The

etiology of occlusion of smaller and surface branches obviously is more diverse

and most commonly involves cardiogenic emboli or material from an ipsilateral

site of carotid atherosclerosis. Other sources of emboli include spontaneous


dissection of a carotid artery, material from breast metastasis, a marantic embolus,

fungal endocarditis, and paradoxical emboli due to a patent foramen ovale.

o Embolization occurs with equal frequency in the right and left MCA.

Angiography reveals that these occlusions are usually found in the first 24 hours,

but the vessels are generally patent within 48 hours. A persistent occlusion has a

less favorable prognosis. The size of the infarct also depends on the collateral

circulation, which is highly variable as a result of congenital vascular patterns and

collateral vascular development secondary to long-standing atherosclerosis.

• Indirect ischemia

o Distal territories of the MCA are quite vulnerable to ischemia because of failure

of perfusion due to arrhythmia and other causes of hypotension. Such compromise

in circulation is especially significant in patients with carotid artery stenosis.

o The prevalence of such strokes is uncertain, but they are not thought to be

uncommon, given the high correlation of carotid stenosis with distal territory

stroke.

• Atherosclerosis - Primary atherosclerosis of the MCA and branches accounts for only 7-

8% of symptomatic MCA disease. Furthermore, many of these cases probably represent

recanalized embolism and not true atherosclerosis.

• Thrombosis - Approximately 2-7% of ischemic events in the MCA territory are due to

thrombotic occlusion. The diagnosis can be excluded using repeat angiography, but this is

of questionable utility.

• Amyloid angiopathy - This is a rare etiology for lobar cortical strokes in elderly patients.
• Other - Dissection and stenosis of the MCA are rarely documented as causes of MCA

stroke.

• Etiology based on age - Hemorrhagic stroke is the most common etiology in younger

persons (aged 18-45 y), with intracranial hemorrhage accounting for 41% and

subarachnoid hemorrhage accounting for 17% of strokes in persons in the younger age

group. The remaining 42% of strokes due to ischemia generally require a more

exhaustive workup to elucidate an etiology. Consider carotid or vertebral dissection,

collagen-vascular disease, and coagulopathies. Studies reveal that dissection is an

underrecognized cause of stroke in younger populations. Still, even with advances in

diagnostic options, 20% of strokes in younger persons continue to be of unknown

etiology.

Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from

http://emedicine.medscape.com/article/323120-overview

DIAGNOSTIC EXAMINATIONS

Imaging Tests

Imaging tests can produce a detailed picture of the brain. These tests include computed

tomography (CT or CAT) scans and magnetic resonance imaging (MRI).

CT Scans
A CT scanner sends a series of X-rays through the head that are analyzed by a computer to create

a detailed picture of a "slice" of the area being studied. Each X-ray lasts a fraction of a second.

During a CT scan of the head, the head is positioned inside a CT scanner's cylinder. The entire

scanner can tilt, and the X-ray scanning cylinder within it can rotate to obtain the views needed.

For a head scan, 10 to 30 slices are usually taken. The results are highly-detailed images of the

head, including the brain, eyes, bones of the skull and sinuses within the bones around the nose.

This is often one of the first tests given to patients who may have had a stroke. These scans

provide important information about the cause of the stroke and the location and extent of brain

injury. CT scans are clearer pictures of the brain than regular X-rays.

Sometimes a special dye (contrast material) that contains iodine is injected into the blood during

a CT scan of the head. The dye makes blood vessels and certain structures inside the head more

visible on the CT scan images. This is known as CT angiography.

MRI

An MRI produces a picture of the brain using a large magnetic field. It also can show the

location and extent of brain injury, but the image is sharper and more detailed. An MRI can

distinguish between the blockage of blood flow due to a clot, which causes transient ischemic

attack and ischemic stroke, and bleeding, which causes hemorrhagic stroke. This type of

diagnostic technique is often used to diagnose small, deep injuries. After the first 24 hours, MRI

can identify the exact size and location of the area affected by a stroke. This information may

help the doctor determine how well the person may recover from a stroke.
An MRI is more sensitive than a CT scan in identifying changes caused by lack of oxygen to

brain cells during the first 72 hours after a stroke. An MRI is more accurate than a CT scan of the

head in identifying multiple small strokes within the brain. An MRI is also better for detecting

strokes in the lower, back part of the brain (cerebellum) and the part of the brain that connects

with the spinal cord (brain stem). An MRI seems to be more accurate in detecting strokes caused

by clots (ischemic strokes) during the first 3 days after a stroke, but the test is less accurate if it is

done in the first 24 hours after symptoms first begin.

Electrical Activity Tests

Electrical activity tests record the electrical impulses of the brain. These tests include an

electroencephalogram (EEG) and evoked response tests. In an EEG, electrodes are put on a

person's scalp to pick up electrical impulses, which are printed out as brain waves. An evoked

response test measures how the brain handles different sensory information, using electrodes that

record electrical impulses related to hearing, body sensation or vision.

Blood Flow Tests

Blood flow tests can reveal problems in the flow of blood to the brain, normally through the use

of ultrasound technology. During these tests, a probe is placed over the artery in question -

usually the arteries of the neck or at the base of the skull - and the amount of blood flow is
measured. Such tests include B-mode imaging, Doppler testing and duplex scanning, which

gives detailed information about the condition of arteries.

Angiography

Angiography (also known as arteriography) is another type of blood flow test. In this, special

dyes are injected into the blood vessels and an X-ray is taken. This test evaluates the size and

location of blockages and can be especially valuable in diagnosing aneurysms and malformed

blood vessels and providing information before surgery.

Carotid angiography is the best test available to identify and measure the blockage in the carotid

arteries of the neck. It is usually done after a carotid ultrasound has shown that there probably is

a blockage in the artery and if surgery (endarterectomy) is being considered to remove the

blockage and reopen the artery. In this test, a tiny tube (catheter) is inserted into an artery (often

in the arm) and threaded through other blood vessels to reach the carotid artery. A dye is then

injected through the tube and into the artery. The dye outlines the blood vessel and X-rays are

taken to evaluate the degree of narrowing and the condition of a plaque. If a plaque is rough,

clots are more likely to form in the blood vessel. When the dye is injected, some people feel a

burning sensation in the face and head, a brief headache, flushed on one side of the face or

nauseous. The test usually takes from one to three hours. The patient may be given a drug to help

relax during the test.

Cerebral angiography uses the same technique to study the arteries of the brain. It is usually done

at the same time as carotid arteriography to evaluate blood flow through the brain. The results

will help decide whether surgery to reopen a blocked artery (carotid endarterectomy) is
appropriate. Angiography carries the risk that the procedure itself may cause a piece of plaque to

break away and travel through the blood to the brain, causing a stroke during the procedure.

Duplex Scans

Duplex scans are a sensitive form of ultrasound done of the neck when narrowing of the carotid

arteries due to plaque buildup is suspected. It is often the first test used when you are being

evaluated for surgery to reopen a blocked artery (carotid endarterectomy). In carotid artery

ultrasound scanning, high-pitched sound waves are bounced off the blood vessels and tissues of

the neck to create an image of the arteries. Duplex scanning, which is a newer technique than

traditional carotid artery ultrasound and now used more often, is able to measure blood flow at

many points in the blood vessel at one time. It is used more often than older carotid ultrasound

methods.

During duplex scanning, an instrument is moved over both sides of the neck. The resulting two-

dimensional picture shows clearly the amount of blockage in the artery. This method also shows

color pictures that indicate how fast blood is flowing in any point in the blood vessel. Although

carotid ultrasonography is quicker, safer, less painful and less expensive than carotid

arteriography, it may not always be as accurate in determining the amount of blockage of blood

flow as some other tests. However, carotid ultrasonography is often the first test used and can be

used to decide if further tests are needed.

Magnetic Resonance Angiography

Magnetic resonance angiography (MRA) is a form of MRI that can measure blood flow through

blood vessels. The test uses a strong magnetic field and radio signals to create pictures of the
blood flow through blood vessels. With an MRA, both the blood flow inside of the vessel and the

condition of the blood vessel walls can be seen. An MRA takes pictures quickly that can be seen

individually or together as a three-dimensional picture.

• An MRA is often used to determine if narrowing of blood vessels (especially the carotid

arteries), abnormally formed blood vessels or an aneurysm is present.

• MRAs are relatively safe and easy to perform, and they cost less than some other tests.

People with pacemakers or certain metal implants cannot have an MRA done. Pregnant

women should not have an MRA done.

• The pictures of the carotid arteries that are produced by an MRA are not as clear as those

produced using carotid arteriography.

• MRA is no more sensitive than carotid ultrasonography/duplex scanning, but it is more

expensive.

• MRAs do not produce clear pictures when the blood flow through the vessel is very rapid

or when the vessel has severe narrowing.

• Holes (ulcerations) within plaque may not always be seen with an MRA.

Echocardiography

Echocardiography (ECHO) is a sophisticated type of blood flow test that uses high-pitched

sound waves to produce an image of the heart. The sound waves are sent through a device called

a transducer and are reflected off the various structures of the heart. These echoes are converted

into pictures of the heart that can be viewed on a monitor similar to a TV screen. An

echocardiogram is used to evaluate how well the heart chambers fill with blood and pump blood
to the rest of the body. ECHO can also be used to estimate the amount of blood pumped out of

the left ventricle with each heartbeat (called the ejection fraction).

An ECHO can help evaluate heart size and heart valve function, identifying areas of poor blood

flow in the heart, areas of heart muscle that are not contracting normally, previous injury to the

heart muscle caused by impaired blood flow or evidence of congestive heart failure, especially in

people with chest pain or a possible heart attack. In addition, ECHO can identify some heart

defects that have been present since birth (congenital heart defects).

There are several different types of echocardiograms:

• Transthoracic echocardiogram (TTE). This is the standard, most commonly used method

of echocardiography. Views of the heart are created by moving the transducer to different

places on the chest or abdomen wall.

• Transesophageal echocardiogram (TEE). This is a special type of test in which the

instrument that emits sound waves (transducer) is passed down the esophagus instead of

being moved over the outside of the chest wall. A TEE may show clearer pictures of the

heart because the transducer is located closer to the heart and the lungs and bones of the

chest wall do not block the sound waves. A TEE requires a sedative and anesthetic

applied to the throat to ease discomfort.

Other Tests
Another diagnostic test is the lumbar puncture (spinal tap), in which a needle is inserted into the

spinal canal to collect samples of the clear, fluid that surrounds the brain and spinal cord. The

pressure of this fluid is measured, and the samples are analyzed for color, blood cell counts,

protein, glucose and other substances. Some of the fluid may be placed under conditions that

promote the growth of infectious organisms (cultured), such as bacteria or fungi, to check for

infection.

Source: Cedars-Sinai, 2011, Diagnostic Testing, http://www.cedars-sinai.edu/Patients/Programs-

and-Services/Stroke-Program/Stroke-Resources/Diagnostic-Testing.aspx

Duplex scanners

Duplex scanners display real-time grey-scale images which allow the operator to display the

speed of blood flowing in a selected part of the image. Figure 5 shows a duplex scan of a

superficial femoral artery in the upper thigh.

