Laura Tidwell

MSN 621

Alverno College

April 2011

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Table of Contents“Compass” retrieved from Microsoft Windows 2007

Clipart

“Compass” retrieved from Microsoft Windows 2007 Clipart

Increase awareness of the pathophysiological factors that make Incontinence a concern for healthcare professionals, specifically nurses.

“What we think determines what we see-even though it often seems the other way around” (Carlson, 2006, p. 13)

1. Review skin Pathophysiology

2. Relate harmful effects of urine and feces due to incontinence.

3. Discuss Case Based patient Scenario, with multiple concerns, and how those concerns have implications for an incontinent patient.

4. Conceptualize inflammation processes and the risks as they relate to incontinence.

Risks for IncontinenceRisks for Incontinence

You are Here

Neural Control of IncontinenceNeural Control of Incontinence

Inflammation Inflammation

Stress ResponsesStress Responses

Potential ComplicationsPotential Complications

Moisture LesionsMoisture Lesions Elderly patients

at RiskElderly patients at Risk

Diabetes at a GlanceDiabetes at a Glance

Click Topic to Learn More

Case StudyCase Study

Epidermis & DermisEpidermis & Dermis

Case Study OutcomeCase Study Outcome

Urine & FecesUrine & Feces

Common Disorders &

Genetic Risk

Common Disorders &

Genetic Risk

One of your 4 patients is an 82 year old woman, admitted with increased confusion and failure to thrive. She is a Type 2 Diabetic with a Stage 1 ulcer on her R buttock and a Stage 2 ulcer on her L buttock. She has Ensure ordered 3 X Daily with meals to help supplement her nutritional needs. Her activity level is up to chair 3 X Daily with meals. She transfers with assist of 2. The total recorded intake in the last 24 hours is: 50cc between 0000-0759, Zero between 0800-1559, 100cc between 1600-2359 which adds up to 150cc. When you enter the room at 3 pm she is sleeping in her chair, she has been up since lunch at 1200 and has not been toileted since 1130 am, she wears a depends. There has been zero recorded output in 24 hours.

“Nurse” retrieved from Microsoft Windows 2007 Clipart

Cc=ml

1 Ensure = 355cc

150cc=less than 1/2 can

Ensure 3 X daily orders

150cc Input Recorded

Past 24 Hours

“Normal” Urinary output = 30-60cc per hour.

Zero Output Recorded past 24 Hours

If the patient is Incontinent does that mean we don’t track her output? .

“Confusion” retrieved from Microsoft Windows 2007 Clipart

Stage 1 & Stage 2 pressure ulcers

Patient is Diabetic

Is Incontinence Normal? Urinary Incontinence is

widely accepted as “normal”, it can often be cured and it can always

be relieved by good management

Hold Moisture in, Right?

Excessive and continuous skin moisture can pose a risk to compromise the integrity of the skin by causing the skin

tissue to become macerated and therefore be at risk for epidermal erosion.

superficial, partial skin loss and shiny wet skin caused by by incontinence

McDonagh, D. (2008). Moisture lesion or pressure ulcer? A review of the literature. Journal of Wound

Care, 17(11), 461. Retrieved from EBSCOhost, February 28, 2011. Permission granted.

Stimulation of Parasympathetic neurons (the bladder fills) = Contraction of detrusor muscle = urination

(Porth, 2009)

(Misconception Junction, 2010) Permission granted under  Wikimedia Commons

This is mediated by acetylcholine. Receptors that respond to acetylcholine are called

Cholinergic Receptors

There are receptors found in the parasympathetic endings of the detrusor muscle. The detrusor muscle is the 2nd layer in the lining of the bladder, made up of smooth muscle fibers.

(Porth, 2009)

“Muscle Fiber” retrieved from Microsoft Windows 2007 Clipart

FDOH, 2010. Permission Granted

The relaxation and storage function of the bladder is controlled by the Sympathetic Nervous System.

Stimulation of sympathetic neurons = Relaxation of detrusor muscle

The bladder is supplied with a1 and B2 adrenergic receptors. The B2 receptors are in the detrusor muscle and they relax it, until the volume when the micturition (passage of urine) reflex is triggered by the increasing bladder volume. The activation of a1 receptors produces the contraction of the

internal sphincter.

