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Transcript of Laura Tidwell MSN 621 Alverno College April 2011.
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.
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http://upload.wikimedia.org/wikipedia/commons/thumb/3/3d/Neutrophil.png/60px-Neutrophil.png
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Normal_Epidermis_and_Dermis_with_Intradermal_Nevus_10x.JPG
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