The operator has placed a 'gate' in the image of the artery, and the blood velocity waveform is

displayed. In the common and superficial femoral arteries, the waveform normally has a forward

component followed by a reverse component and a second smaller forward component. This is

called a triphasic waveform because of the three phases. More distally in the superficial femoral

artery, the second forward component may be absent, giving a biphasic waveform with two

phases.
The duplex scanner detects the moving blood by using the Doppler effect. Ultrasonic echoes

returning to the probe from stationary structures come back with the same frequency. However,

if the target is moving towards or away from the probe, the echoes return with a higher or lower

frequency. The scanner detects any change in frequency, and can calculate the actual speed of

the target provided the angle between the direction of the ultrasonic beam and the direction of

movement is known. The operator therefore aligns a marker along the direction of flow in the

blood vessel and positions a cursor at the height of the peak systolic blood velocity. The scanner

then calculates the speed of the blood (Figure 5).

The frequency shift caused by the Doppler effect depends on the frequency of the transmitted

ultrasound and the speed of the blood. It happens that the frequency shift is normally in the audio

range, so most duplex scanners send the signal to a pair of audio speakers, and this enables the

operator to hear the signal in addition to seeing the display.

Colour Doppler scanners

Colour Doppler scanners detect and display moving structures by superimposing colour onto the

grey-scale image. The operator positions a box on the image, and colour is superimposed

wherever the scanner detects a moving structure, usually blood. Figure 6 shows a colour Doppler

image of the popliteal artery behind the knee. The colour fills the lumen of the vessel, showing

that the blood is moving right up to the vessel wall.The hue of the colour shows the direction and

magnitude of the blood velocity. In this image, red and yellow indicate flow away from the

probe, with dark red representing low velocities and orange and yellow indicating higher

velocities. Flow towards the probe is indicated in blue and green, with green indicating higher

velocities. The hue can therefore be used to identify sites where the artery becomes narrower and
the blood has to move faster to achieve the same volume flow rate. When the blood velocity

exceeds the limit of the colour scale, aliasing occurs. The equipment interprets high velocity in

one direction as lower velocity in the other direction, and there is a sudden transition from

yellow to green or vice versa (Figure 4). This can be useful for identifying the raised velocities

associated with significant narrowing of the arteries.

Colour Doppler can also be used to display venous blood flow. The blood moves more slowly in

the veins so different settings are used. Most scanners come with a menu of recommended

settings for different applications, including peripheral arterial and peripheral venous studies.

Source: (N.A.)(N.D.)Retrieved from http://www.worldwidewounds.com/2000/sept/Michael-

Lunt/Doppler-Imaging.html

Carotid doppler ultrasound is a non-invasive test that uses sound waves to measure the flow of

blood through the large carotid arteries that supply blood to the brain. These arteries can become

narrowed due to arteriosclerosis or other causes, and this can lead to transient ischemic attack

(mini-stroke) or cerebral vascular accident (stroke). The carotid doppler test can help doctors

determine stroke risk and the need for preventive measures.

Why Do I Need To Have a Carotid Doppler Test?:

A carotid doppler test may be performed if you have had a stroke, or, if based on your doctor's

evaluation, you are considered to be at increased risk of having a stroke due to decreased blood

flow in the carotid arteries.


What Preparations Are Necessary For Carotid Doppler Test?:

This is a non-invasive procedure, and no special preparations are necessary.

How is a Carotid Doppler Test Performed?:

The ultrasound technician will apply a jelly-like substance to both sides of your neck, where the

carotid arteries are located. This helps lubricate the skin and allow the ultrasound sensor to move

more freely. The sensor is moved back and forth over the neck and generates sound waves that

bounce off the arteries. The echo that bounces back is measured, and the changes in frequency

can measure the flow of blood. The flow will be different in areas that are narrowed.

What Can I Expect After I Have After a Carotid Doppler Test?:

This test takes an average of 15 to 30 minutes for most people, though it can vary. Once the test

is completed, you will be free to resume normal activities with no restrictions.

When Will the Results of a Carotid Doppler Test Be Ready?:

The completed test is recorded on a videotape by the ultrasound technician. The tape is reviewed

by a diagnostic radiologist who measures the blood flow and determines the amount and location

of any narrowing of the carotid arteries. The radiologist will send a report to your doctor. The

results should be available within a few days at most.

What are the Next Steps After Carotid Doppler Test?:

Your doctor will review the written report provided by the radiologist. Further treatment

recommendations will be based on the results of this test along with other factors as determined

by your individual condition. One procedure that may be recommended is acarotid

endarterectomy. This surgical procedure is done to open up constricted arteries and increase

blood flow to the brain. There are other treatments that may also be recommended.
Source: (N.A.)(N.D.)Retrieved from

http://seniorhealth.about.com/od/stroke/p/carotid_doppler.htm

TREATMENT

If the neurologic deficit progresses over the following minutes or hours, heparinization

may be of value in limiting or arresting further deterioration. Since the signs of progressing

stroke may be stimulated by an intracerebral hematoma, the latter must be excluded by

immediate CT scanning or angiography before the patient is heparinized.

Early management of a complete stroke consists of attention to general supportive

measreus. During the acute stage, there may be marked brain swelling and edema, with

symptoms and signs of increasing intracranial pressure, an increasing neurologic deficit, or

herniation syndomre. Corticosteroids have been prescribed in an attempt to reduce vasogenic

cerebral edema. Prednisone (up to 100 md/d) or dexamethasone (16mg/d) has been used, but the

evidence that corticosteroids are of any benefit is conflicting. Dehydrating hyperosmolar agents

have also been prescribed in efforts to reduce brain swelling, but there is little evidence of any

lasting benefit. Likewise, clinical benefit from treatment with vasodilators such as parpavarine is

minimal. Neither hypercapnia nor hypocapnia has been shown to have any benefit. Barbiturates

are known to decrease neuronal metabolism and energy requirements and have been reported to

improve functional recovery in experimental stroke models; their use in humans, however is

experimental. Attempts to lower the blood pressure of hypertensive patients during the acute

phase has a stroke should be avoided, since there is loss of cerebral autoregulation and lowering

the blood pressure may further compromise ischemic areas.


Anticoagulant drugs have no role in the management of patients with a completed stroke,

except when there is cardiac stroke, except when there is cardiac source of embolization.

Treatment is then started with intravenous heparin while warfarin is introduced. The target is an

international normalized ratio of 3:4 for the prothrombin time. If the CT scan shows no evidence

of hemorrhage and the cerebrospinal fluid is clear, anticoagulant treatment may be started

without delay. Some physicians prefer to wait for 2 to 3 days before intiating anticoagulant

treatment; the CT scan is then repeated and anticoagulant therapy is initiated if it again shows no

evidence of hemorrhagic transformation.

Thrombolytic therapy by administration of tissue plasminogen activator within 3 hours

after onset (often difficult to determine) of stroke improves clinical outcome. Preliminary studies

suggest that calcium channel blocking drugs such as nimopidine (30mg orally every 6 hours for

four weeks) reduce deficit produced by cerebral ischemia and the morbidity and mortality rates

from stroke. Multicenter studies are now in progress to study further the effects of these agents in

acute cerebral ischemia.

Blockage of glutamate, an excitatory neurotransmitter, reduces sensitivity of central

neurons to ischemia. The N-methyl-D-aspartate (NMDA) type of glutamate receptors is linked to

calcium permeable channels, and studies in animals have shown that specific NMDA-receptor

antagonists reduce stroke size, deficits, and the percentage of severely ischemic neurons. The

role of this therapeutic approach in humans is currently under study.

Physical therapy has an important role in the management of patients with impaired

motor function. Passive movements at an early stage will help prevent contractures. As

cooperation increases and some recovery begins, active movements will improve strength and

coordination. In all cases, early mobilization and active rehabilitation are important.
Occupational therapy may improve morale and motor skills, while speech therapy may be

beneficial in patients with expressive dysphagia or dysarthia. When there is severe and persisting

motor deficit, a device such as a leg brace, toe spring, frame or cane may help the patient move

about, and the provision of other aids to daily living may improve the quality of life.

Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis &

treatment (45th ed.). New York: Lange Medical Books/Mcgraw-Hill.

Recent Studies

S ã rk ã m ö et al investigated whether listening daily to music or speech can improve

auditory sensory memory in patients who have suffered neural damage. Fifty-four patients in the

acute recovery phase following MCA stroke were divided into a music group, an audio book

group, and a control group. In order to index the patients' auditory sensory memory, magnetic

mismatch negativity (MMNm) responses to variations in the frequency and duration of sound

were measured over a 6-month follow-up period, using whole-head magnetoencephalography.

The authors found a significant increase in the frequency MMNm amplitude in the music

and audio book patients over that of the controls. Moreover, the audio book group showed a

greater increase in the duration MMNm amplitude than did the other 2 groups. Sarkamo et al

also found a correlation in the music group between frequency MMNm amplitude changes and

improvements in verbal memory and focused attention. The authors concluded that following

neural damage, patients can undergo long-term plastic changes in early sensory processing by

listening to music and speech. They suggested that such changes may help to restore higher

cognitive functions in these patients.


Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from

http://emedicine.medscape.com/article/323120-overview

Frequency of Middle Cerbral Artery Stroke

UNITED STATES

The frequency of middle cerebral artery stroke (MCA stroke) is reported to be more than

80 cases per 100,000 people. According to Barnett and colleagues, most strokes occur in the

MCA territory of cerebral circulation.2

INTERNATIONAL

A systematic review of stroke incidence worldwide found that between 1970 and 2008,

stroke incidence decreased 42% in high-income countries and increased more than 100% in low-

to middle-income nations; between 2000 and 2008, the overall stroke incidence in low- to

middle-income countries was 20% higher than that in high-income countries. 3 This review did

not distinguish between middle cerebral artery strokes and other CVAs.

MORTALITY/MORBIDITY

A significant number of patients (15-30%) die from acute stroke within the first 30 days

after the event. Survival after hemorrhagic stroke is less common, with only a 20% survival rate.

Death in the first week after stroke is directly due to the stroke in 90% of cases. Pulmonary

embolism is the most common cause of death within 2-4 weeks of stroke. Pneumonia is the most

common cause of mortality within 2-3 months after the event. Thereafter, cardiac disease is the

most common cause of death.


RACE

Ethnic minorities, specifically African and Mexican Americans, are at a significantly

higher risk for ischemic stroke. One study revealed the total prevalence to be 191 strokes per

100,000 people surveyed in the black population, 149 strokes per 100,000 people surveyed in the

Hispanic population, and 88 strokes per 100,000 people surveyed in the white population.

SEX

Males are affected by middle cerebral artery strokes more often than are females, with a male-to-

female ratio of 3:1.

AGE

Risk of middle cerebral artery stroke (MCA stroke) increases with age. The highest incidence of

MCA strokes is in the seventh and eighth decades of life. Stroke in younger persons (aged 18-45

y) is far less common than in elderly persons. Hemorrhagic stroke is the most common etiology,

with intracranial hemorrhage accounting for 41% and subarachnoid hemorrhage accounting for

17% of strokes in persons in the younger age group. Studies reveal that dissection is an

underrecognized cause of stroke in younger populations. Still, even with advances in diagnostic

options, 20% of strokes in younger persons continue to be of unknown etiology.

RISK FACTORS OF ISCHEMIC INFARCT book based

HYPERTENSION

When the ventricles contract, they force blood into large, thick-walled elastic arteries that

expand as the blood is pushed into them. The high pressure in these arteries forces blood to

continually move into areas where the pressure is lower. The pressure is highest in the large
arteries and continues to drop throughout the pathway, reaching zero or negative pressure at the

venae cavae.

Peripheral resistance is the amount of friction encountered by the blood as it flows

through the blood vessels. It is increased by many factors, but probably the most important is the

constriction, or narrowing of blood vessels, especially arterioles, as a result of sympathetic

nervous system activity or atherosclerosis. Increased blood volume or blood viscosity(thickness)

also raise peripheral resistance. Any factor that increases either the cardiac output or peripheral

resistance causes an almost immediate reflex rise in blood pressure. Many factors can alter blood

pressure, such as: age, weight, time of day of, exercise, body position, emotional state and

various drugs, to name a few.