(Porth, 2009)

(Author, N., 2011) Permission granted under  Wikimedia Commons

Receptors found in Detrusor Muscle are responsible for

Urination

ParasympatheticWere you right?

Receptors are responsible for Relaxation (filling) of bladder

Sympathetic

Click in Above Boxes

(Porth, 2009)

Stroke & Advanced Age

Loss of ability to perceive bladder filling

Parkinson disease(Commonly Genetic)

Detrusor contractions are elicited suddenly

Spinal cord Injury

Storage reflexes are provoked during filling

Click in boxes to learn more

Injury to sacral cord or spinal roots

Bladder fills but does not contract

Pelvic Surgery

Increased filling and impaired sphincter control

Diabetic neuropathies & Multiple Sclerosis

Bladder overfilling occurs due to a loss of ability to perceive bladder filling

(Porth, 2009)

Click ON Frame to learn more

Studies have suggested a genetic component of Stress Urinary Incontinence and Pelvic Organ Prolapse (Allen, 2010).

Possible link to genetics predisposing patients to recurrent UTIs which can be a contributing factor (especially in elderly) to

urinary incontinence (Zaffanello, et al., 2010).

Atropic Vaginitis

An inflammation of the vagina (and the outer urinary tract) due to the thinning and shrinking of the tissues. This is all

due to a lack of the reproductive hormone estrogen, which happens

naturally during peri-menopause, and increasingly so in post-menopause.

Atropic Vaginitis

An inflammation of the vagina (and the outer urinary tract) due to the thinning and shrinking of the tissues. This is all

due to a lack of the reproductive hormone estrogen, which happens

naturally during peri-menopause, and increasingly so in post-menopause.

Endocrine

Bladder stasis and infection are long

term complications of Diabetes Mellitus (Which our patient

has)

Endocrine

Bladder stasis and infection are long

term complications of Diabetes Mellitus (Which our patient

has)

(Porth, 2009)(Author, N. 2010)

FDOH, 2010. Permission Granted

About the barrier it forms

Intact skin forms a physical barrier with its closely packed cells, multiple layering, continuous shedding of cells and presence of

protective keratin (Porth, 2009)

About the barrier it forms

Intact skin forms a physical barrier with its closely packed cells, multiple layering, continuous shedding of cells and presence of

protective keratin (Porth, 2009)

About bacteria on the skin

The skin has simple chemicals that create a salty, acidic environment and antibacterial proteins, such as enzymes that

inhibit the colonization of microorganisms and aid in their destruction (Porth, 2009)

About bacteria on the skin

The skin has simple chemicals that create a salty, acidic environment and antibacterial proteins, such as enzymes that

inhibit the colonization of microorganisms and aid in their destruction (Porth, 2009)

Can this barrier be broken?

Some pathogens can penetrate the anatomic layers and cause physiologic changes that result in infectious disease (Porth, 2009)

Can this barrier be broken?

Some pathogens can penetrate the anatomic layers and cause physiologic changes that result in infectious disease (Porth, 2009)

Click boxes to learn more

Epidermis (Physical Barrier)

Closely packed cells, multiple layering

(Kilbad, 2008) Permission granted under  Wikimedia Commons

(US-Gov.2005-2009). Permission granted under Wikimedia Commons.

 .

Vasculature

Epidermis Body’s 1st line of defense

Dermis

(Vasculature) within this layer

Connective tissue layer that separates the Epidermis from the Subcutaneous fat layer. Supports the Epidermis and is the Primary source of nutrition. Blood Vessels are within this layer.

The arterial vessels nourish the skin. The Dermis is well supplied with Sensory Neurons

Prevention of: pathogenic organisms, excessive water loss

The skin is the largest organ of the body, it is about 2 mm thick and weighs approximately six pounds.

Is Well Supplied with Sensory Neurons

Yes! Sensory Impairment happens

at this level!

Is the body’s 1st line of defense

No….that is the Epidermis

The Blood Vessels are within this

Layer

Yes!The Blood Vessels are within this

Layer!

(Kilbad, 2008) Permission granted under  Wikimedia Commons

Click boxes to test your knowledge!

