INTEGUMENTARY

SYSTEM
 ASSESSMENT
DIAGNOSTIC TESTS
A. Skin biopsy
1. Description
 Obtaining a small piece of skin
tissue for histopathologic study
 Methods include punch,
incisional, and shave
1. Implementation preprocedure
 Obtain informed consent
 Cleanse site as prescribed
DIAGNOSTIC TESTS
A. Skin biopsy
1. Implementation postprocedure
 Place specimen, when obtained by physician, in the appropriate container
and send to pathology laboratory for analysis
 Use surgically aseptic technique for biopsy site dressings
 Assess the biopsy site for bleeding and infection
 Instruct the client to keep dressing in place for at least 8 hours, and then
to clean the site daily, as prescribed, and use antibiotic ointment as
prescribed
DIAGNOSTIC TESTS
DIAGNOSTIC TESTS
B. Skin cultures
1. Description
a. Noninvasive procedure
b. A small skin culture sample is
obtained, using a sterile
applicator and the appropriate
type of culture tube (bacterial
or viral)
c. Viral culture is placed
immediately on ice
d. Sample is sent to laboratory to
identify an existing organism
DIAGNOSTIC TESTS
B. Skin cultures
1. Implementation:
Obtain skin culture
samples prior to
instituting antibiotic
therapy
2. Implementation
postprocedure: Send
skin culture sample
to the laboratory
 DIAGNOSTIC TESTS
C. Wood’s light
examination
1. Description: Skin is viewed under
ultraviolet light through a special
glass (Wood’s glass) to identify
superficial infections of the skin
2. Implementation preprocedure:
Darken room prior to the
examination
3. Implementation postprocedure:
Assist the client during adjustment
from the darkened room
DIAGNOSTIC TESTS
 DIAGNOSTIC TESTS
D. Skin testing
1. Description
a. The administration of an allergen to the skin’s surface or into the dermis
b. Administered by patch, scratch, or intradermal techniques
DIAGNOSTIC TESTS
1. Implementation
preprocedure
a. Discontinue systemic
corticosteroids or
antihistamine therapy for
48 hours prior to the test,
as prescribed
b. Obtain informed consent
c. Have resuscitation
equipment available if a
scratch test is performed,
as it may induce an
anaphylactic reaction
Nursing Assessment
History:
 presence of skin lesions
 duration; speed of spread
 associated symptoms
 occupation
 medications used
 allergies
 immediate environment (presence of animals,
plants, infections)
Physical Examination
 Color- deviations from the normal range
within the individual’s race
 Skin temperature- regulated by
vasoconstriction or vasodilation
 Moisture- dry, moist or oily
 Elasticity, Mobility, and Turgor
 Texture of skin
 SKIN
INFECTIONS
BACTERIAL Skin Infections
 Impetigo
Caused by staphylococci,
streptococci or multiple
bacteria
Most frequently involved
areas are face, hand, neck and
extremities
More common among
children
Impetigo
Clinical Manifestations
Small, red macules
becoming discrete,
thin walled vesicles that
rupture and covered with
honey-yellow crust
 Medical Management
maintain proper hygiene
topical antibiotics (3x daily) or systemic
antibiotics are prescribed
(mupirocin, retapamulin, and fusidic acid)

Nursing Intervention
Prevent spread of the disease- use of personal towels;
wash hands
Use compresses of Burow’s solution to remove the crusts
to allow faster healing; dry by exposure to air
 Folliculitis
Infection of the hair follicle of different degrees
Staphylococcus is the main pathogenic
organism

Most common in back of neck , armpits, axillae or buttocks

Folliculitis
 Folliculitis
Tests might include:
 Scraping of the skin to look for yeast under the microscope
 Obtaining a swab for culture to determine the cause of infection
A dermatologist can help :
 Control your folliculitis
 Avoid scarring or other damage to the skin
 Make scars less noticeable
 Folliculitis
Medications
 Lotions, gels or pills to control bacterial infection. For mild
infection caused by bacteria
 Creams, shampoos or pills to fight fungal infections. Antifungals
are for infections caused by yeast rather than bacteria.
 Creams or pills to calm inflammation.
Furuncles (Boils): deep bacterial
inflammation of a hair follicle
Signs and Symptoms
 A painful, red bump that starts out small and can enlarge to more than 2
inches (5 centimeters)
 Reddish or purplish, swollen skin around the bump
 An increase in the size of the bump over a few days as it fills with pus
 Development of a yellow-white tip that eventually ruptures and allows the
pus to drain out
Carbuncles- A carbuncle is a cluster of boils that form a
connected area of infection. Compared with single boils,
carbuncles cause a deeper and more severe infection and are
more likely to leave a scar.
Risk Factors:

Close contact with a person who has a staph infection.

Diabetes. This disease can make it more difficult for the body to
fight infection, including bacterial infections of your skin.
Other skin conditions. Because they damage your skin's
protective barrier, skin problems, such as acne and eczema, make
pt more susceptible to boils and carbuncles.
Compromised immunity.
Prevention
Wash your hands regularly with mild soap. Or use an alcohol-
based hand rub often. Careful hand-washing is your best defense
against germs.
Keep wounds covered. Keep cuts and abrasions clean and covered
with sterile, dry bandages until they heal.
Avoid sharing personal items. Don't share towels, sheets, razors,
clothing, athletic equipment and other personal items. Staph
infections can spread via objects, as well as from person to person.
If you have a cut or sore, wash your towels and linens using
detergent and hot water with added bleach, and dry them in a hot
dryer.
Treatment
Incision and drainage. Your doctor may drain a large boil or
carbuncle by making an incision in it. Deep infections that can't be
completely drained may be packed with sterile gauze to help soak up
and remove additional pus.
Antibiotics.

Self care
Warm compresses. Apply a warm washcloth or compress to the
affected area several times a day, for about 10 minutes each time.
This helps the boil rupture and drain more quickly.

Never squeeze or lance a boil yourself. This can spread the

infection.