Neural factors: the autonomic nervous system. The parasympathetic division of

autonomic nervous system has little or no effect on blood pressure, but sympathetic division is

important and is responsive to many different factors. The major action of sympathetic nerves on

the vascular system is to cause vasoconstriction, or narrowing of the blood vessels, which

increases blood pressure. The sympathetic center on the medulla of the brain is activated to cause

vasoconstriction in many different circumstances. When we stand up suddenly after lying down,

the effect of gravity causes the blood to pull in the vessels of the legs and feet and the blood

pressure drops. This activates pressoreceptors (called baroreceptors) in the large arteries of the

neck and chest. They send of warning signs that result in reflexive vasoconstriction, which

increases blood pressure back to homeostatic levels. When blood volume suddenly decreases, as

in hemorrhage, blood pressure drops, and the heart begins to beat more rapidly ( as it tries to
compensate). However, because venous return is reduced by blood loss. The heart also beats

weakly and inefficiently. In such cases, the sympathetic nervous system causes vasoconstriction

to increase the blood pressure so that venous return increase and circulation can continue.

Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco, Calif.:

Benjamin Cummings ;.

MANAGEMENT, DIAGNOSTICS, CLINICAL MANIFESTATIONS HPN

MANILA, Philippines—High blood pressure has been established as a major risk factor for

stroke and the unfortunate thing about it is that most hypertensive patients have no symptoms.

The statistics are grim:

• Less than half of hypertensive patients are aware that they have high blood pressure.

• Only about a quarter are taking antihypertensive medications.

• Only about 10 percent, or even less, have adequately controlled high blood pressure.

Trivialize hypertension

What is quite tragic is that many hypertensive patients are aware that they have high blood

pressure, but since they have no symptoms, they trivialize their hypertension. Sadly, many of

these potential victims of the “silent killer” see no need and no strong motivation to take their

medicines religiously to make sure that their blood pressures are controlled to optimal levels.
Not until they develop a serious stroke or a heart attack do they realize what their wanton

disregard for their hypertension has cost them. And by then, it’s too late already.

The effective strategy therefore is quite obvious. If we can only make the 90 percent with

untreated or uncontrolled hypertension aware of the risk they are unduly exposed to, we can

significantly reduce the incidence of stroke and other cardiovascular complications in our

country.

Increase awareness

Hopefully, the I-Stroke campaign, spearheaded by Dr. Joey Navarro and Otsuka, and the

“Marunong and Nagtatanong” information campaign collaborated in by the Philippine Heart

Association, Stroke Society of the Philippines, Philippine Society of Hypertension and

Therapharma, will significantly increase awareness on hypertension and stroke among Filipinos

and stem the tide of what could produce a population with many disabled stroke victims.

According to the World Health Organization, 15 million people worldwide will suffer from

stroke this year. Five million will die and another five million will be permanently disabled. In

the Philippines, stroke affects 486 out of 100,000 Filipinos or roughly half a million Filipinos,

according to Dr. Navarro in his study published in The Philippine Journal of Neurology.

However, access to specialist care may be a problem.

At risk for stroke


“There are less than 300 neurologists in the country or one for every 300,000 patients. This puts

many Filipinos at risk for stroke and its life-threatening complications,” explains Dr. Johnny

Lokin, newly elected president of the Philippine Neurological Association.

Once an individual develops signs and symptoms of stroke or brain attack, he should not delay

going to the hospital ER because time is of the essence to prevent more severe complications.

The symptoms of stroke are sudden weakness of the facial muscles, arm or leg, usually on one

side of the body.

One may also feel sudden numbness on one side of the body, confusion, difficulty in speaking or

understanding speech, blurring of vision in one or both eyes, difficulty in walking, dizziness, loss

of balance or a severe headache.

The PNA and SSP are encouraging the establishment of specialized acute stroke units in all

tertiary hospitals to make sure that stroke patients are promptly and adequately treated with

medications and interventions that can prevent more severe, irreversible damage to the brain.

Currently, there are about 16 of these acute stroke units nationwide. Hopefully, most medical

centers will have such facility which will be a big boost in treating stroke patients and preventing

its complications.

Source: Castillo, Rafael M.D.,(2007,December).Inquirer lifestyle.Stroke prevention

campaigns.Retrieved from http://showbizandstyle.inquirer.net/lifestyle/lifestyle/view/20071201-

104135/Stroke_prevention_campaigns
MYOCARDIAL INFARCTION AND ATHEROSCLEROSIS

Myocardial infarction (heart attack) is a serious result of coronary artery disease. Coronary

artery disease occurs from atherosclerosis, when arteries become narrow or hardened due to

cholesterol plaque build-up. Further narrowing may occur from thrombi (blood clots) that form

on the surfaces of plaques. Myocardial infarction occurs when a coronary artery is so severely

blocked that there is a significant reduction or break in the blood supply, causing damage or

death to a portion of the myocardium (heart muscle). Depending on the extent of the heart

muscle damage, the patient may experience significant disability or die as a result of myocardial

infarction.

In addition to atherosclerosis, myocardial infarction may result from a temporary contraction or

spasm of a coronary artery. When this occurs, the artery narrows and the blood flow from the

artery is significantly reduced or stopped. Though the cause of coronary artery spasm is still

unknown, the condition can occur in both normal blood vessels and those partially blocked by

plaques.

Source: Heart Disease- Myocardial Infarction (Heart Attack), 2011,

http://www.imaginis.com/heart-disease/heart-disease-myocardial-infarction-heart-attack-1

CORONARY ARTERY BYPASS GRAFT (CABG)

Coronary artery bypass graft surgery involves the bypass of a blockage in one or more of

the coronary arteries using the saphenous veins, mammary artery, or radial artery as conduits or
replacement vessels. Before surgery, coronary angiography precisely locates lesions and points

of narrowing within the coronary arteries.

During traditional CABG surgery, a median sternotomy incision is made so that the heart

and aorta can be seen. The client is placed on cardiopulmonary bypass (CPB) and the heart is

stopped (cardioplegia) using a solution of iced saline containing potassium. After the bypasses

have been performed, the client is taken off of the machine, and the heart takes over again. Three

different types of “less invasive” CABG surgery are also performed: (1) off-bypass CABG

performed through a median sternotomy with a smaller incision; (2) minimally invasive direct

CABG (MIDCABG) performed through a left anterior thoracotomy without cardiopulmonary

bypass; and port-access CABG with femoral-to-femoral bypass and cardioplegia with a limited

incision. Many institutions are performing MIDCABG surgery. In off-bypass CABG, the surgery

is performed on a beating heart after a reduction in cardiac motion with several different

medications and devices. The benefit of this type of CABG surgery is the avoidance of the use of

CPB because of the many potential complications of CPB.

Saphenous veins can be used as the new coronary artery. The distal end of the vein is

saturated to the aorta, and the proximal end is swen to the coronary vessel distal to the blockage.

The veins are reversed so that their valves do not interfere with blood flow. The internal

mammary artery (IMA) can also be grafted to a coronary artery. It is more routinely used to

revascularize the portion of the myocardium supplied by the left anterior descending (LAD)

artery. The disadvantage of the IMA is that more time is required to remove it and the mammary

artery is shorter. An advantage is that IMA grafts have greater chance of remaining patent.

Radial arteries have also been used in repeat CABG and when radiation therapy to the chest

makes it impossible to use the IMA. The radial artery has had excellent patency rates.
For clients who need revascularization of the anterior coronary arteries, MIDCABG is a

less invasive approach. The IMAs are used as conduits, and the client does not need to be placed

on CPB. MIDCABG surgery is less costly than traditional CABG surgery and is associated with

fewer postoperative complications. A small study comparing outcomes in CABG to minimally

invasive bypass procedures found that fewer cardiac and pulmonary complications were reported

in the minimally invasive group.

Source: Black, J., & Hawks,J.(2009).Medical Surgical Nursing:Clinical Management for

Positive Outcomes.St. Louis, Missouri: Saunders Elsevier

VALVE REPLACEMENT

When valvuloplasty is not a viable alternative (eg, when the annulus or leaflets of the

valve are immobilized by calcifications, severe fibrosis or fusion of the chordate tendinea,

papillary muscles, and leaflets below the valve), vavle replacement is performed. General

anesthesia and cardiopulmonary bypass are used for valve replacement s. Most procedures are

performed through a median sternotomy, although the mitral valve may be approached through a

right thoracotomy incision. Mitral, and more rarely aortic ,valve replacement can be performed

with minimally invasive techniques thatv do not involve cutting through the sternum.

Instead,incisions are only made in the upper or lower half part of the sternum or between ribs;

these incisions are 2 to 4 inches long. Some of these minimally invasive procedures are robot

assisted and the surgeon, watching a video display, uses a joystick to control the robot and
surgical instruments. With these procedures,patients have less bleeding,pain,risk for infection

and scarring. Hospital stays average3 days and recovery may be as short as 3 weeks.

After the valve replacement is visualized, the leaflets of the aortic or pulmonic valve are

removed, but some or all the mitral valve structures ( leaflets, chordae, and papillary muscles.)

are left in place to help maintain the shape and function of the left ventricle after the mitral valve

replacement. Sutures are placed around the annulus and then through the valve prosthesis. The

replacement valve is slid down the suture into position and tied into place. The incision is closed

and the surgeon evaluates the function of the heart and the quality of the prosthetic repair. The

patient is weaned from cardiopulmonary bypass, the surgical repair is often assessed in color

flow Doppler TEE and the surgery is completed.

Before the surgery, the heart gradually adjusts to the pathology but the surgery abruptly

“corrects” the way blood flows through the heart. Complications unique to valve replacement are

related to sudden changes in intracardiac blood pressures. All prosthetic valve replacement create

a degree of stenosis when they are implanted in the heart. Usually the stenosis is mild and does

not affect heart function. If valve replacement was for a stenotic valve blood flow through the

heart is often improved. The signs and symtoms of the backward heart failure resolve in a few

hours or days. If valve replacement was for a regurgitant valve into which blood had been

regurgitating to achieve it’s optimal postoperative function. The signs and symptoms of of heart

failure resolve gradually as the heart function improves. Patients are at risk for may

postoperative complications such as bleeding,thromboembolism,infection,heart

failure,hypertension,dysrhythmias,hemolysisa nd mechanical obstruction of the valve.


Source: Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-

surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &

Wilkins.

ATRIAL FIBRILLATION

Atrial fibrillation (A Fib) is the most common supraventricular dysrythmias encountered in the

emergency department affecting 1% to 2% of the general population, especially older adults.

Atriall fibrillation is characterized by rapid chaotic atrial depolarization from reentrant pathway.

Ectopic atrial foci produce impulses between 350 and 600 beats/min. at extremely rapid rates,

however, the entire atrium may not be able to recover from one depolarization wave before next

begins, resulting in mechanical and electrical disorganization of the atria without effective atrial

contraction. Small irregular baseline undulations that vary in the size and shape, called f waves,

are identified which differ from the formed “saw-toothed” waves atrial flutter. Similar to atrial

flutter, the AV node is bombarded with more impulses than it can conduct so a rapid ventricular

response comparable to the atrial rate cannot occur. Most if these impulses are blocked; however,

as a result of the erratic atrial impulses, the ventricular rhythm is very irregular. The ventricular

rante ranges from 100 to 180 beats/min.