Sensory PerceptionMeasures a patients' ability to detect and respond to

discomfort or pain, their ability to cognitively react to pressure-related discomfort.

Do you remember what our patient was admitted with?Increased confusion

&Failure to Thrive

Increased confusion&

Failure to Thrive

And…..she has an existing Stage 1 to her R buttock, Stage 2 to her L buttock

How long has she been up to the chair?

3 hours

How long has she been up to the chair?

3 hours

Click to check your answer

(Click box)

Urine is slightly acidic, it contains urea, sodium chloride, and organic salts, all of which can irritate

the skin.

Feces is waste from the Digestive Tract. It consists of food residue and bacteria. Imagine that on your skin!

Fecal Incontinence is associated with an increased risk of skin damage. The alkali (increased pH), bacterial and enzymatic

content of fecal material may irritate and damage the skin (Hurnauth,

2011) .

Fecal incontinence left untreated can lead to excoriation and breakdown which may become infected. (Author, N. 2008).

Enzymes are proteins that are made from amino acids, and they work to facilitate chemical

reactions.

The elevated pH of stool increases the activity of proteases and lipases (both are enzymes) found in stool, which causes

increased permeability of the skin, which makes it more susceptible to other agents such as bile salts (found in

urine).

That’s IF our patient was Incontinent of Feces…..As for Bacteria, remember this?

Some pathogens can penetrate the anatomic layers and cause physiologic changes that result

in infectious disease

As for Bacteria, remember this?

Some pathogens can penetrate the anatomic layers and cause physiologic changes that result

in infectious disease

Moisture lesion: superficial, partial skin loss, multiple irregular shaped spots and shiny wet skin caused by urinary incontinence

Grade IV pressure ulcer and moisture lesion caused by unrelieved pressure and fecal incontinence

Combined lesion: irregular wound shape, grade III pressure ulcer and moisture lesion

McDonagh, D. (2008). Moisture lesion or pressure ulcer? A review of the literature. Journal of Wound Care, 17(11), 461. Retrieved from EBSCOhost, February 28, 2011. Permission granted.

Activity

Level of physical activity, very little or no activity can encourage breakdown of tissue. 

Mobility

Capability to adjust body position independently.

Friction and Shear

The amount of assistance needed to move, the sliding motion can cause shear which means the skin and bone are moving in opposite directions .

Restricted Mobility

She requires assist of 2 to get up, this restricts her ability

to toilet herself

Restricted Mobility

She requires assist of 2 to get up, this restricts her ability

to toilet herself

Click box

(Author, N., 2011) Permission granted under  Wikimedia Commons

Absolutely! How did you know?

This is a Pressure

Ulcer, though it will

be complicated

by Incontinence it is caused by pressure

Click on area of breakdown in picture, likely due to Incontinence

Epithelial Barriers

Microbes

The classic response to inflammation includes redness, swelling, heat, pain or discomfort, and loss of function

Inflammation is the body’s response to

immune reactions, injury, or ischemic damage.

(Porth, 2009)

Arterioles

Arterioles

Involves

Involves

Vasodilation

Vasodilation

(Opening of capillary beds) which results in:

(Opening of capillary beds) which results in:

The area becoming congested(Edema)

The area becoming congested(Edema)

Redness &

Warmth

Redness &

Warmth

(Porth, 2009)

Protein rich fluid (exudate) into extravascular spaces Increased concentration of blood constituents

(red cells, leukocytes, platelets, and clotting factors)

Stagnation of flow Clotting of blood at the site of injury aids in the spread of

infection The osmotic pressure causes fluid to move into tissues

producing:

Increased permeability of microvasculature Increased permeability of microvasculature

That leads to:

That leads to:

Pain Swelling (edema)

Impaired Function

(Porth, 2009)

Phagocytic leukocytes (WBCs that kill the

bacteria or eat it) move into the area of injury or

infection

Phagocytic leukocytes (WBCs that kill the

bacteria or eat it) move into the area of injury or

infection

Chemical Mediators

released from tissue cells

Chemical Mediators

released from tissue cells

Neutrophils migrate from blood vessels

to the inflamed tissue

Neutrophils migrate from blood vessels

to the inflamed tissue

(Porth, 2009)

Neutrophils

Because they received the

message from the chemical

mediators that were released

Monocytes

(Histamine) from Basophils

Become Macrophages once they move from the blood into the tissue

Macrophages now present the antigen to other cells in hopes of finding a cell that will recognize

the antigen

Macrophages

All photos: (Author, N., 2011) Permission granted under  Wikimedia Commons

Exudate is produced in the _______ Stage of Inflammation:

Cellular

Try again, WBCs move into the area during this

stage

Cellular

Try again, WBCs move into the area during this

stage

Vascular

Great Job!