Prevent contamination. Wash your hands thoroughly after treating

a boil. Also, launder clothing, towels or compresses that have
touched the infected area, especially if you have recurrent infections.
Viral Infections
Herpes Zoster
(Shingles)
caused by varicella zoster virus
painful vesicular eruption along area
of distribution of sensory nerves
from one or more posterior ganglia
**reactivation of latent varicella virus
and reflects lowered immunity
Viral Infections
Symptoms
 Pain, burning or tingling
 Sensitivity to touch
 A red rash that begins a few days after the pain
 Fluid-filled blisters that break open and crust over
 Itching

Some people also experience:

 Fever
 Headache
 Sensitivity to light
 Fatigue

***Pain is usually the first symptom of shingles. For some people, the pain can be
intense. Depending on the location of the pain, it can sometimes be mistaken for
problems with the heart, lungs or kidneys. Some people experience shingles pain
without ever developing the rash.
Complications
 Complications from shingles can include:
 Postherpetic neuralgia. For some people, shingles pain
continues long after the blisters have cleared.
 Vision loss. Shingles in or around an eye (ophthalmic shingles)
can cause painful eye infections that may result in vision loss.
 Neurological problems. Shingles may cause inflammation of
the brain (encephalitis), facial paralysis, or problems with
hearing or balance.
 Skin infections. If shingles blisters aren't properly treated,
bacterial skin infections may develop.
Diagnosis: Culture
Medical Management
No treatment unless immunosuppressed,
treatment is given-Acyclovir (Zovirax)
Analgesic for pain relief

Shingles can cause severe pain, health care provider also may prescribe:
 Capsaicin topical patch (Qutenza)
 Anticonvulsants, such as gabapentin (Neurontin, Gralise, Horizant)
 Tricyclic antidepressants, such as amitriptyline
 Numbing agents, such as lidocaine, in the form of a cream, gel, spray or
skin patch
 An injection including corticosteroids and local anesthetics
Prevention
 A shingles vaccine may help prevent shingles. People who are
eligible should get the Shingrix vaccine,

Nursing Management
Isolate patient
Administer medications
Avoid scratching or rubbing area
Wear lightweight, loose cotton clothing
Herpes Simplex
 2 types:
Herpes Simplex
Type 1- orolabial
most common type
causes burning,
tingling, and itching;
followed by tiny vesicle
 Herpes Simplex
 Herpes Simplex
Type 2 - genital
area
transmitted
primarily through
sexual contact;
lesions are painful
and frequently
crack open

Genital herpes is a common sexually transmitted infection (STI). The

herpes simplex virus (HSV) causes genital herpes. Genital herpes
can often be spread by skin-to-skin contact during sexual activity.
Manifestations
 painful grouped vesicles
accompanied
by systemic symptoms

Complications:
 herpetic whitlow
 fetal anomalies
 eczema herpeticum
Manifestions:
 Pain or itching around the genitals
 Small bumps or blisters around the genitals, anus or mouth
 Painful ulcers that form when blisters rupture and ooze or bleed
 Scabs that form as the ulcers heal
 Painful urination
 Discharge from the urethra, the tube that releases urine from the body
 Discharge from the vagina
Herpetic Whitlow
Causative agent: HSV
2-20 days incubation
Clinical manifestations:
pain, erythema, vesicles, crusting,
desquamation
Heals in 2-3 weeks
Infectious for 20 days
Conservative
treatment
Eczema herpeticum
 Is diagnosed clinically
when a patient with
known atopic
dermatitis presents with
an acute eruption of
painful, monomorphic
clustered vesicles
associated with fever and
malaise.
 Viral infection can be
confirmed by viral swabs
taken by scraping the
base of a fresh blister.
Eczema herpeticum
Treatment
 Treatment for recurrent episodes is most effective when started
within 48 hours of when symptoms begin.
 Antiviral medicines commonly given include acyclovir,
famciclovir and valacyclovir.
 Taking a lower daily dose of one of these medicines can also
decrease how often symptoms occur (‘outbreaks’).
 Fungal Infection
 Tinea
Infection -
RINGWORM
Types:
Tinea Pedis – Foot

 Tinea corporis -
ringworm of the
body
Fungal Infection
 Tinea Capitis-scalp

 Tinea Cruris –
 groin
Fungal Infection

Tinea Unguium – nails

Tinea corporis
Ringworm of the body (tinea corporis) is a rash caused by a fungal infection.

It's usually an itchy, circular rash with clearer skin in the middle.

Symptoms
 Signs and symptoms of ringworm may include:
 A scaly ring-shaped area, typically on the buttocks, trunk, arms and legs
 Itchiness
 A clear or scaly area inside the ring, perhaps with a scattering of bumps whose color
ranges from red on white skin to reddish, purplish, brown or gray on black and brown
skin
 Slightly raised, expanding rings
 A round, flat patch of itchy skin
 Overlapping rings
Causes
Ringworm is a contagious fungal infection caused by common mold-like parasites that liv
on the cells in the outer layer of your skin. It can be spread in the following ways:
 Human to human.
 Animal to human.
 Object to human.
 Soil to human. (rare)
Management
Tinea Pedis
*Soaks of Burow’s solution or potassium
permanganate solution: remove the crusts, scales,
and debris & reduce inflammation
*Topical antifungal agents: miconazole, clotrimazole
*Keep feet dry as possible!

Tinea Corporis
*Topical/oral antifungal agents: Itraconazole,
fluconazole,
*Use clean towel and washcloth daily
Prevention
Ringworm is difficult to prevent. The fungus that causes it is common, and the
condition is contagious even before symptoms appear. Take these steps to reduce
your risk of ringworm:
 Educate. Be aware of the risk of ringworm from infected people or pets.
 Keep clean. Wash hands often. Keep shared areas clean, especially in schools, child
care centers, gyms and locker rooms. If participated in contact sports, shower right
after practice or a match and keep uniform and gear clean.
 Stay cool and dry. Don't wear thick clothing for long periods of time in warm,
humid weather. Avoid excessive sweating.
 Avoid infected animals. The infection often looks like a patch of skin where fur is
missing.
 Don't share personal items. Don't let others use clothing, towels, hairbrushes,
sports gear or other personal items. And don't borrow such things.
Treatment
 antifungal medications — such as a lotion, cream or ointment that you apply to the
affected skin.

Self care
 For a mild case of ringworm, try these self-care tips.
 Keep the affected area clean and dry.
 Apply an over-the-counter antifungal lotion, cream or ointment such as clotrimazole
(Lotrimin AF) or terbinafine (Lamisil AT) as directed on the packaging.
Parasitic Infections
Pediculosis - caused
by Pediculus humanus louse

Types:
Pediculosis Capitis – scalp
Peduculosis

Pediculosis corporis – body

 Pediculosis pubis- genital area
Medical management
Lindane (Kwell)- applied on infested and hairy areas.
5% Permethrin (Elimite)
Antipruritics
Systemic antibiotics and topical corticosteroids
It is removed after 8 hours by thorough washing.
May be repeated after 1 week.