Examination of the ECG reveals erratic unidentifiable P waves and underlying ventricular

rhythm that reveals to be irregular. Because of atrial disorganization “atrial kick” is lost, thereby

decreasing cardiac outputby as much as 30%. With increasing ventricular rates allowing less

filling time, cardiac output declines even further and may result in dyspnea, angina pectoris,

heart failure and shock. The clinet may have a pulse deficit between apical and radical pulses.
Atrial fibrillation most commonly occurs because of the following:

Coronary artery disease, congestive heart failure, valvular heart disease (particularly mitral and

aortic), sick sinus syndrome, advanced age, longstanding hypertension, pericarditis

During atrial fibrillation, blood pools in the ‘quivering” atria because of lack of adequate

contraction of atrial appendages. Pooling blood is prone to clot, forming a mural thrombus, ,

which increases the risk of cerebral and peripheral vascular emboli. Most clients with sudden

onset of atrial fibrillation are given anticoagulant to reduce risk of thrombus formation and

embolic events. Approximately 20% to 25% OF CEREBRAL vascular accidents are due to

cardiogenic emboli.

Source: Black, J., & Hawks,J.(2009).Medical Surgical Nursing:Clinical Management for

Positive Outcomes.St. Louis, Missouri: Saunders Elsevier

DIABETES MELLITUS TYPE II

Type 2 diabetes affects approximately 90% to 95% of people with the disease. It occurs

commonly among people who are older than 30 years of age and obese and Kidney Diseases,

although its incidence is rapidly increasing in younger people because of the growing epidemic

of obesity in children, adolescents, and young adults. The two main problems related to insulin in

type 2 diabetes are insulin resistance and impaired insulin secretion. Insulin resistance refers to a

decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell

surfaces and initiates a series of reaction involved in glucose metabolism. In type 2 diabetes,

these intracellular reactions are diminished, making insulin less effective at stimulating glucose

uptake by the tissues and at regulating glucose release by the liver. The exact mechanism that
lead to insulin resistance and impaired insulin secretion in type 2 diabetes are unknown, although

genetic factors are thought to play a role.

To overcome insulin resistance and to prevent the buildup of glucose in the blood,

incease amounts of insulin must be secreted to maintain the glucose level at a normal or slightly

elevated level. This is called metabolic syndrome, which includes hypertension,

hypercholesterolemia, and abdominal obesity. However of the beta cells cannot keep up with the

increased demand for insulin, the glucose level rises and type 2 diabetes develops.

Despite the impaired insulin secretion that is characteristic to type 2 diabetes, there is enough

insulin present to prevent the breakdown of fat and the accompanying production of ketone

bodies. Therefore, DKA does not typically occur in type 2 diabetes. However, uncontrolled type

2 diabetes may lead to another acute problem—hyperglycemic hyperosmolar nonketonic

syndrome. Because type 2 diabetes associated with a slow, progressive glucose intolerance, its

onset may go undetected for many years. If the patient experiences symptoms, they are

frequently mild and may include fatigue, irritability, polyuria, polydipsia, poorly healing skin

wounds, vaginal infections, or blurred vision.

For most patient (approximately 75%), type 2 diabetes is detected incidentally (eg, when routine

laboratory tests ophthalmoscopic examinations are performed). One consequence of undetected

diabetes is that long-term diabetes complications (eg, eye disease, peripheral neuropathy,

peripheral vascular disease) may have developed before the actual diagnosis of diabetes is made,

signifying that the blood glucose has been elevated for a time before diagnosis.
Source: Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-

surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &

Wilkins.
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 of glucose becoming progressively less efficient when

responding to further glucose elevations. This phenomenon, termed desensitization, is reversible

by normalizing glucose levels. The ratio of proinsulin (a precursor to insulin) to insulin secreted

also increases.

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

biologic activity of insulin in both the liver and peripheral tissues. The state is known as insulin

resistance, People with type 2 diabetes mellitus have a decreased sensitivity to glucose which

results in continued hepatic glucose production even with high blood 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: (1) decreased glucose utilization, (2) increased fat mobilization, and (3)

increased protein utilization

Decreased Glucose Utilization


Cells that require insulin as a carrier for glucose can take only about 25% of the glucose they

require for fuel. Nerve tissues, erythrocytes, and the cells of the intestines, liver, and kidney

tubules do not require insulin for glucose transport. However, adipose tissues, along with skeletal

and cardiac muscle requires insulin for glucose transport. Without adequate amounts of insulin,

much if the ingested glucose cannot be used.

With inadequate amounts of insulin, blood glucose levels rise. The 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 kidney excretes the excess glucose.

Glucose appears in the urine (glycosuria), acts as an osmotic diuretic and causes excretion of

increased amounts of water, resulting in fluid volume deficit.

Increased Fat Mobilization

In type 1 diabetes mellitus and occasionally with severe stress in type 2 diabetes mellitus, the

body turs to fat stores for energy production when glucose is unavailable. Fat metabolism causes

breakdown in products called ketones to form. Ketones accumulate in the blood and are excreted

through the kidneys and lungs. Ketone levels can be measured in the blood and urine; high levels

can indicate uncontrolled diabetes mellitus

Ketones interfere with the body’s acid-base balance by producing hydrogen ions. The pH

can decrease, and metabolic acidosis can develop. In addition, when ketones are excreted,

sodium is also eliminated, sodium is also eliminated, resulting in sodium depletion and further

acidosis. The excretion of ketones also increases osmotic pressure, leading to increase fluid loss.

Also, when fats are the primary source of energy, body lipid levels can increase to five times

normaly, leading to increased atherosclerosis.


Increased Protein Utilization

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

down and rebuilt. In people with type 1 diabetes mellitus, without insulin to stimulate protein

synthesis, the balance is altered, which leads to increased catabolism (destruction). Amino acids

are converted to glucose in the liver, further elevating glucose levels. If this condition goes

untreated, clients with type 1 diabetes mellitus appear emaciated. The pathophysilogic processes

of diabetes mellitus continue, leading to may acute and chronic complications.

Clinical Manefistations

An elevated blood glucose level, called hyperglycemia, leads to common clinical manifestations

associated with diabetes mellitus. In type 1 diabetes mellitus, the onset of clinical manifestations

may be subtle with the possibility of life-threatening situations likely to happen (i.e., diabetic

ketoacidosis). In type 2 diabetes mellitus, the onset of clinical manifestations may develop so

gradually that clients may notice few or no clinical manifestations for a number of years.

The clinical manifestations of diabetes mellitus are increased frequency of urination

(polyuria), increased thirst or fluid intake (polydipsia), and, as the disease progresses, weight loss

despite hunger and increased food intake (polyphagia).

Diagnosis of Diabetes mellitus

Physical examination, medical history, and laboratory tests are employed to evaluate clients with

diabetes mellitus. Clinical manifestations suggest the presence of diabetes mellitus, but

laboratory tests are needed to make a definitive diagnosis.


Fasting Blood Glucose Level

A fasting blood glucose sample is drawn when the client has not ingested any nutrients other that

water for at least 8 hours. This blood sample generally reflects glucose level from hepatic

production. If the client is receiving a dextrose intravenous solution, results of the test must be

analyzed with that variable in the mind. In clients who are known to have diabetes mellitus, food

and insulin are withheld until after the specimen is obtained. The diagnosis of diabetes mellitus is

made when a client’s fasting blood glucose level is greater than 126 mg/dl. Values between 110

and 125mg/dl indicate an IFG. The fasting blood glucose measurement provides the best

indication of overall glucose homeostasis and is preferred method of diagnosing diabetes

mellitus.

Casual Blood Glucose Level

Clients may also be diagnoses with diabetes mellitus based on clinical manifestations and a

casual (random) blood glucose level greater than 200mg/dl. A casual blood glucose sample can

be drawn any time of the day without regard to fasting. Elevated blood glucose levels may occur

after meals, after stressful events, in sample drawn from an IV site, or in cases of diabetes

mellitus.

Postload Blood Glucose Level

A postload or postprandial (after a meal) glucose level can also be drawn and used to diagnose

diabetes mellitus. Postload blood glucose samples are drawn every 2 hours after a standard meal

and reflect the efficiency of insulin-mediated glucose uptake by peripheral tissues. Normally,
blood glucose level should return to fasting levels within 2 hours. A 2-hour postload glucose

level greater than 200mg/dl during oral glucose tolerance test (OGTT) is confirmation for a

diagnosis of diabetes mellitus.

In older adults, postload levels are higher, typically increasing by 5 to 10 mg/dl decade

after age 50 years because of the normal decline in glucose tolerance associated with aging.

Smoking and drinking coffee can lead to falsely elevated values at 2 hours, whereas strenuous

exercise can lead to falsely decreased values.

Laboratory Tests related to Diabetes Mellitus

Glycosylated Hemoglobin Level

Glucose normally attaches itself to the haemoglobin molecule on a red blood cell. Once

attatched, it cannot dissociate. Therefore the higher the blood glucose levels, the higher the levels

of glycosylated haemoglobin (HbA1c). The term HbA1c is referred to as an A1C. The A1C is an

average blood glucose level measured over the previous 3 months. It is stated as a percentage

and is useful in evaluating long-term glycemic control. To avoid diabetes-related complications,

The ADA recommended keeping A1C level below 7%.

The ADA recommends that A1C testing be done routinely on all people with diabetes

mellitus. The A1C test should be done semiannually in client’s who have met the primary target

goal for glycemic control (<7%) and quarterly in clients who have not met the primary glucose

for goal for glycemic control. Conditions that increases erythrocyte turnover, such as bleeding,
pregnancy, or asplenia (absence of spleen as after splenectomy), lead to falsely low A1C

concentrations. High aspirin does, alcohol ingestion, uremia, elevated haemoglobin levels, and

heparin therapy can cause falsely elevated A1C levels.

Glycosylated Albumin Level

Glucose also attaches to proteins, primarily albumin. The concentration of glycosylated albumin

(fructosamine) represents the average blood glucose level over the previous 7 to 10 days. This

measurement is useful when short-term determinations of average blood glucose level are

desired. The reliability and clinical capability continue to be evaluated

Connecting Peptide (C-Peptide) Level

When the proinsulin produced by pancreatic beta-cells is broken apart by an enzyme, two

products are formed, insulin and connecting peptide, commonly called C-Peptide. Because C-

peptide and insulin are formed in equal amounts, this test indicates the amount of endogenous

insulin production. Clients with type 1 diabetes mellitus usually have no or low concentration of

C-peptide. Clients with type 2 diabetes mellitus tend to have normal or elevated levels of C-

peptide.

Ketonuria

Urine levels of ketones can be tested by clients’ use of dip-strips or tablets. The presence of

ketones in the urine (a condition called ketonuria) indicates that the body is using fat as a major
source of energy, which may result in ketoacidosis. Test results are indicated by the presence of

color changes, indicating the presence of ketones.

All clients with diabetes mellitus should test their urine for ketones during acute illness or stress,

when blood glucose levels are elevated (>240mg/dl), and when they are pregnant or have

evidence of ketoacidoses (e.g. nausea, vomiting, or abdominal pain).

Some testing strips detect ketones as well as glucose. Although urine testing is important for

checking ketones, urine testing for glucose is not a reliable method for monitoring.

Proteinuria

Microalbuminuria measures microscopic amounts of protein in the urine (proteinuria). The

presence of protein (microalbuminuria) in the urine is an early manifestation of the kidney

disease. Testing the urine for microalbuminuria shows early neurophaty, long before it would be

evidenton routine urinalysis. The ADA recommends that all clients with diabetes mellitus be

tested for microalbuminuria annually. Some clients, however, require more frequent testing to

detect progression of kidney disease related to adverse effects of certain medications on the

kidneys.