Vascular

Great Job!

Pain is typically experienced during the _________ Stage of Inflammation:

Vascular

Nice Job! Fluid moves into

tissues causing Pain

Vascular

Nice Job! Fluid moves into

tissues causing Pain

Cellular

Try Again

Cellular

Try Again

?

?

Tissue DamageTissue

DamageRelease of

Prostaglandins & Leukotrines

Release of Prostaglandins & Leukotrines

Mast cells release Histamine & Acetylcholine

(inflammatory mediators)

Mast cells release Histamine & Acetylcholine

(inflammatory mediators)

Increased venule

permeability

Increased venule

permeability>

WBCs>

WBCsCapillary

endothelium adhesive

proteins

Capillary endothelium adhesive

proteins

Vasodilation

Vasodilationand and

and

Exudate leaks out of venules into

tissues

Exudate leaks out of venules into

tissues

Decreased blood volume

Decreased blood volume

Tissues Swell: edema

Tissues Swell: edema

Pressure on nerves causes pain

Pressure on nerves causes pain

WBCs adhere to capillary

lining

WBCs adhere to capillary

lining

Release cytokines to attract more

WBCs & promote healing

Release cytokines to attract more

WBCs & promote healing

Phagocytize invading organisms + injured

cells

Phagocytize invading organisms + injured

cells

Leads to:And

Which causes

Then:

Results:

Causing:

Then

So they can:

And

Stress Response A decrease in the blood flow to kidneys (decreased volume due

to poor PO intake)

A decrease in the blood flow to kidneys (decreased volume due

to poor PO intake)

Causes Kidneys to

release Renin

Causes Kidneys to

release Renin

Stimulates Angiotensin

1 production

Stimulates Angiotensin

1 production

Angiotensin 1 Converting

Enzyme (ACE)

converts it to Angiotensin

11

Angiotensin 1 Converting

Enzyme (ACE)

converts it to Angiotensin

11

Adrenal Cortex releases

Aldosterone

Adrenal Cortex releases

Aldosterone

Na/K+ ATPase in distal tubule

activated

Na/K+ ATPase in distal tubule

activated

Increase in Blood volumeIncrease in

Blood volumeVasoconstriction to kidneysVasoconstriction to kidneys

Vasoconstriction to Skin

Vasoconstriction to Skin

Confines blood flow to inner core of

body and Subcutaneous

tissue

Confines blood flow to inner core of

body and Subcutaneous

tissue

The Sympathetic Nervous System is turned on:

Hypothalamus releases Cortico-Releasing Hormone

(CRH)

Hypothalamus releases Cortico-Releasing Hormone

(CRH)

Inflammation and immune responses are

suppressed

MaintainingBlood Glucose is the

Body’s goal

Inflammation and immune responses are

suppressed

MaintainingBlood Glucose is the

Body’s goal

Adrenal Cortex releases CortisolAdrenal Cortex

releases CortisolCortisol (promotes glucose productio

n by liver)

Cortisol (promotes glucose productio

n by liver)

Adrenal medulla Releases

Epinephrine

Adrenal medulla Releases

Epinephrine

Which blocks prostaglandin

production, injured tissue can’t call

WBCs

Glucocorticoids are produced in response to stress and are necessary for survival.

They suppress the inflammatory response. Remember, maintaining the blood glucose is the body’s goal.

Cortisol is a glucocorticoid, it stimulates glucose production by the liver, promotes protein breakdown and causes mobilization of fatty acids.

As body proteins are broken down, amino acids are mobilized and transported to the liver, where they are used in the production of glucose (glucogenesis), this is the body’s way of producing energy.