Nursing Intervention
 Prevent the spread of infection
 Treat all family members
Scabies
caused by a mite
called Sarcoptes scabiei
Found in people living in
substandard living condition
 Not an infection but an INFESTATION

Spread thru direct

 physical contact
 Scabies is an itchy skin rash caused by a tiny burrowing mite called Sarcoptes
scabiei. Intense itching occurs in the area where the mite burrows. The need to
scratch may be stronger at night.
 Scabies is contagious and can spread quickly through close person-to-person
contact in a family, child care group, school class, nursing home or prison.
Because scabies spreads so easily, health care providers often recommend
treating the entire family or any close contacts.
 Clinical Manifestation

Severe pruritic, small,

raised burrows. May be
red or brown threadlike
lesions
Most common sites:
between fingers, wrists,
extensor surfaces of
elbows, around nipples,
axillary folds, groin
Medical management
Take warm, soapy bath or shower to remove the
scaling debris from the crusts
Lindane (Kwell) – can cause neurotoxicity; not
safe for infants, pregnant women or in any
patient with wide spread excoriations and open
skin.
Crotamiton (Eurax)
Permethrin 5% cream- highly effective and safe
Oral antihistamines: help control itching
 Nursing Implementation
Treat all family members
Procedure for Lindane (Kwell):
(1)apply a thin layer over the entire
body from neck down
(2) wash off in 8-12 hours
(3) give a second treatment in 24 hours if prescribed.

Wash underclothing and bed and bath linens in hot water on the day of
treatment; dry in dryer or iron after dry; change linens daily.
Atopic Dermatitis

Type 1 immediate
hypersensitivity disorder
Incidence highest in infants
& children
Pruritus & hyperirritability
of the skin are the most
consistent features
 Atopic Dermatitis
Related to large
amounts of histamine
in the skin
Lesions develop
secondary to the
trauma of scratching
Remissions and
exacerbations from
adolescence to age
20
Management
Wear cotton fabrics, wash with mild detergent, humidifying dry heat
in winter
Antihistamines: diphenhydramine/chlorpheniramine maleate
Avoiding animals, dust, sprays and perfumes and other allergens
Keep skin moisturized
Topical corticosteroids
antibiotics as prescribed
Non-infectious Inflammatory
Dermatoses
Psoriasis

 Chronic, recurrent
 AUTOIIMUNE
 GENETICS
 NOT CONTAGIOUS!!
 Abnormally produced
Epidermal cells at 6x to
9x faster than normal
 Affects about 2% of the
population; European
ancestry.
Psoriasis is a skin disease that causes a rash with itchy, scaly patches, most
commonly on the knees, elbows, trunk and scalp.

Psoriasis is a common, long-term (chronic) disease with no cure. It can be

painful, interfere with sleep and make it hard to concentrate. The
condition tends to go through cycles, flaring for a few weeks or months,
then subsiding for a while. Common triggers in people with a genetic
predisposition to psoriasis include infections, cuts or burns, and certain
medications.
Causes
 Psoriasis is thought to be an immune system problem that causes skin cells to
grow faster than usual. In the most common type of psoriasis, known as plaque
psoriasis, this rapid turnover of cells results in dry, scaly patches.

Psoriasis triggers
 Infections, such as strep throat or skin infections
 Weather, especially cold, dry conditions
 Injury to the skin, such as a cut or scrape, a bug bite, or a severe sunburn
 Smoking and exposure to secondhand smoke
 Heavy alcohol consumption
 Certain medications — including lithium, high blood pressure drugs and
antimalarial drugs
 Rapid withdrawal of oral or injected corticosteroids
Common signs and symptoms of psoriasis include:
 A patchy rash that varies widely in how it looks from person to person, ranging
from spots of dandruff-like scaling to major eruptions over much of the body
 Rashes that vary in color, tending to be shades of purple with gray scale on brown
or Black skin and pink or red with silver scale on white skin
 Small scaling spots (commonly seen in children)
 Dry, cracked skin that may bleed
 Itching, burning or soreness
 Cyclic rashes that flare for a few weeks or months and then subside
 Drug Therapy
 Topical corticosteroids: Aristocort, Kenalog, Lidex, Psorcon
 Topical nonsteroidals: Retinoids such as
tazarotene, Vitamin D3 derivatives
Coal tar products
 Medicated shampoos
 Intralesional therapy: Kenalog, Fluoroplex
 Systemic therapy: Methotrexate; Hydroxyurea
 Photochemotherapy: UVA or UVB light;
 (combines UVA light with oral psoralens, or topical tripsoralen)
Nursing Management
1. Education
Drug Therapy
2. Advise patient not to pick at or scratch
affected areas.
3. Teach patient measures to prevent dry skin
Avoid too-frequent washing
Use warm, not hot water
Pat dry affected areas; avoid rubbing
Use emollients to moisturize skin.
4. Encourage verbalization of feelings.
5. Introduce successful coping strategies
 Frostbite

 Damage to tissues and

blood vessels as a result
of prolonged exposure to cold
􀂋 Fingers, toes, nose, and
ears are often affected

Manifestation
Numbness
Paresthesia
Pallor
Severe pain, swelling,
erythema, and blistering
occur once the client is in
a warm environment
Necrosis and gangrene
 Intervention
Handle the tissues gently
Rewarm the affected part rapidly and continuously with a warm water
bath (90 to 107 F) for 15 to 20 minutes or until skin flushing occurs
Avoid slow thawing, interrupted periods of warmth, or massage (tissue
damage)
Do not debride blisters
Leave area exposed initially for continued assessment
Apply bulky dressings, to permit drainage and provide
C A R E O F PAT I E N T S
RENAL DISORDE
 RENAL FUNCTIONS
7 functions of the kidneys
A - controlling ACID-base balance
W - controlling WATER balance
E - maintaining ELECTROLYTE balance
T - removing TOXINS and waste products from the body
B - controlling BLOOD PRESSURE
E - producing the hormone ERYTHROPOIETIN
D - activating vitamin D
URINARY TRACT
INFECTIONS
CYSTITIS – I N F L A M M AT I O N O F B L A D D E R D / T B A C T E R I A L I N F E C T I O N
PREDISPOSING FACTORS:
• High risk: women
• Microbial invasion (E.Coli)
• Increased estrogen levels, estrogen
therapy
• Allergens/irritants
• Poor perineal hygiene
• Synthetic underwear and pantyhose
• Wet bathing suits
• Sexual intercourse
• Bladder distention/renal stones
• Incontinence
• Indwelling foley catheter
CYSTITIS – I N F L A M M AT I O N O F B L A D D E R D / T B A C T E R I A L I N F E C T I O N