Self-Monitoring Blood Glucose

They key to managing diabetes mellitus to keep the blood glucose level as close to normal as

possible or within a target range that is agreed upon between the client and healthcare provider.

Self-monitoring blood glucose (SMBG) provides immediate feedback and data on blood glucose

levels. SMBG is recommended for all clients with diabetes mellitus, regardless whether they are
type 1, type 2, or gestational diabetes. SMBG is a way to know how the body responds to food,

insulin, activity and stress.

The frequency and timing of SMBG depend on the needs and goals of each individual client. For

most clients with type 1 diabetes mellitus and pregnant women taking insulin, SMBG is

recommended three or more times daily. Testing should be done before each meal, before

bedtime, and possibly in the middle of the night. For clients with type 2 diabetes mellitus, the

frequency and timing of SMBG are mutually agreed upon by the client and health care provider.

If the client with type 2 diabetes are taking oral medications, they usually do not have to monitor

as often as someone with type 2 diabetes mellitus taking insulin. Extra times to SMBG level

should include the following:

• When starting a new drug (oral agent) or insulin

• When starting an over-the-counter medication that affects the blood glucose levels (e.g.

steroid)

• When you are under a lot of stress/ sick

• When you think your glucose level is too high or too low

• When you lose or gain weight

• When there is a change in your medication dose, eating plan, or physical activity.

Health promotion action for type 2 diabetes mellitus include the following:

• Following eating habits


• Avoiding foods high in refined sugars and saturated fats

• Maintaining ideal body weight, starting in childhood

• Exercising regularly

• Returning to pre-pregnancy weight or ideal body weight post partum

Health maintenance activities involve the following:

• Screening high risk individuals (i.e., people with family history of diabetes mellitus in the

first or second generation; members of certain racial or ethnic backgrounds [African

American, Native American, Mexican American, Asians/Pacific Islanders]; people older

than age 45 with any other risk factors, people with hypertension or hyperlipidemia;

clients with previous impaired flucose tolerance, women with previous gestational

diabetes mellitus or those who have had a baby weighing more than 9 pounds , and

people with a history of recurrent infection, habitual physical inactivity, or polycysytic

ovary syndrome) by measuring a fasting blood glucose level.

• Performing periodic assessments to determining client’s learning needs and to assess

glycemic control.

• Using strategies shown to reduce complications of diabetes mellitus by removing or

treating coexisting risk factors such as smoking, hypertension, hyperlipidemia, and use of

nephrotoxic drugs.

• Performing daily foot care


• Preventing hypoglycemia or hyperglycemia by closely monitoring blood glucose levels

and taking early action

Health restoration actions include the following:

• Teach meal planning and physical activity programs to reduce obesity

• Prompt treatment of foot abrasions or infections

• Follow-up visits to assess for complications of diabetes mellitus and reinforce learning

needs

• Yearly funduscopic examinations by an ophthalmologist with treatment as needed.

• Treatment of previously described risk factors

• Control of angina and peripheral vascular disease.

Black, J., & Hawks,J.(2009).Medical Surgical Nursing:Clinical Management for Positive

Outcomes.St. Louis, Missouri: Saunders Elsevier

COMPLICATIONS OF DIABETES MELLITUS.

Progressive diabetic nephropathy - consists of proteinuria of varying severity occasionally

leading to nephritic syndrome with hypoalbuminuria, edema, and an increase in circulating

betalipoproteins as well as progressive azotemia. In contrast to all other renal disorders, the

proteinuria associated with diabetic nephropathy does not diminish with progressive renal failure
(patients continue to excrete 10-11 g daily as creatinine clearance diminishes). As renal failure

progresses, there is an elevation in the renal threshold at which glycosuria happens.

Hypertension develops wit progressive renal involvement, and coronary and cerebral

artherosclerosis seems to be accelerated. Approximately two-thirds of adult patients with diabetis

have hypertension. Once diabetic nephropathy has progressed to the stage of hypertension,

proteinuria, or early renal failure, glycemic control is not beneficial in influencing it course. In

this circumstance, antihypertensive medications including ACE inhibitors, and restriction of

dietary protein to 0.6 g/kg body weight per day are recommended. ACE inhibitors have been

shown to protect against deterioration in renal function in IDDM patients with clinical

nephropathy. This beneficial effect appears to be due to improved glomerular hemodynamics

that cannot be explained only by the antihypertensive action of these drugs. One long term study

using captopril (25 mg three times daily) showed a 50% reduction in the risk of the combined

end points of death, dialysis and transplantation in IDDM subjects with diabetic nephropathy and

clinical proteinuria. During initiation of ACE inhibitor therapy, the rare occurrence of persistent

hyperkalemia (above 6 meq/L) is an indication to stop this medication.

When the serum creatinine reachers 3mg/dL, consultation with a nepgrologist or a

diabetologist experienced in the treatment of diabetic nephropathy is recommended. When the

serum createnine reaches 5 mg/dL, consultation with personnel at a center where renal

transplantation is performed is indicated.

Dialysis has been of limited value in the treatment of renal failure due to diabetic

nephropathy. At present, experience in renal transplantation – especially from related donors-is

more promising and is the treatment of choice in cases where there are no contraindications such

as severe cardiovascular disease.


Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis &

treatment (45th ed.). New York: Lange Medical Books/Mcgraw-Hill.

• Stroke

Stroke is a term used to describe neurologic changes caused by an interruption in the

blood supply to a part of the brain. Ischemic stroke is caused by a thrombotic or embolic

blockage of blood flow to the brain. Bleeding into the brain tissue or the subarachnoid space

causes a hemorrhagic stroke. Ischemic strokes account for about 83% of all strokes. The

remaining 17% of strokes are hemorrhagic. Cerebrovascular disorders are the third leading cause

of death in the United States and account for about 150,000 mortalities annually. An estimated

550,000 people experience a stroke each year. When second strokes are considered in the

estimates, the incidence increases to 700,000 per year in the United States alone. Stroke is a

leading cause of adult disability and a leading primary diagnosis in long-term care. More than 4

million stroke survivors are living with varying degrees of disability in the Unites States. Along

with a high death rate, strokes produce significant morbidity in people who survive them. Of

stroke survivors, 31% require assistance with self-care, 20% require assistance with ambulation,

71% have some impairment in vocational ability up to 7 years following the stroke, and 16% are

institutionalized.

Etiology and Risk Factors

Blood flow to the brain can be decreased in several ways. Ischemia occurs when the

blood supply to a part of the brain is interrupted or totally occluded. Ultimate survival or

ischemic brain tissue depends on the length of time it is deprived plus the degree of altered brain
metabolism. Ischemia is commonly due to thrombosis or embolism. Thrombotic strokes are more

common than embolic strokes.

Risk factors:

The incidence of stroke and stroke mortalities has gradually declined in many

industrialized countries in recent years as a result of an increased recognition and treatment of

risk factors. Modifiable risk factors can be reduced or eliminated through lifestyle changes.

Hypertension is the most important modifiable risk factors for both ischemic and hemorrhagic

stroke. Adequate blood pressure control is associated with a 38% reduction in stroke incidence.

Cardiovascular disease and atrial defibrillation are also associated with an increased risk

of stroke. Diabetes Mellitus increases the risk of stroke and morbidity and mortality after stroke.

• Diabetes Mellitus

There are 18.2 million people in the United States who have diabetes mellitus (DM). The

prevalence of this medical disorder increases with age. Half of all cases occur in people over the

age of 55, and it is estimated that 18% of the United States population over the age of 60 have

DM.Patients with DM are more prone to develop vascular diseases, including strokes. In addition

to being a deadly disorder in diabetics, stroke is a disabling disorder. Most stroke survivors are

left with some physical and/or cognitive deficits. Stroke is the leading cause of permanent

disability in the United States and it is the second leading cause of cognitive decline. Thus

healthcare providers who care for patients with DM should be knowledgeable about the

interrelationship between DM and stroke, as well as interventions that can minimize their

patients’ risk of primary and secondary stroke. In this article we will discuss epidemiologic
relationships between DM and stroke, effects of DM on outcome from stroke, and stroke

prevention strategies for the diabetic patient.

Epidemiology of diabetes mellitus and stroke

In adults with stroke, DM is often present as a co-morbid condition. Prospective, community

based epidemiologic studies conducted in the United States and Europe suggest that

approximately one fifth of stroke patients have DM.

An initial diagnosis of DM is often made at the time of acute hospitalization for stroke. For

example, in the Copenhagen Stroke Study, 75% of the diabetics had known DM prior to their

stroke, whereas DM was diagnosed in the remaining 25% of patients during hospitalization for

their stroke.

A risk factor is an antecedent condition that is considered to be a component of a disease

pathway. Risk factors may, or may not, be related to the etiology of the disease. Case control

studies of stroke patients and prospective epidemiologic studies have confirmed an independent

effect of diabetes on ischemic stroke in both men and women, with an increased relative risk in

diabetics ranging from 1.8 to nearly 6-fold.

Since diabetics have an increased susceptibility to developing atherosclerosis, it is very likely

that DM is a risk factor that plays an essential role in producing the vascular pathology

underlying ischemic stroke. Since diabetics have an increased susceptibility to developing

atherosclerosis, it is very likely that DM is a risk factor that plays an essential role in producing

the vascular pathology underlying ischemic stroke. Other established independent risk factors for

ischemic stroke include cigarette smoking, chronic hypertension, hyperlipidemia, and atrial

fibrillation. A substantial number of strokes are attributable to these risk factors. The population-
attributable risk is an estimate of the percentage of excess stroke in a population that is

attributable to a given risk factor. The population-attributable risk takes into account both the

prevalence and potency of a risk factor. In the United States chronic hypertension has the highest

population-attributable risk, estimated to be associated with 50 % of all strokes. DM is estimated

to have a population-attributable risk of approximately 35%. This figure for DM is greater than

the estimates of the population-attributable risk for cigarette smoking (12.3%) and atrial

fibrillation (9.4%). Intracerebral hemorrhage (ICH) accounts for approximately 15% of strokes

in the United States. Most casecontrol studies examining the relationship between DM and ICH

have not concluded that DM is an independent risk factor for ICH. A cohort study, however,

conducted on over 20,000 middle-aged male cigarette smokers found that the presence of DM

marginally increased the risk of ICH.

A meta-analysis that combined this cohort study with 9 case-control studies suggested that DM

is a risk factor for ICH (RR=1.30; 95% CI, 1.02 to 1.67) DM is not, however, as potent a risk

factor for ICH as chronic hypertension since epidemiologic studies have consistently shown a

stronger association between chronic hypertension and ICH.

Subarachnoid hemorrhage (SAH) is usually due to rupture of an intracranial aneurysm. SAH

accounts for 5% of strokes in the western hemisphere. DM has not been found to be

independently associated with aneurysmal SAH in epidemiologic studies.

DM independently associated with some subtypes of ischemic stroke.