. “Magnifying Glass” retrieved from Microsoft Windows 2007 Clipart

In a person with diabetes, the body raises the blood glucose but they are unable to utilize that energy depending on the type/severity of their disease, due to the body’s specific problem with making or utilizing insulin.

Insulin is the only hormone known to have a direct effect on lowering Blood Glucose levels.

It promotes glucose uptake by cells (for energy).

Lets summarize: So the body can produce glucose for energy, even if her PO intake is inadequate in response to stress.

But………. in a Diabetic, the Glucose that was produced for energy cannot be utilized properly, in addition to the Immune Response being suppressed by the Cortisol production?

“Injection” retrieved from Microsoft Windows 2007 Clipart

(Porth, 2009)

What happens to our patient when the sympathetic nervous system is turned on?

Remember the SNS turns on when chemical mediators are released from the cells

(cellular stage of inflammation).

Increased BLOOD Glucose

Great!

Increased BLOOD Glucose

Great!

She will heal faster

No, energy is taken away from inflammation and immune responses when the SNS is

activated

She will heal faster

No, energy is taken away from inflammation and immune responses when the SNS is

activated

Impaired healing

Yes!!! That is NOT

what we want for

our patient!

Impaired healing

Yes!!! That is NOT

what we want for

our patient!Inflammation and immune

responses are suppressed

Impressive!!!

Inflammation and immune responses are suppressed

Impressive!!!

Cytokines stimulate the migration and activation of the immune and inflammatory

cells

They also affect the thermoregulatory center in the hypothalamus to produce fever, the most obvious sign

of an acute phase response

They are produced by those Macrophages we talked about, they recruit and direct migration of

immune and inflammatory cells.

They are used extensively in intercellular communication. In addition, cytokines activate those cells,

stimulating them to produce more cytokines

SIRS is a serious condition related to systemic inflammation. There is an

abnormal regulation of various cytokines

Click boxes to learn about Sirs(Porth, 2009)

When there is a “Cytokine Storm” what do you think is happening?

Does this seem a potential complication for a patient with Incontinence?

There’s an abnormally high amount of cytokines

being produced which could indicate SIRS

RIGHT!

There’s an abnormally high amount of cytokines

being produced which could indicate SIRS

RIGHT!

There may be a rise in patient’s Temperature

RIGHT AGAIN!

There may be a rise in patient’s Temperature

RIGHT AGAIN!

Yes

Absolutely! She has a portal of

entry for invading organisms with skin breakdown

Yes

Absolutely! She has a portal of

entry for invading organisms with skin breakdown

No

Try Again, does this patient have a breakdown in

her Skin Barrier?

No

Try Again, does this patient have a breakdown in

her Skin Barrier?

Late sign of infectionSlight elevations may indicate serious infection

or diseaseThey often have a lower baseline temperatureThey often increase their temperature during an

infection but it may fail to reach a level that is equated with significant fever

It has been suggested that 20%-30% of elders with Serious Infection present with an absent or

blunted febrile response(Porth, 2009) “Elderly” retrieved from Microsoft Windows 2007 Clipart

Slower reepithelialization of open wounds

More Vulnerable to: Chronic Wounds Diabetic Wounds Ischemic Ulcers

Due To: Immobility Diabetes Mellitus Vascular Disease “Elderly” retrieved from Microsoft Windows 2007 Clipart

Slower Healing Processes

Was our Patient Elderly?

Changes in the Micturition cycle that accompany the aging process

makes the Elderly population more prone to Incontinence.

Diuretics: Increased excretion of Sodium & Chloride in Urine =

Higher Acidity

Diuretics: Increased excretion of Sodium & Chloride in Urine =

Higher Acidity

Tranquilizers, Hypnotics: Side effects include: Increased Urinary Retention,

Incontinence

Tranquilizers, Hypnotics: Side effects include: Increased Urinary Retention,

Incontinence

Antidepressants: Side effects include Nocturia, Frequency of Urination

Antidepressants: Side effects include Nocturia, Frequency of Urination

Anticholinergic: Prevent acetylcholine from combining with

parasympathetic receptors

Anticholinergic: Prevent acetylcholine from combining with

parasympathetic receptors

(Spratto & Woods, 2003, pp. 19-161)

Click in boxes to learn more about medication effects

Medications usually cause Transient Urinary Incontinence-Temporary

It is believed that approximately 30% of all cases of urinary incontinence in older people are transient.