MANIFESTATIONS:
• Urinary frequency and urgency
• Flank pain
• Fever, chills, anorexia, generalized body
malaise
• Dysuria (painful urination), bladder spasms
• Burning sensation upon urination
• Hematuria, cloudy, dark, foul-smelling urine
CYSTITIS

DIAGNOSTIC EXAMINATIONS
• Urine culture and sensitivity – (+) E. Coli 90
• Urinalysis
– Increased WBC
– Increased CHON
– Increased pus cells
CYSTITIS
NURSING
MANAGEMENT
• Force fluids (2-3
liters/day)
• Provide warm sitz bath
to promote comfort
• Provide acid-ash diet:
cranberries, grape
juice, plums
CYSTITIS
NURSING
MANAGEMENT
• Strict asepsis in foley
catheter insertion,
maintain close system
• Meticulous perineal
care
• Avoid caffeine and
alcohol
CYSTITIS
NURSING MANAGEMENT
• Monitor for gross hematuria, color, odor of urine
• Administer medicines as ordered:
– Penicillins
– Cephalosphorins (SE: Nausea Headache)
– Tetracycline (teeth stains, photosensitivity)
– Sulfonamides: Cotrimoxazole (Bactrim), Sulfisoxazol
– Nitrofurantoin (Macrodantin)
– Pyridium: decreases pain, promotes relaxation of sph
CYSTITIS
NURSING MANAGEMENT
• DISCHARGE TEACHING: importance of hydration
• VOID after SEXUAL INTERCOURSE
• Instruct female to:
– Proper perineal hygiene
– Front to back cleaning
– Void every 2-3 hours (especially pregnant women)
– Bubble bath
– (-) talcum powder, perfume
CYSTITIS
NURSING MANAGEMENT
• Wear cotton pants, avoid tight clothes or pantyhose w
• Avoid sitting in a wet bathing suit for prolonged peri
• Use estrogen vaginal creams to restores pH, use wate
lubricants for coitus (esp. for menopausal women)
PYELONEPHRITIS - A C U T E O R C H R O N I C I N F L A M M AT I O N O F R
T O T U B U L A R D E S T R U C T I O N , I N T E R N A L A B S C E S S A N D R E N A L FA I L U R E .

• PREDISPOSING FACTORS
• Microbial invasion : E.
coli/Streptococcus
• Urinary retention/stagnation
• Pregnancy
• Diabetes mellitus
• Exposure to renal toxins: use of
nephrotoxic agents
PYELONEPHRITIS
MANIFESTATIONS:
• ACUTE:
– Urinary frequency and urgency
– Costovertebral angle pain and tenderness
– Fever and chills, anorexia, body malaise
– Burning upon urination
– Dysuria, nocturia, hematuria
• CHRONIC
– fatigue and or weakness
– Weight loss
– Polyuria
– Polydypsia
– HPN
PYELONEPHRITIS
NURSING MANAGEMENT:
• CBR especially during acute attack
• Forced fluids
• Provide an acid ash diet
• Provide warm sitz bath for comfort
• Administer medications:
– NITROFURANTOIN
– PYRIDIUM (urinary analgesics)
– PREVENT COMPLICATIONS : renal
failure
NEPHROLITHIASIS
• Formation of stones elsewhere in the urinary tract
NEPHROLITHIASIS
• TYPES OF STONES
• Calcium
• Oxalate
• Uric acid
PREDISPOSING FACTORS
– High calcium and oxalate diet
– Hereditary
– Hyperparathyroidism (hypercalcemia)
– Use of diuretics, dehydration
– Obstruction and urinary stasis, UTI,
prolonged catheterization
– Obesity
– Sedentary lifestyle, prolonged
immobility
NEPHROLITHIASIS
• DIAGNOSTIC PROCEDURES
• Urinalysis – (+)RBC, WBC, Pus
• KUB – reveal site or location of
stones
• Stone analysis: reveals
composition of stone
• Cystoscopy exam: urinary
obstruction
• IVP: reveals obstruction
NEPHROLITHIASIS
NEPHROLITHIASIS
• MANIFESTATIONS:
• Pain – obstruction, tissue trauma, hemorrhage and
• Renal colic (dull, aching or sudden sharp severe pa
lumbar region radiating to the testicles (M) and bla
• Ureteral colic radiating to the genitalia
• Nausea vomiting, pallor, diaphoresis, cool, moist s
• Alternating urinary frequency and retention
• Signs and symptoms of UTI
NEPHROLITHIASIS
• DIAGNOSTIC PROCEDURES:
• KUB ultrasound
• CT scan
• Renal ultrasound – LOCATES STONES
• IVP – location and composition of stones
• Cystoscopy – urinary obstruction
• UA – increased wbc, rbc, bacteria
• Stone analysis: type, no. and composition
NEPHROLITHIASIS
• NURSING INTERVENTIONS:
• Monitor VS, IO, signs and symptoms of infection
• Force fluids
• Strain all urine with gauze, WOF presence of stone
lab for analysis
• Warm sitz bath, warm compresses on flank area
• Turn immobilized patient every 2 hours
• Administer narcotic analgesics, antibiotics, allopur
NEPHROLITHIASIS
NEPHROLITHIASIS
• CALCIUM PHOSPHATE STONES
– Acid ash, decrease calcium, decrease
phosphate, vitamin D
• CALCIUM OXALATE
– Acid ash, decrease calcium, decrease
oxalate (tea, almonds, cashews,
chocolate, cocoa, beans, spinach and
rhubarb)
• STRUVITE/TRIPLE PHOSPHATE (Mg
& NH3)
– Caused by urea splitting by bacteria
– Acid ash, decrease phosphate (dairy
products, red and organ meats, whole
grains)
NEPHROLITHIASIS
• URIC ACID
– Alkaline ash, decrease
purines (organ meats,
gravies, red wines, sardines)
• CYSTINE
– Alkaline ash, decrease
methionine (AA that forms
cystine): meat, milk, cheese,
eggs
NEPHROLITHIASIS
SURGICAL
INTERVENTIONS:
• Nephrectomy
• Cystoscopy
• EXTRACORPOREAL
SHOCKWAVE
LITHOTRIPSY (ESWL)
• URETEROLITHOTOMY
ACUTE RENAL FAILURE (ARF)
- S U D D E N I N A B I L I T Y O F T H E K I D N E Y S T O E X C R ET E N I T R O G E N O U S WA S T E P R O
AZOTEMIA