The cerebrovascular system is comprised of large and small caliber arteries. The components of

the large arterial circulation are the extracranial and intracranial segments of the carotid and

vertebral arteries, and the other arteries that comprise the Circle of Willis (basilar artery, middle
cerebral arteries, anterior cerebral arteries, and the posterior cerebral arteries). Infarction

occurring in the distribution of these arteries is usually of thrombo-embolic origin. Small caliber

arteries comprise the microcirculation. These arteries are 100µm-400µm in diameter and they

supply blood to the white matter of the cerebral and cerebellar hemispheres, the thalami, the

basal ganglia, and brainstem parenchyma. Occlusion of a small artery is thought to be produced

by degenerative arterial pathology within the vessel wall. These arteriopathies include

microatheromas, lipohyalinosis, and fibrinoid necrosis. A brain infarction produced by an

occluded small artery is commonly called a lacunar infarction. DM has been independently

associated with two forms of large artery disease and with small artery infarctions detected by

neuroimaging studies. Diabetes accelerates the development of carotid artery atherosclerosis. In

a population-based cohort study of 1192 men and women examined at a 5-year interval,

progression of intima-media thickness on ultrasound studies of the common carotid artery (CCA)

and internal carotid artery (ICA) was approximately twice the rate in diabetics compared with

non-diabetics. Progression rate in the ICA was greater in patients with undiagnosed diabetes

compared to patients with diagnosed diabetes.

Intracranial large artery atherosclerotic disease produces stenotic lesions within the

arteries that comprise the Circle of Willis. This arteriopathy is responsible for approximately

10% of all ischemic strokes. DM was found to be an independent risk factor for intracranial large

vessel occlusive disease in a hospital-based study of 166 patients with a first ischemic stroke or

TIA due to a stenotic intracranial artery.

In addition, the diabetic patients were more likely than non-diabetic patients to have had

a larger number of diseased vessels than non-diabetics. The greatest extent of intracranial large

vessel occlusive disease was seen in diabetics with high lipoprotein (a) levels, suggesting a
synergistic interaction between these two factors. DM is a well established risk factor for small

artery occlusive disease affecting the retina, kidneys, and cranial nerves. The role of DM in

cerebral small vessel occlusive disease is less well characterized. Autopsy studies have yielded

conflicting results, some of them suggesting a relationship between diabetes and lacunes, and

others no significant relationship. No prospective epidemiologic studies have been conducted to

examine whether or not DM is an independent risk factor for stroke due to small vessel

occlusion.

Diabetes mellitus negatively affects outcome from stroke

DM not only significantly increases the risk of stroke, but also is a predictor of reduced survival

following stroke. Higher mortality rates from stroke have been reported in diabetics, compared to

non-diabetics in most 3,14-17 but not all studies. These studies demonstrate that the higher

mortality rate is present throughout the entire post-stroke time period. Mortality rates are higher

in diabetics during acute hospitalization for stroke, one year, and one decade after the stroke. DM

may affect the rate of recovery of neurologic function following a stroke. Lithner et al. reported

that four days after hospital admission, more stroke patients with DM than without DM were still

confined to bed. In the Copenhagen Stroke Study, patients with DM recovered more slowly than

non-diabetic patients; however the amount of neurological deficit at hospital discharge was

equivalent between the two groups.

Stroke prevention in diabetics

Prevention of stroke is divided into primary and secondary prevention. Primary prevention refers

to prevention of a first stroke. Secondary prevention refers to prevention of stroke following a


TIA or an initial stroke. The clinician who cares for patients with DM can invoke multiple

interventions to prevent primary and secondary strokes in these patients, some of which are

outlined below.

Treatment of hyperglycemia

Glycemic control may have a protective effect in primary stroke prevention. The UKPDS-35

study was a prospective study of 3642 patients with a median follow-up of 10.4 years for all

cause mortality. The study investigators found stroke risk was decreased by 12% for every 1%

reduction in hemoglobin A1C, although this was not statistically significant (p=.035).

In this study, the hemoglobin A1C was reduced from a median of 7.9% to 7.0%. It is

possible that the impact on stroke risk would have been more profound if patients with worse

initial diabetic control had been treated more aggressively.

In the Veterans Administration feasibility trial, there was no benefit found on stroke

incidence with intensive versus conventional insulin treatment in type 2 DM.

Despite the findings of these two studies, and the remaining uncertainty as to whether

tight diabetic control can significantly reduce risk of a first stroke, tight control has been shown

to prevent other vascular complications in the diabetic, and it may be inferred that stroke risk

may be reduced. In addition, improved diabetic control may reduce the progression of large

vessel atherosclerotic disease in the diabetic. The Atherosclerosis Risk in Communities Study

Investigators (ARIC) found that patients with previously undiagnosed DM were found to have an

even greater rate of progression of carotid atherosclerosis than known diabetics, suggesting that

early diagnosis and treatment of DM may help to prevent progression of large vessel disease. No

clinical trial assessing the utility of aggressive control of hyperglycemia in diabetic stroke
patients, with secondary stroke as an outcome, has been conducted. Thus we do not know

whether tight glucose control decreases the risk of recurrent stroke.

Source: Antonios N., Silliman S., 2005, Diabetes Mellitus and Stroke, from

http://www.dcmsonline.org/jax-medicine/2005journals/Diabetes/diab05g-stroke.pdf

GOUTY ARTHRITIS

Gout

Gout is a heterogeneous group or conditions related to a genetic defect or purine metabolism that

results in hyperuricemia. Over secretion of uric acid, or a combination of both, occurs. The

prevalence of gout is reported to be less than 1% to 15.3%, and it appears to be on the rise. The

incidence increases with age and body mass index. It occurs more commonly in males than in

females (Wortmann & Kelley, 2005).

In primary hyperuricemia, elevated serum urate levels or manifestations of urate deposition

appear to be consequences of faulty uric acid metabolism. Primary hyperuricemia may be caused

by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ

meats), or heredity. In secondary hyperuricemia, gour is a clinical feature secondary to any of a

number genetic or acquired processes, including conditions in which there is an increase in cell

turnover (leukemia, multiple myeloma, some types of anemias, psoriasis) and an increase in cell

breakdown. Altered renal tubular function, either as a major action or as an unintended side
effect of certain pharmacologic agents (eg, diuretics such as thiazides and furosemide), low-dose

salicylates, or ethanol, can contribute to uric acid underexcretion.

Pathophysiology

Hyperuricemia (serum concentration greater than 7mg/dl) can but does not always cause

monosodium urate crystal deposition (Becker & Jolly, 2005). However, as uric acid levels

increase, the risk becomes greater. Attacks of gout appear to be related to sudden increase or

decreases of serum uric acid levels. When the urate crystals precipitate within a joint, an

inflammatory response occurs, and an attack of gout begins. With repeated attacks,

accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the

body, such as the great toe, the hands, and the ear. Renal urate lithiasis (kidney stones), with

chronic renal disease secondary to urate deposition, may develop.

The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors

other than crystals may be related to the inflammatory reaction. Recovered monosodium urate

crystals are coated with immunoglobulins that are mainly IgG. IgG enhances crystal

phagocytosis, thereby demonstrating immunologic activity.

Clinical Manifestations

Manifestations of the gout syndrome include acute gouty arthritis (recurrent attacks of severe

articular and periarticular inflammation), tophi (crystalline deposits accumulating in articular

tissue, osseous tissue, soft tissue, and cartilage), gouty nephropathy (renal impairment), and uric

acid urinary calculi. Four stages of gout can be identified: asymptomatic hyperuricemia, acute

gouty arthritis, intercritical gout, and chronic tophaceous gout. The subsequent development of

gouty is directly related to the duration and magnitude of the hyperuricemia. Therefore, the
commitment to lifelong pharmacologic treatment of hyperuricemia is deferred until there is an

initial attack of gout.

Medical Management

A definitive diagnosis of gouty arthritis is established by polarized light microscopy of the

synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear

leukocytes in the fluid. Colchicine (oral or parenteral), an NSAID such as indomethacin, or a

corticosteroid is prescribed to relieve an acute attack of gout. Management of hyperuricemia,

tophi, joint destruction, and renal disorders is usually initiated after the acute inflammatory

process has subsided. Uricosuric agents, such as probenecid (Benemid), correct hyperuricemia,

and dissolve deposited urate. When reduction of serum urate level is indicated, uricosuric agents

are the medications of choice. If the patient has, or is at risk for, renal insufficiency or renal

calculi (kidney stones), allopurinol, a xanthine oxidase inhibitor, is also effective (Wortmann &

Kelley, 2005). Corticosteroids may be used in patients who have no response to other therapy. If

the patient experiences several acute episodes or there is evidence of tophi formation,

prophylactic treatment is considered. Specific treatment is based on the serum uric acid level.

Nursing Management

Although severe dietary restriction is not necessary, the nurse should encourage the patient to

restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake.

Maintenance of normal body weight should be encouraged. In an acute episode of gouty arthritis,

pain management with prescribed medications is essential, along with avoidance of factors that

increase pain and inflammation, such as trauma, stress, and alcohol. During the intercritical
period, the patient feels well and may abandon preventive behaviours, which may result in an

acute attack. Acute attacks are most effectively treated if therapy is begun early in the course.

Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-surgical

nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

PARKINSON’S DISEASE

Parkinson’s disease is a slowly progressing neurologic movement disorder that eventually leads

to disability. It is the fourth most common neurodegenerative disease, and 50,000 new cases are

reported each year in the United States (Chen and Fernandez, 2007; Thomure, 2006). The

disease affects men more often than women. Symptoms usually first appear in the fifth decade of

life; however, cases have been diagnosed as early as 30 years of age.

The degenerative or idiopathic form of Parkinson’s disease is the most common; there is

also a secondary form with a known or suspected cause. Although the cause of most cases is

unknown, researchers suggest several causative factors , including genetics, atherosclerosis,

excessive accumulation of oxygen free radicals, viral infection, head trauma, chronic use of

antipsychotic medications, and some environmental exposures.

Pathophysiology

It is associated with decreased levels of dopamine resulting from destruction of pigmented

neuronal cells in the substantia nigra in the basal ganglia region of the brain. Fibers or neuronal
pathways project from the substantia nigra to the corpus striatum, where neurotransmitters are

key to the control of complex body movements. Through neurotransmitters acetylcholine

(excitatory) and dopamine (inhibitory), striatal neurons relay messages to higher motor centers

that control and refine motor movements. The loss of dopamine stores in this area of the brain

results in more excitatory neurotransmitters than inhibitory transmitters, leading to an imbalance

that affects voluntary movement.

Clinical symptoms do not appear until 60% of the pigmented neurons are lost and the

striatal dopamine level is decreased by 80%. Cellular degeneration impairs the extrapyramidal

tracts that control the semiautomatic functions and coordinated movements; motor cells of the

motor cortex and extrapyramidal tracts are not affected. Researchers are working on uncovering

the exact mechanisms of neurodegeneration; current theories suggest that it results from

oxidative stress in a portion of the neuron known as Lewy bodies, protein aggregation, or a

combination of the two mechanisms (Barker and Barasi, 2008).

Clinical Manifestations

Parkinson’s disease has a gradual onset, and symptoms progress slowly over a chronic,

prolonged course. The cardinal signs are tremor, rigidity, bradykinesia (abnormally slow

movements), and postural instability.

Tremor

Although symptoms are variable, a slow, unilateral resting tremor is present in the majority of

patients at the time of diagnosis. Resting tremor characteristically disappears with purposeful

movement but is evident with the extremities are motionless. The tremor may manifest as a

rhythmic, slow turning motion (pronation-supination) of the forearm and the hand and a motion
of the thumb against the fingers as if rolling a pill between the fingers. Tremor is present while

the patient is at rest; it increases when the patient is walking, concentrating, or feeling anxious.

Rigidity

Resistance to passive limb movement characterizes muscle rigidity. Passive movement of an

extremity may cause the limb to move in jerky increments, referred to as lead-pipe or cog-wheel

movements. Involuntary stiffness of the passive extremity increases when another extremity is

engaged in voluntary active movement. Stiffness of the arms, legs, face, and posture are

common. Early in the disease, the patient may complain of shoulder pain due to rigidity.