“Urinary Incontinence is widely accepted as “normal” in old age, although its consequences are

devastating; it can often be cured and it can always be relieved by good management”

(Ham & Sloane, 1997, p. 323)

One of your 4 patients is an 82 year old woman admitted with increased confusion and failure to thrive. She is a Type 2 Diabetic with a Stage 1 ulcer on her R buttock and a Stage 2 ulcer on her L buttock. She has ensure ordered 3 X Daily with meals that she doesn’t like. Her activity level is up to chair 3 X Daily with meals. She transfers with assist of 2. The total recorded intake in the last 24 hours is: 50cc between 0000-0759, Zero between 0800-1559, 100cc between 1600-2359. When you enter the room at 3 pm she is sleeping in her chair, she has been up since lunch at 1200 and has not been toileted since 1130 am, she wears a depends. There has been Zero recorded output in 24 hours.

Now she has a Temperature of 99.9 when her vitals are taken. She denies pain in the area of her pressure ulcers. She is assisted back to bed and the dressing to the L buttock which is saturated, is removed. The wound is cleaned and the bandage replaced.

The Nurse remembers that heat is a sign of inflammation, the patient’s temperature is rising which could indicate:

Systemic InflammationShe thinks about the possibility that the patient

cannot relate any sensation of pain in the areas of skin breakdown, due to:

Sensory ImpairmentAnd begins to wonder if the next nurse will notify

the physician of the discharge during her dressing change because this could indicate:

InfectionClick links to Learn More

Did the patients’ diet have significant

implications in maintaining her health status?

Did the patients’ diet have significant

implications in maintaining her health status?

Risk factors for a Systemic Inflammatory

Response?

Risk factors for a Systemic Inflammatory

Response?

If our patient was incontinent, was it

important for us to know that?

If our patient was incontinent, was it

important for us to know that?Are Elderly

patient’s at higher risk for

complications from

Incontinence?

Are Elderly patient’s at higher

risk for complications

from Incontinence?

“Driving” retrieved from Microsoft Windows 2007 Clipart

Yes to all(Click)

Congratulations! Your patient is in educated hands!

Yes to all(Click)

Congratulations! Your patient is in educated hands!

For the Nurse caring for this patient, it is Friday.

For the patient that suffered a systemic inflammatory

response, a poor outcome could have been prevented.

How can we manage all those factors?

Recognize signs/symptoms of inflammation

Recognize signs/symptoms of inflammation

Report changes in discharge/drainage to

physician

Report changes in discharge/drainage to

physicianMaintain or increase

Nutritional statusMaintain or increase

Nutritional status

Toilet patient regularly, in an effort to: Prevent

Incontinence

Toilet patient regularly, in an effort to: Prevent

Incontinence

Click boxes to learn More

ASSESS patient’s Skin on Admission ,Q Shift &

PRN

ASSESS patient’s Skin on Admission ,Q Shift &

PRNAccurate Documentation of I &

OAccurate Documentation of I &

O

An estimated 15-30% of community-dwelling elders and 50% of institutionalized elders have severe urinary incontinence

(Porth, 2009). 30% of this group also experience fecal incontinence (Ham & Sloane, 1997)

The economic and social costs, annually, more than $3 billion is spent managing incontinence in nursing homes alone (Porth, 2009, p.

889)

Incontinence increases social isolation, frequently leads to institutionalization of elderly persons, and predisposes to

infections and skin breakdown (Porth, 2009, p. 889)

Thank you for watching, I hope that you’ll consider the Potential Complications, involved in Incontinence and the Bottom Line for your patient.

Allen, P. (2010). Study: Incontinence, prolapse may have genetic basis. Urology Times, 26(39).

Author, N. (2008). Skin care and incontinence in the elderly. Nursing & Residential Care, 10(10).