PREDISPOSING FACTORS:
• PRE RENAL: involves decrease in GFR (n=125
– Hemorrhage
– Shock
– Chronic diarrhea
– CHF
– Hypotension
– septicemia
ACUTE RENAL FAILURE (ARF)
- S U D D E N I N A B I L I T Y O F T H E K I D N E Y S T O E X C R ET E N I T R O G E N O U S WA S T E P R O
AZOTEMIA

PREDISPOSING FACTORS:
• INTRA RENAL: involves renal pathology
– Pyelonephritis
– DM
– AGN
– Acute tubular necrosis: common SE post hemoly
ACUTE RENAL FAILURE (ARF)
- S U D D E N I N A B I L I T Y O F T H E K I D N E Y S T O E X C R ET E N I T R O G E N O U S WA S T E P R O
AZOTEMIA

• POST RENAL: (+) mechanical obstruction

• BPH
• Nephro/urolithiasis
• Tumor
• Urinary strictures
A C U T E R E N A L FA I L U R E ( A R F )
A C U T E R E N A L FA I L U R E ( A R F )
CHRONIC RENAL FAILURE (CRF)
IRREVERSIBLE LOSS OF KIDNEY FUNCTION

• PREDISPOSING
FACTORS
– DM and HPN
(common causes)
– Recurrent
pyelonephritis
– Exposure to renal
toxins
– Tumor
RENAL TOXINS
CHRONIC RENAL FAILURE ( ARF)

• STAGES:
• Diminished renal reserve volume
– Asymptomatic, normal BUN and CREA
• Renal insufficiency
• End stage renal disease (ESRD)
– Presence of oliguria, azotemia
CHRONIC RENAL FAILURE ( ARF)

• MANIFESTATIONS:
• URO:
– Azotemia (elevated BUN and creatinine)
– Oliguria
– Nocturia
– Hematuria
– dysuria
CHRONIC RENAL FAILURE ( ARF)

• MANIFESTATIONS:
• NEURO:
– Lethargy
– Headache
– Disorientation, confusion, restlessness
– Memory impairment
– Decreased LOC
CHRONIC RENAL FAILURE ( ARF)

• MANIFESTATIONS:
• RESPIRATORY:
– Depressed or diminished cough reflex
– Kussmaul’s respiration
• HEMATOLOGY:
– Anemia
– Leukopenia
– Bleeding tendencies (thrombocytopenia)
– All blood cells decreased
– Increased susceptibility to infection
CHRONIC RENAL FAILURE ( ARF)

• MANIFESTATIONS:
• CARDIOVASCULAR CHANGES
– Pulmonary hypertension
– CHF
– pericarditis
• GI DISTRESS
– Anorexia
– Nausea and vomiting
– Diarrhea, constipation
– Stomatitis
– Uremic fetor
CHRONIC RENAL FAILURE ( ARF)

• MANIFESTATIONS:
• INTEGUMENTARY:
– Pruritus
– Uremic frost

• METABOLIC/ELECTROLYTE IMBALANCE
– Hyperkalemia
– Hyperphosphatemia
– Metabolic acidosis
CHRONIC RENAL FAILURE ( ARF)
CHRONIC RENAL FAILURE ( ARF)
CHRONIC RENAL FAILURE (CRF)

• NURSING MANAGEMENT
• Enforce CBR
• Administration of O2 as ordered
• High CHO diet, low CHON, fats; high vitamin a
• Provide meticulous skin care
– Wash with warm water
– Soap irritates and dries skin
CHRONIC RENAL FAILURE ( ARF)

• ADMINISTER MEDICATIONS
– Anti hypertensive medications: monitor orthost
hypotension
– SODIUM BICARBONATE
– Kayexalate enema
– Hematinics
– Antibiotics
– Supplementary vitamins and minerals
– Phosphate binders
– Calcium gluconate
CHRONIC RENAL FAILURE ( ARF)

• ASSIST IN HEMODIALYSIS

fistula
CHRONIC RENAL FAILURE ( ARF)

HEMODIAL
• Process of c
• Involves DI
particles fr
compartme
across a SM
flows throu
compartme
and the dia
fluid comp
CHRONIC RENAL FAILURE ( ARF)

HEMODIALYSIS
• Cleanses the blood of accumulated waste products
• Removes the by-products of protein metabolism such
creatinine and uric acid from the blood
• Removes excess body fluids
• Maintains or restores the buffer system of the body
• Corrects electrolyte levels in the body
CHRONIC RENAL FAILURE ( ARF)
HEMODIALYS
CHRONIC RENAL FAILURE ( ARF)

• SECURE consent and explain procedure to client

• Maintain strict aseptic technique
• Obtain baseline data – before and every 30 minutes
procedure
• Monitor: vital signs, weight, blood exams (secure a
procedure), check input and output
• Have client void pre-procedure
• Inform client about bleeding (blood is heparinized)
• Assess the patency of the blood access device before
after dialysis
CHRONIC RENAL FAILURE ( ARF)

• MONITOR FOR SIGNS OF COMPLICATIONS:

• Bleeding
• Embolism
• Disequilibrium syndrome
• Septicemia
• Shock
• Hepatitis
• Avoid BP taking, phlebotomy, IV meds at the site o
extraction to prevent compression
CHRONIC RENAL FAILURE ( ARF)

• MONITOR FOR SIGNS OF COMPLICATIONS:

• Palpate for thrills, auscultate for bruits
• Instruct that minimal bleeding is expected since blo
heparinized
• Avoid use vasodilators, sedatives and tranquilizers
hypotension unless ordered.
• Withhold medications that can be removed by dialy
ADEK, digoxin, some antibiotics)
• Prepare at bedside bulldog clips to prevent embolis
• Auscultate for bruits and palpate for thrills (if + pa
END
 NURSING
MANAGEMENT OF
SHOCK
SHOCK
• Condition in which widespread
perfusion to the cells is inadequate to
deliver oxygen and nutrients to support
vital organs and cellular function.
(VonRueden, Bolton & Vary, 2008)
• A complex, life threatening condition or
syndrome characterized by inadequate
blood flow to the tissues and cells of the
body.
WHAT HAPPENS IN SHOCK?
WHAT HAPPENS IN SHOCK?
INITIAL STAGE
• The cardiac output is insufficient
to supply the normal nutritional
needs of tissues but not low
enough to cause serious symptoms
COMPENSATORY STAGE
• The cardiac output is reduced further but
due to compensatory vasoconstriction,
the BP tends to remain within the
normal range. Blood flow to the skin
and kidney decrease while blood flow to
CNS and myocardium is maintained.
PROGRESSIVE STAGE
• The unfavorable change become more and more
apparent – falling BP, increase vasoconstriction,
increased heart rate and oliguria.
• If compensatory mechanisms are unable to cope
with the reduced output, shock becomes
progressively more severe and passed onto the
next stage.
IRREVERSIBLE STAGE
• In this stage of shock, no type of therapy
can save the patient’s life – BP
decreases, blood volume can be normal
in this stage. Fluid transfusion may
restore BP only temporarily. BP still
declines until eventually DEATH occurs.
CLINICAL FINDINGS
IN SHOCK
MANIFESTATIONS AMONG ELDERLY
HYPOVOLEMIC SHOCK
• Caused by reduction of
fluid 15% to 30% of
blood (750- 1500ml of
blood in 70kg person).
Loss of blood externally
by blooding or shifts of
internal fluids by
dehydration AND severe
edema
 CAUSES OF HYPOVOLEMIC
SHOCK
• SEVERE BLEEDING
• SEVERE PERSISTENT
VOMITING
• SEVERE DIARRHEA
• SEVERE EDEMA or ASCITES
• DIURESIS
• SEVERE BURNS
• INADEQUATE FLUID
PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK
CLINICAL MANIFESTATIONS OF HYPOVOLEMIC SHOCK

• Hypotension
• Cold clammy skin
• Pallor
• Tachycardia
• Tachypnea
• Restlessness
• Anxiety
• Weakness
• Altered sensorium
• Oliguria <20 ml/hr – possibly in progressive stages
CLINICAL MANIFESTATIONS OF HYPOVOLEMIC SHOCK

• Metabolic acidosis
• Nausea, vomiting thirst
• Irritability
• Shallow respirations
• Increased serum electrolyte, blood glucose,
serum creatinine, sodium, potassium
• Unconsciousness and unresponsive to pain
 MANAGEMENT OF
HYPOVOLEMIC SHOCK

•Treatment of underlying cause (stop bleeding by

pressure of surgery for internal organs), medication to
treat diarrhea.
•Fluid and blood replacement: use large vein and two IV
lines, use CRYSTALLOID solutions or albumin, blood
products (PRBCs for hemoglobin to carry O2 to tissues).
•Modified Trendelendburg position
•Pharmacologic therapy: vasopressors, antimotility,
antiemetic
MANAGEMENT OF HYPOVOLEMIC SHOCK
 MANAGEMENT OF
HYPOVOLEMIC SHOCK

•Administering blood and

fluids safely
•Oxygenation delivery
•Comfort and rest provided
to patient
 CARDIOGENIC SHOCK
• occurs when the heart’s ability to pump
blood is impaired.
• Results from inadequate perfusion of body
tissue with oxygenated blood that is
insufficient to sustain life. CARDIAC
OUTPUT is decreased
 CAUSES OF CARDIOGENIC
SHOCK
• Acute myocardial infarction
• Congestive heart failure
• Pulmonary embolism
• Cardiac tamponade
• Cardiomyopathy
CLINICAL MANIFESTATIONS OF CARDIOGENIC SHOCK

• Same with hypovolemic shock

• DYSRHYTHMIA
• Chest pain
• Respiratory distress
• Ventricular failure
• Mechanical complication during
ventricular septal rupture
 MANAGEMENT OF
CARDIOGENIC SHOCK

• Oxygen delivery
• Thrombolytic therapy
• Correction of acidosis
• Antidysrhythmic agents
• Pain management
• Hemodynamic monitoring
• ECG monitoring
• IV fluid administration
• Reduce anxiety and ensure comfort
SEPTIC SHOCK
• Most common type of
circulatory shock caused
by widespread infection
• Despite the increased
sophistication of
antibiotic therapy, the
incidence of septic shock
has continued to rise
during the past 60 years.
 CAUSES OF SEPTIC SHOCK
• Invasive procedures
• Older population and
resistance to antibiotics
• Virus, fungi, gram
negative bacteria
• Chronic diseases: DM,
AIDS
• Improper wound care
and management
• Severe burns
• UTI, abortion
CLINICAL MANIFESTATIONS
OF SEPSIS
CLINICAL MANIFESTATIONS
OF SEPSIS
 CLINICAL MANIFESTATIONS
SEPTIC SHOCK

• HYPERTHERMIA
• Severe headache
• Anuria
• Respiratory distress
• Decreased cardiac output
• Hypotension
• Skin cold and pale
• Multiple organ failure
EARLY TREATMENT OF
SEPSIS PATIENTS
 MANAGEMENT OF
PATIENTS IN SEPTIC SHOCK

• Fluid replacement therapy

• Nutrition therapy (enteral nutrition possibly)
• Use aseptic technique
• Monitor injection sites for infection
• Assess culture and sensitivity from any sites
• Administer antibiotic therapy
• Assess clinical manifestations of infection
 NEUROGENIC SHOCK
• Inability of nervous system to control
dilation of blood vessels.
• Neurogenic shock results from generalized
vasodilation and loss of vasomotor tone
due to
• Massive increase in vascular capacity
• Pooling of blood in periphery
• Decreased venous return to heart
 PATHOLOGY OF
NEUROGENIC SHOCK

• Vasodilation occurs when loss of balance

between parasympathetic and sympathetic
stimulation
• Sympathetic stimulation causes
vasoconstriction
• BLOOD VOLUME is normal but
parasympathetic stimulation causes
vasodilation and fluid shifts occur
 CAUSES OF NEUROGENIC SHOCK
• Brain traumatic injury
• Brain damage
• Spinal cord injury
• Deep spinal anesthesia
• During lumbar puncture
• Severe pain, hypoglycemia,
emotional stress
• Drugs causing vasomotor
center depression
• Anti snake venom
CLINICAL MANIFESTATIONS OF
NEUROGENIC SHOCK