Bradykinesia

One of the most common features of Parkinson’s disease is bradykinesia, which refers to the

overall slowing of active movement. Patients may also take longer to complete activities and

have difficulty initiating movement, such as rising from a sitting position or turning in bed.

Postural instability

The patient commonly develops postural and gait problems. A loss of postural reflexes occurs,

and the patient stands with the head bent forward and walks with a propulsive gait. The posture

is caused by the forward flexion of the neck, hips, knees, and elbows. The patient may walk

faster and faster, trying to move the feet forward under the body’s center of gravity (shuffling

gait). Difficulty in pivoting causes loss of balance (either forward or backward). Gait impairment

and postural instability place the patient at increased risk for falls.

Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-surgical

nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
COPING OF PATIENTS WITH STROKE

UNIVERSITY OF MARYLAND STUDY FINDS CERTAIN COPING STRATEGIES

IMPACT RECOVERY FROM STROKE

Following a stroke, almost two-thirds of people turn to religion on a regular basis and

about 12 percent frequently use humor to cope with the stress that results from having a stroke.

That's according to researchers at the University of Maryland School of Medicine in Baltimore,

who also found that about two-thirds of stroke patients use acceptance as a way to move forward

and deal with their new challenges.

Results of the study, which showed that certain coping strategies enable people to adjust

better to life after a stroke, were presented at the American Heart Association's 27th International

Stroke Conference in San Antonio, Texas, on February 7, 2002.

The study evaluated the coping style and psychological adjustment of 56 stroke survivors

treated at the University of Maryland Medical Center (34 women and 22 men) one year after

their stroke. The most common strategies among the patients were turning to religion,

acceptance, and positive reinterpretation and growth, which means that they tried to find

something positive from their experience, shifted their priorities, and gained new appreciation for

their family and friends. Almost half of the patients studied used positive reinterpretation and

growth on a daily basis.

While many patients use a variety of coping strategies, the researchers looked at the most

dominant ones used on a regular basis by patients in the study.


"Individuals who used humor and positive reinterpretation were more outgoing, active,

and positive a year after their stroke," says the study's lead author, Lynn Grattan, Ph.D., an

associate professor of neurology at the University of Maryland School of Medicine and a

neuropsychologist at the University of Maryland Medical Center.

"Turning to religion can also help patients cope effectively following a stroke, especially

if they are using it to seek strength to deal with the challenges they face," says Dr. Grattan.

The researchers also found that stroke patients who avoided addressing the issues related

to their stroke had higher levels of depression one year after the stroke. These individuals used

"behavioral disengagement" as a coping strategy, acting as though their stroke didn't happen and

diverting their attention away from activities that would help them with rehabilitation and

recovery. For example, they may have skipped follow-up doctor or physical therapy

appointments or ignored recommendations on diet, exercise and other lifestyle changes to

prevent a future stroke. Behavioral disengagement was used frequently by seven percent of

patients in the study.

A stroke can lead to feelings of frustration, anxiety, anger, apathy or depression. By

avoiding the emotional and behavioral aspects of what they went through, Dr. Grattan says

patients who disengage are not dealing with natural feelings of loss and are not allowing

themselves to take steps that could improve their condition.

"We believe these findings are important to keep in mind as we work with patients early

in the recovery process," according to Dr. Grattan.

"Two people with the same stroke-related disabilities can have very different outcomes.

One person may return to work and social activities, while the other may end up on permanent
disability. We believe pre-stroke personality and coping strategies play a major role in how well

patients recover," she adds.

Dr. Grattan says health care providers should first assess the patient's dominant coping

style and tailor therapy to that individual. "Through counseling, stroke support groups and other

methods, we can encourage patients to use the most effective coping strategies, especially during

the year following a stroke, to maximize their adjustment and recovery," she says.

In a related study, Dr. Grattan and her colleagues found that patients who had adjusted

most successfully one year after their stroke had received support from family and friends. The

most useful types of support included driving them to doctor appointments, picking up

prescriptions, and empathic listening, which means listening with sensitivity to the person's

needs ad point of view without being judgmental.

Stroke is the leading cause of serious disability among adults. About 600,000 people

suffer from a stroke each year in the U.S.

The following University of Maryland School of Medicine researchers collaborated with

Dr. Grattan on the study: Natasha Kabitski, Marjan Ghahramanlou, Christopher Vaughan,

Marcella Wozniak, Steven Kittner and Thomas Price.

Source: Levitt, E.B.February 7,2002.University of Maryland study finds certain coping strategies

impact recovery from stroke.Retrieved from

http://www.umm.edu/news/releases/stroke_recovery.htm
Coping Mechanism of Stroke Patients

Recovery from a stroke is easier if you make simple changes that help you cope better. You can

stay independent and productive by taking control of your health and daily life. All that is needed

to live a normal life is a plan for a new life.

Physical Strength and Conditioning

Patients need to keep their movements strong and lively. You also need to keep blood pressure

and cholesterol under control to prevent complications or another stroke. Both practices help a

patient cope with the condition of restricted blood flow and circulation, and the weakening of

muscles from inactivity. Regular walking strengthens muscles and the cardiovascular system.

Weight lifting or tai chi can make you stronger and raise your conditioning so you can have a

more active life.

Diet

Liveliness in daily activities depends upon a controlled weight and low blood pressure and

cholesterol. Eat a healthful diet low in salt, fat and sugars. Vegetables, fiber-rich whole grain

breads and chicken or fish are good for controlling your weight and cardiovascular system.

Nutritional charts and healthy recipes can be a part of typical eating.

Daily Living

Daily living can be difficult after a stroke if you do not make changes to your home. With less

control, balance and vision on one side of your body, walking through the home can be

obstructed by a narrow doorway or end in slips or falls. A patient needs clear access to each part

of the house. If necessary, paths are wide enough for walking with a walker or cane, or moving
in a wheelchair. Reorganizing the furniture so all pathways are clear is a wise choice. Danger can

be avoided by removing throw rugs. Modifications also might be a good choice. Instead of

leaning on furniture or fixtures, you can install grab bars for walking stairs or entering the

bathtub or ramps to enter heightened areas.

Communications

When a patient has had a stroke in the left side of the brain, a disruption of communications

occurs due to loss of blood flow to the language center in the brain. This condition is called

aphasia. A patient with aphasia has difficulty forming words to speak or write, or can not

understand when others talk to them. Telling family and friends about the condition that is in the

way of communicating helps you cope with the difficulties in relating. Regular speech practice

can improve language ability.

Engagement and Activity

Patients can be depressed or upset by living with the effects of a stroke. Life is made more vital

by staying engaged with family and friends, and staying active, to keep the emotions stable.

Encourage friends and family to check in with you and do social activities with you. Join a

support group with stroke patients who understand your condition. For vitality and pleasant

satisfaction, live a physically active life and do the things you enjoy.

Source: Benjamin,A.(N.D.)Coping mechanism of stroke patients.Retrieved from

http://www.ehow.com/about_5479458_coping-mechanism-stroke-patients.html
COPING OF FAMILIES WITH STROKE PATIENT

Suffering a Stroke: Family Members are Victims of Stroke Too

The victims of stroke are not the only ones who must deal with the devastating

consequences of this condition; their families also do as well. Sometimes families have to deal

with the shock of seeing a once capable individual suddenly deteriorate and need help for the

simplest things. Other times they may blame themselves for not spotting the vague signs of

stroke in the very short window of time that could have prevented further brain damage. Since

many stroke victims need to be convinced to go to the hospital if they are still conscious, a

family member may feel guilt over not being more convincing sooner. Many family members

have to alter their own plans such as employment or education to compensate for the family need

to care for the stroke victim. The families themselves are often overlooked when they have to

take a stroke victim to rehabilitation and doctors appointments, plus care for all the duties of the

household.

Relationships can be disrupted as family members may have to take on unfamiliar roles. Perhaps

the stroke victim supported the family or cared for another relative, and this upsets the balance of

the household when the rest of the family often have to pick up the victim's responsibilities and

learn how to be a caretaker at the same time. A large part of how your family works and interacts

with each other - whether as caretaker, breadwinner, cook, or emotional support, is altered

quickly and replaced with tremendous responsibility. Some issues that families must deal with
include knowing how to handle the stroke victims employment, especially if they are self

employed and it is unclear if the person will be able to return to work in that capacity.

Should the family sell the business? Hire a new person to help out? How long do they hold on to

the family business if it is losing money? Does the victims insurance issue from the business, and

will it be affected if the business is sold or closed? Can you afford to keep the business and the

home if the business is not generating money? It is not much easier to decide about a job either,

perhaps they will rehabilitate to a reasonable degree, but what if it takes a few years? This sort of

problem makes long term financial decisions very difficult, such as what is to be done about the

children's' education if the school of choice may not be an option if adequate income may not

exist, yet the child cannot necessarily plan on scholarships due to financial need if this cannot be

determined what the need will be upon starting school.

Since many stroke victims may feel frustration and perhaps an altered personality, they may be

very short tempered with those who care for them. While the victim themselves is reliant upon

the family often for basic things such as being driven somewhere or caring for financial tasks or

tasks that require coordination, it is hard to feel and act grateful for help doing something they

likely feel they should be able to do themselves. This makes caring for a stroke victim very

stressful, especially since the responsibility doesn't let up for the family members. This can

severely affect the family by affecting their own health as they are often too busy to care for their

own needs and they never get a day off. It is also difficult dealing with a stroke altered

personality that you may not necessarily like. A formerly kind and patient person may have their

higher cortical functions altered enough to just not act like the person you know, and often, the
complete opposite - impulsive, emotional, harsh, and anxious.

However, the same stroke victim may be able to carry on short conversations with others in a

pleasant manner, such as a phone call, a visit, or dealing with a stranger for a short period of

time. Because of this, personality changes may not be recognized by non-family members who

do not see the person as altered. Doctors may be greeted pleasantly and treated well by the stroke

victim and therefore not take caretakers concerns seriously when they state that the stroke victim

acts differently at home. Such isolation is often burdensome to caretakers who feel like the stroke

victim has only changed their behavior towards them. Not recognizing that polite chit chat and

manner towards others and coping with day to day needs and emotions are not the same,

caretakers are left confused about the emotions they see and often feel little can be done to fix

things.

WHAT CAN YOU DO TO HELP STROKE VICTIMS AND THEIR FAMILIES

If you have a friend or family member who cares for a stroke victim, often they can use a day or

afternoon off, even if just to take a nap. You may not be a professional caretaker, but when

possible, try to provide

something to alleviate some responsibility such as preparing a meal or offering to go to the

store or drive them somewhere. Even coming over with a few favorite movies of the stroke

victim or some favorite music to listen to will give the caretaker a bit of a break, often help cheer
up the stroke victim and will not require you to make too much conversation with the stroke

victim themselves if you do not know them very well or do not know what to say. While difficult

to do in practice, try not to take any remarks the stroke victim makes to you too seriously if they

seem altered.

It is also important for family members to try to take turns so that all the burdens do not fall on

one person. While you may be taking more than your share, if you are not dealing with the care

of the person each day like the main caretaker is, then you are not dealing with the same

emotional burdens that the main caretaker does. Even having a another person in the house

alleviates some of the burden so that the caretaker can concentrate on other duties without being

overly concerned about the whereabouts of a stroke victim if some else just comes by to visit or

read the paper on occasion.