Author, N. (2010). Retrieved on April 9, 2011 from: http://en.wikipedia.org/wiki/Atrophic_vaginitis

Author, N. (2011). Retrieved on April 9, 2011 from:

http://upload.wikimedia.org/wikipedia/commons/thumb/3/3d/Neutrophil.png/60px-Neutrophil.png

Author, N. (2011). Retrieved on April 10, 2011 from:

http://upload.wikimedia.org/wikipedia/commons/thumb/5/57/Illu_bladder.jpg/300px-Illu_bladder.jpg

Bowne, P. 2004. Inflammation Tutorial. Retrieved on March 26, 2011 from http://faculty.alverno.edu/bowneps

 

Carlson, R. (2006). YOU CAN BE HAPPY no matter what (p. 13). Novato, Ca: New World Library.

Florida Department of Health (FDOH). (2010). Retrieved April 27, 2011 from:

http://www.doh.state.fl.us

Ham, R., & Sloane, P. (1997). Primary Care Geriatrics: A Case-Based Approach 3rd edition (pp.

323-329). St. Louis, Mo: Mosby.

Hurnauth, C. (2011). Management of faecal incontinence in acutely ill patients. Nursing

Standard, 25(22), 48-56.

Kilbad. (2008, October 18). Normal Epidermis and Dermis with Intradermal Nevus. Retrieved

April 8, 2011 from:

http://upload.wikimedia.org/wikipedia/commons/thumb/b/b4/Normal_Epidermis_and_Dermis_

with_Intradermal_Nevus_10x.JPG/800px-

Normal_Epidermis_and_Dermis_with_Intradermal_Nevus_10x.JPG

McCann, S., & Zamarripa, C. (2010). Incontinence and skin breakdown: a guideline for improved

outcomes... Dermatology Nursing Institute's Annual Congress, September 2009, Washington,

DC.Dermatology Nursing, 22(2), 23. Retrieved from EBSCOhost. February 28, 2011.

McDonagh, D. (2008). Moisture lesion or pressure ulcer? A review of the literature. Journal of

Wound Care, 17(11), 461. Retrieved from EBSCOhost, February 28, 2011.

Misconception Junction. (2010). Retrieved April 26, 2011 from:

http://www.misconceptionjunction.com/wp-content/uploads/2010/10/brain-763982-1.jpg

Mosby. (1998). Mosby's Medical, Nursing, & Allied Health Dictionary (p. 946). St. Louis, MO:

Mosby.

Microsoft Clip Art images. Retrieved March 23, through April 27, 2011 from

http://office.microsoft.com/en-us/clipart.com

Porth, C., & Matfin, G. (2009). Cell and Tissue Characteristics (p. 59). Philadelphia, PA:

Lippincott Williams & Wilkins.

Porth, C., & Matfin, G. (2009). Diabetes Mellitus and the Metabolic Syndrome (p. 1047-1076 ).

Philadelphia, PA: Lippincott Williams & Wilkins.

Porth, C., & Matfin, G. (2009). Inflammation, Tissue Repair, and Wound Healing

(pp. 378-389). Philadelphia, PA: Lippincott Williams & Wilkins.

Porth, C., & Matfin, G. (2009). Pathophysiology Concepts of Altered Health States: Disorders of

the Bladder and Lower Urinary Tract (p. 889). Philadelphia, PA: Lippincott Williams & Wilkins

Portz, D. (2009). What Kind of Rash Is It? Retrieved March 14, 2011 from Bowne, P.S., 2004-10,

PATHO Interactive Physiology Tutorials: Http://faculty.alverno.edu/bowneps

Spratto, G. R., & Woods, A. L. (2003). PDR (pp. 19-161). Clifton Park, NY: Delmar Learning.

Svedrup. (2004). MRNA-interaction. Retrieved April 9, 2011 from:

http://upload.wikimedia.org/wikipedia/commons/f/fb/MRNA-interaction.png

US-Gov. (2005-2009). Skin. Retrieved April 8, 2011 from:

http://upload.wikimedia.org/wikipedia/commons/3/34/Skin.jpg

Voegeli, D. (2010). Care or harm: exploring essential components in skin care regimens.

British Journal of Nursing, 19(13).

Zaffanello, M., Malerba, G., Cataldi, L., Antoniazzi, F., Franchini, M., Monti, E., & Fanos, V.

(2010). Genetic risk for recurrent urinary tract infections in humans: a systematic

review. Journal Biomedicine & Biotechnology, 1-10.