• Nervousness
• LOC changes
• Confusion
• Skin warm but dry
• Respiratory depression
• hypotension
 MANAGEMENT OF
NEUROGENIC SHOCK

• Control spinal cord injury clinical

manifestations
• Position patient carefully in spinal anesthesia
• Elevate HOB when using spinal anesthesia to
prevent agent from spreading to the brain
• Monitor patient closely for signs of internal
bleeding that could lead to hypovolemic shock
• Apply anti-embolic stocking and check for
lower extremity pain and tenderness/redness
 ANAPHYLACTIC SHOCK
• Occurs rapidly as a result of
antigen exposure or severe
allergic reaction.
• It is life threatening.
ANAPHYLACTIC SHOCK
ANAPHYLACTIC SHOCK
ANAPHYLACTIC SHOCK
 MANAGEMENT OF
ANAPHYLACTIC SHOCK

• Stop antibiotic/remove the cause

• Give epinephrine, antihistamine STAT
• Nebulize patient
• Infuse IV fluids
• Close monitoring for allergens
• Assess previous reaction and response
AN 82-YEAR-OLD MAN IS ADMITTED AFTER
BEING INVOLVED IN A MOTOR VEHICLE
COLLISION. HE HAS SEVERE CHEST AND
ABDOMINAL INJURIES. HIS HEAD AND
EXTREMITIES ARE ONLY MINIMALLY
TRAUMATIZED. HE UNDERGOES SURGERY FOR
A SPLENIC RUPTURE. AFTER EIGHT HOURS,
HE BECOMES HYPOTENSIVE AND FEBRILE,
AND IS INTUBATED BECAUSE OF
RESPIRATORY FAILURE. HE RAPIDLY
DEVELOPS DISSEMINATED INTRAVASCULAR
COAGULATION (DIC). WHICH OF THE
FOLLOWING IS THE MOST LIKELY DIAGNOSIS?
A. ANAPHYLACTIC SHOCK
B. CARDIOGENIC SHOCK
C. HYPOVOLEMIC SHOCK
D. NEUROGENIC SHOCK
E. SEPTIC SHOCK
THE CORRECT ANSWER IS E.

RATIONALE:
THE CLINICAL SETTING OF TRAUMA
PRODUCES THE OBVIOUS CAUSE OF
HEMORRHAGE FOR SHOCK, BUT YOU SHOULD
BE AWARE THAT THE DIFFERENTIAL MAY
ACTUALLY BE MORE COMPLEX AND INCLUDE
OTHER CAUSES AS WELL. IN THIS CASE,
ABDOMINAL TRAUMA AND SURGERY HAVE
PROBABLY INTRODUCED GUT ORGANISMS
INTO THE BLOODSTREAM, LEADING TO THE
DEVELOPMENT OF SEPTIC SHOCK SEVERAL
HOURS LATER.
•END
BURNS
compiled and prepared by
Dr. Franklin S. Casison
• Learning Objectives

At the end of the lecture, students will be a

1. Define, identify and assess BURN.
2. classify types of burn
3. compute for the percentage of burn
4. know and apply the nursing and medica
management for burns.
• BURN

- is an injury to the skin or other organic tis

primarily caused by heat or due to radiation,
radioactivity, electricity, friction or contact with
chemicals.
• Thermal (heat) burns occur when some or all o
in the skin or other tissues are destroyed by:
hot liquids (scalds)
hot solids (contact burns), or
flames (flame burns).
• Different Types of Burns:

- A burn injury usually results from an energy transfer to

a) Thermal burns: due to external heat sources which r
temperature of the skin and tissues and cause tissue
or charring. Hot metals, scalding liquids, steam, and
when coming in contact with the skin, can cause the
b) Radiation burns: due to prolonged exposure to ultra
of the sun, or to other sources of radiation such as x-
c) Chemical burns: due to strong acids, alkalies, deterg
solvents coming into contact with the skin and/or ey
d) Electrical burns: from electrical current, either altern
current (AC) or direct current (DC)
• Classifications of Burns:

- classified as first-, second-, or third-degree, depen

how deep and severe they penetrate the skin's surf

A. First-degree (superficial) burns

- affect only the epidermis, or outer layer of skin.
- burn site is red, painful, dry, and with no blisters.
- Example: Mild sunburn

* Long-term tissue damage is rare and usually cons

increase or decrease in the skin color.
• Classifications of Burns:

- classified as first-, second-, or third-degree, depen

how deep and severe they penetrate the skin's surf

A. First-degree (superficial) burns

- affect only the epidermis, or outer layer of skin.
- burn site is red, painful, dry, and with no blisters.
- Example: Mild sunburn