NOM, Yahoo! Contributor Network (2007). Suffering a Stroke: Family Members are Victims of

Stroke Too. Retrieved from:

http://www.associatedcontent.com/article/221766/suffering_a_stroke_family_members_are_pg

3.html?cat=5

GERIATRICS WITH STROKE

Older person with hypertension, severe arteriosclerosis, diabetes, gout, anemia,

hypothyroidism, silent myocardial infarction, TIA’s and dehydration and those who smoke are
among the high risk candidates for cerebrovascular accident, the third leading cause of death in

this age group. Although a ruptured blood vessel can be responsible for this problem, most

CVAs in elderly are caused by partial or complete cerebral thrombosis. Light headedness,

dizziness, headache, drop attack (feeling of being strongly and suddenly pulled to the ground),

and memory and behavioural changes are some of the warning signs of CVA. A drop attack is a

fall caused by a complete muscular flaccidity in the legs but with no alteration in consciousness.

Eliopoulos C. (2001), Gerontologiccal Nursing (5th ed.), Lippincontt Williams and Wilkins 530

walnut st. Philadelphia

OTHER DIAGNOSTICS

MCHC

Mean corpuscular hemoglobin (MCH) is the average amount of hemoglobin per red blood cell

in a blood sample. MCH is used to help diagnose the type (cause) and severity of anemia. When

MCH is low, this can mean a person has iron-deficiency anemia. This type of anemia can be

caused by insufficient iron in the diet or by blood loss. Blood loss, such as what might occur with

tumors in the colon and other parts of gastrointestinal tract, can cause low iron levels and a low

MCHC.

High MCH levels may indicate the presence of macrocytic anemia and can have a variety of

causes, including liver disease, and deficiencies of vitamin B12 and folic acid (folate). MCH is

part of a Complete Blood Count (CBC) test.

Dixon,S.July 15, 2009.Mean corpuscular hemoglobin.Retrieved from

http://coloncancer.about.com/od/glossary/g/MCH.htm
RDW

Red cell distribution width (abbreviated as RDW) is a measurement of the amount that

red blood cells vary in size. A cell is the smallest, most basic unit of life, that is capable of

existing by itself. Red blood cells help carry oxygen in the blood.

Electronic instruments are capable of analyzing the blood sample and detecting the pulses

that are produced by red blood cells. The stronger the pulses are, the greater the red blood cells

are in size. Likewise, the weaker the pulses are, the smaller the red blood cells are in size.

The normal RDW level is 10.2 to 14.5%. It is important to keep in mind that the ranges

mentioned above will be different depending on the machine used to do the blood test. Always

use the normal range printed on the lab report to decide what range is normal.

A high RDW (over 14.5%) means that the red blood cells vary a lot in size. There are

many possible reasons why the RDW level can be too high. To determine what the possible

cause of a high RDW level is, a comparison is made to the mean corpuscular

volume (abbreviated MCV). The MCV is the average amount of space occupied by each red

blood cell.

If both the RDW and MCV levels are increased, there are several possible causes. One

possible cause is liver disease. The liver is the largest organ in the body and is responsible for

filtering (removing) harmful chemical substances, producing important chemicals for the body,

and other important functions. Another cause of high RDW & MCV levels is hemolytic anemia.

Hemolytic anemia is a condition in which the red blood cells are destroyed earlier than they
should be.

The RDW and MCV levels can both be increased if there is too little vitamin B12 or folic

acid (a type of vitamin) in the body. A vitamin is one of a group of substances made up partly of

carbon (an element) that are essential in small amounts for normal bodily functioning and

chemical processes in the body to take place.

Another scenario is that the RDW level can be high, but the MCV level can be low. This

can happen because of iron deficiency anemia. Iron deficiency anemia is a decrease in

hemoglobin in the blood that is caused by an inadequate supply of iron. Hemoglobin is substance

present in red blood cells that help carry oxygen to cells in the body. Iron is needed to make

hemoglobin, which is why a decreased amount of iron leads to a decreased amount of

hemoglobin.

Another cause of a high RDW level and a low MCV level is thalessemia intermedia.

Thalessemia intermedia is another type of blood disorder in which there is impaired production

of one or more of the elements that make up hemoglobin. If the red blood cells are fragmented

(broken) into smaller parts, this can cause the RDW to be high and the MCV to be low. In this

situation, the red blood cells vary in size when they are broke up (which is why the RDW level is

high) but the cells do not take up much space (which is why the MCV level is low).

A final possibility is that the RDW level is increased and the MCV level is normal. This can

be caused by the beginning stages of a decrease in vitamin B12 or folic acid (a type of vitamin)

in the body. It can also be caused by the beginning stages of iron deficiency anemia, which was

described two paragraphs ago.


A low RDW (below 10.2%) means that the red blood cells vary very little in size. One

reason for a low RDW level is macrocytic anemia. Macrocytic anemia is a blood disorder in

which not enough red blood cells are produced, but the ones that are present are large. Another

cause of a low RDW level is microcytic anemia. Microcytic anemia is a condition in which

abnormally small red blood cells are present. In these two disorders the red blood cells do not

vary much in size because they are either all small or all large. This is what causes the RDW

level to be low.

Source: (N.A.)(N.D.)Red cell distribution width.Retrieved from

http://www.medfriendly.com/redcelldistributionwidth.html

HbA1c

In the blood stream are the red blood cells, which are made of a molecule, haemoglobin. Glucose

sticks to the haemoglobin to make a 'glycosylated haemoglobin' molecule, called haemoglobin

A1C or HbA1C. The more glucose in the blood, the more haemoglobin A1C or HbA1C will be

present in the blood.

Red cells live for 8 -12 weeks before they are replaced. By measuring the HbA1C it can tell you

how high your blood glucose has been on average over the last 8-12 weeks. A normal non-

diabetic HbA1C is 3.5-5.5%. In diabetes about 6.5% is good.

The HbA1C test is currently one of the best ways to check diabetes is under control; it is the

blood test that gets sent to the laboratory, and it is done on the spot in some hospital clinics.

Remember, the HbA1C is not the same as the glucose level.


Testing of HbA1c

If your diabetes is controlled (basically an HbA1C lower than 7%), every 3-6 months.

But if the last reading is above 7% and you are in reasonable health, you will need to achieve a

lower level if possible, and the next reading should be sooner. This assumes you will make

changes to improve your control. There is no point in having your HbA1c measured if you are

not trying to achieve good control of your diabetes, although the level does predict the likelihood

of complications from your diabetes.

Glucose levels fluctuate from minute to minute, hour to hour, and day to day. Thus for hour to

hour control, or day to day, a glucose level is the best guide.

The HbA1C level changes slowly, over 10 weeks, so it can be used as a 'quality control' test.

In diabetes glucose tend to rise more than usual, dropping with exercise, rising after food, rising

a lot more after sweet food, and can make it hard to control.

Diabetes may be defined as having an HbA1c>6.5% (Pulse 2010). So,

• >6.5% = diabetes

• <6.0% = not diabetic

• in between....6.0-6.5...may be this is 'pre-diabetes' or 'at risk of diabetes'.

HbA1C. (2011). Retrieved from Diabetic Retinopathy:

http://medweb.bham.ac.uk/easdec/prevention/what_is_the_hba1c.htm
Lilian Anekwe (2010). Diabetes work to soar under HbA1c switch. Retrieved from Pulse Today:

http://www.pulsetoday.co.uk/story.asp?storycode=4125181

Urinary tract infection (UTI)

The urinary tract is comprised of the kidneys, ureters, bladder, and urethra A urinary

tract infection (UTI) is an infection caused by pathogenic organisms (for example,

bacteria, fungi, or parasites) in any of the structures that comprise the urinary tract.

However, this is the broad definition of urinary tract infections; many authors

prefer to use more specific terms that localize the urinary tract infection to the

major structural segment involved such as urethritis (urethral

infection), cystitis (bladder infection), ureter infection, and pyelonephritis (kidney

infection).

Other structures that eventually connect to or share close anatomic proximity to the

urinary tract (for example, prostate, epididymis, and vagina) are sometimes

included in the discussion of UTIs because they may either cause or be caused by

UTIs. UTIs are common, more common in women than men, leading to

approximately 8.3 million doctor visits per year

Although some infections go unnoticed, UTIs can cause problems that range from dysuria

(pain and/or burning when urinating) to organ damage and even death.
The kidneys are the active organs that, during their average production of about 1.5 quarts

of urine per day, function to help keep electrolytes and fluids (for example,

potassium, sodium, water) in balance, assist removal of waste products (urea), and

produce a hormone that aids to form red blood cells. If kidneys are injured or

destroyed by infection, these vital functions can be damaged or lost.

The most common causes of UTI infections (about 80%) are Escherichia coli bacterial

strains that usually inhabit the colon. However, many other bacteria can

occasionally cause an infection (for example,Klebsiella, Pseudomonas, Enterobacter,

Proteus, Staphylococcus, Mycoplasma, Chlamydia, Serratia and Neisseria spp) but are

far less frequent causes than E. coli. In addition, fungi (Candida and Cryptococcus)

and some parasites (Trichomonas, Schistosoma) also may cause UTIs;

Schistosoma causes other problems, with bladder infections as only a part of its

complicated infectious process.

There are many risk factors for UTIs. In general, any interruption or impedance of the usual flow

of urine (about 50 cc per hour in normal adults) is a risk factor for a UTI. For example, kidney

stones, urethral strictures or any anatomical abnormalities in the urinary tract increases infection

risk. This is due in part to the flushing or wash-out effect of flowing urine; in effect the

pathogens have to "go against flow" because the majority of pathogens enter through the urethra

and have to go retrograde (against a barrier, urine flow) to reach the bladder, ureters, and
eventually the kidneys. Many investigators suggest that women are far more susceptible than

men to UTIs because their urethra is short and its exit (or entry for pathogens) is close to the

anus and vagina, which can be sources for pathogens.

People who require catheters have an increased risk (about 30% of patients with indwelling

catheters get UTIs) as the catheter has none of the protective immune systems to eliminate

bacteria and offers a direct connection to the bladder.

The caregiver should obtain a detailed history from the patient, and if a UTI is suspected, a urine

sample is usually obtained. The best sample is a midstream sample of urine placed in a sterile

cup because it usually contains only the pathogenic organisms instead of the transient organisms

that may be washed from adjacent surfaces when the urine stream begins. Male patients with

foreskin should retract the foreskin before providing a midstream urine sample. In some patients

who cannot provide a midstream sample, a sample can be obtained by a catheter. The urine

sample is then sent for urinalysis.

Most UTIs cause no complications if they spontaneously resolve quickly (a few days) or if

treated early in the infection with appropriate medications. However, there are a number of

complications that can occur if the UTI becomes chronic or rapidly advances. Chronic infections

may result in urinary strictures, abscesses, fistulas, and kidney damage. Rapid advancement of

UTIs can lead to dehydration, kidney failure,sepsis, and death

A good prognosis is usual for spontaneously resolved and quickly treated UTIs. The prognosis

begins to decline if the UTI is not quickly recognized or treated. Elderly and immunodepressed

patients may not have the UTI recognized early; their prognosis may range from fair to poor,

depending on how much damage is done to the urinary tract or if complications like sepsis occur.
Like adults, most adequately treated children will have a good prognosis. Children and adults

with recurrent UTIs may develop complications and a worse prognosis; recurrent UTIs may be a

symptom of an underlying problem with the urinary tract structure.

Many methods have been suggested to reduce or prevent UTIs. Some of these are considered

home remedies and have been discussed (see above home remedies section). There are other

suggestions that may help prevent UTIs. Good hygiene for males and females is useful; for

females, wiping from front to back helps keep pathogens that may reside or pass through the anal

opening away from the urethra;

Incomplete bladder emptying and resisting the normal urge to urinate can allow pathogens to

survive and replicate easier in a non-flowing system.