* Long-term tissue damage is rare and usually cons

increase or decrease in the skin color.
B. Second-degree -(partial thickness) burns or D
- burns involve the epidermis and part of the der
of skin.
- burn site: appears red, blistered, and may be sw
and painful.
C. Third-degree / Fourth-degree (full thickness
- burns destroy the epidermis and dermis.
- burns may also damage the underlying bones,
and tendons.
- burn site appears white or charred.
- no sensation in the area since the nerve endin
destroyed.
• Burns affecting 10 percent of a child's body and
affecting 15 to 20 percent of an adult's body ar
considered to be major injuries and require
hospitalization and extensive rehabilitation.
Assessment:
- thorough ABCD assessment,
- followed by a full head to toe and focused asses
vital to ensure clinical issues/deterioration are id
early and appropriate management initiated. (S
Acute management CPG for further details of b
assessment)
- Assessment of the pediatric patient with a burn
should occur on admission and regularly throug
- Detailed information regarding completion and
documentation of ABCD, head to toe and focus
assessments (Nursing Assessment Clinical Guid
A. Airway and Breathing
Assessment and monitoring of airway patency and brea
be carefully observed as patients at risk of inhalation bu
deteriorate up to 72 hours post burn injury, particularly
1. Sustained burns in an enclosed space (at risk due to
inhalation)
2. Have facial burns / Facial swelling
3. Singed nasal hairs
4. Blackened sputum
5. Stridor or hoarseness of voice
6. Respiratory distress/increased work of breathing.
B. Circulation
1. Children who sustain burns injuries are at increased
circulatory compromise due to significant fluid loss
these patients must be closely monitored for:
2. Signs and symptoms of hypovolemia / hypothermia
3. Other circulatory concerns include:
- Circumferential burns should be identified, monitored
compromise ( neurovascular observations nursing guid
affected area elevated where ever possible.
- Consider the need for an ECG and continuous cardiac
the burn is of electrical origin.
c. Pain assessment
Detailed information regarding pediatric pain assessm
located on the Pain Assessment Nursing Clinical Guide
Information regarding procedural pain management c
on the Procedural Pain Management Clinical Guideline
D. Wound assessment
a. Burn injuries can take up to 10 days to truly present
extent of injury so reassessment is vital.
b. As burn injuries heal accurate wound assessment wi
wound management is altered as needed to ensure
wound care continues to be delivered to the patient
c. Assessment of Total Body Surface Area (TBSA) burn
Lund Browder chart. Areas of erythema and superfic
not included in calculations of TBSA.
d. Assessment of depth of burn injury / wound healing
e. Accurate documentation of wound assessment shou
recorded.
• Calculation of Burned Area: Total Body S
Area (TBSA)
1. Wallace Rule of Nine (Wallace)
2. Lund and Browder Chart - most accurat
because it adjusts for age
NOTE: Superficial burns are not involved in
calculation.
Percentages:
• Calculation of Burned Area: Total Body Surface Area (TBSA)
1. Rule of 9’s
2. Wallace Rule of Nine
Lund Browder Chart
Burn symptoms
- vary depending on the severity or degree of the
- often worse during the first few hours or days a
burn.
Burn symptoms include:
1. Blisters.
2. Pain.
3. Swelling.
4. White or charred (black) skin.
5. Peeling skin.
BURN Diagnosis:
- involves estimating the percentage of the body
by the burn and its depth. Your provider may clas
burn as:
Minor: First- and second-degree burns that cove
10% of the body are considered minor and rarely
hospitalization.
Moderate: Second-degree burns that cover abou
the body are classified as moderate. Burns on th
feet, face or genitals can range from moderate to
Severe: Third-degree burns that cover more than
body are considered severe.
COMPLICATIONS:
A. Third-degree burns that are deep and affect a
portion of skin are very serious and can be life
threatening.
B. Even first- and second-degree burns can beco
infected and cause discoloration and scarring
degree burns don’t cause scarring.
Potential complications of third-degree burns inclu
Arrhythmia, or heart rhythm disturbances, caused
electrical burn.
Dehydration.
Disfiguring scars and contractures.
Edema (excess fluid and swelling in tissues).
Organ failure.
Pneumonia.
Seriously low blood pressure (hypotension): may
Severe infection that may lead to amputation or s
Nursing Diagnosis for BURN:
a) Impaired skin integrity
b) Risk for infection
c) Imbalanced nutrition
d) Impaired physical mobility
e) Disturbed body image
Collaborative Management:
A. First Aid
-an important initial aspect of care as it assists with
well as minimizing the progression of tissue damage
- is effective for up to three hours post time of injury
first aid was not initiated and it is still within the 3 ho
post burn injury, first aid should be completed as ou
prior to any wound care:
-The area of tissue damage should be cooled with co
water for 20 minutes.
-Ensure the unburnt areas of the patient are covered
prevent hypothermia.
B. Fluids
- Burn injuries greater than 10% TBSA and including
result in circulatory compromise secondary to fluid
damaged tissue, widespread vasodilation as well a
capillary permeability and fluid shifts (third spacin
- This can result in hypovolemia leading to burns sh
- Therefore it is vital that adequate fluid is administ
patient in combination with ongoing circulatory a
balance assessment.
- A Strict Fluid Balance must be maintained at all times
intake (both intravenous and oral) and strict measurem
output (weigh nappies, weigh pans/bottle, measure ID
- Fluid resuscitation is required in patients who have >1
and may need two large bore Intravenous cannulas ins
- Fluid resuscitation is calculated utilizing the modified
formula. Expected urine output is 1ml/kg/hr. unless oth
by the medical team.
- U&E’s should be monitored 8 hourly while patient is r
resuscitation.
- Fluid resuscitation rates will need to be adjusted to ac
the patients urine output.
- A Strict Fluid Balance must be maintained at all times
intake (both intravenous and oral) and strict measurem
output (weigh nappies, weigh pans/bottle, measure ID
- Fluid resuscitation is required in patients who have >1
and may need two large bore Intravenous cannulas ins
- Fluid resuscitation is calculated utilizing the modified
formula. Expected urine output is 1ml/kg/hr. unless oth
by the medical team.
- U&E’s should be monitored 8 hourly while patient is r
resuscitation.
- Fluid resuscitation rates will need to be adjusted to ac
the patients urine output.
C. Analgesia
- Initial and ongoing pain management is vital to en
comfort, maximize healing and minimize risk of me
trauma/post-traumatic stress.
- Initial pain relief should be administered immedia
an accurate pain assessment
- Pre-emptive analgesia may be necessary prior to r
positioning, physiotherapy and follow up outpatie
appointments.
- Burn pain experienced by patients is likely to incre
procedures such as dressing changes.
D. Burns dressing
Staff should adhere to the aseptic technique proc
aspects of wound care outlined below.
Removal of previous dressing
Removal of the previous dressing should not dam
healing burn wound and should be as atraumatic a
The use of an adhesive remover, normal saline or w
assist with gentle removal of previous dressings.
E. Wound Management
1) Clean the wound using a soft wipe with water, n
pH neutral soap or cetrimide (please note cetrim
be used on face or scalp). Enough pressure shou
to debride the damaged skin and remove exuda
and slough.
2) Consider the need for a wound swab and compl
necessary.
3) Debridement of any blisters present allows for w
assessment and appropriate dressing applicatio
4) The wound and surrounding skin should be dry b
application of the dressing.
Nurse Katee is caring for Adam, a 22-year-old client,
facility. Which nursing intervention would be approp
identifying nursing interventions aimed at promoting
preventing contractures? Select all that apply.
A. Clustering activities to allow uninterrupted perio
B. Maintaining correct body alignment at all times.
C. Monitoring intake and output, using a urometer i
D. Using a footboard or pillows to keep feet in the c
position.
E. Performing active and passive range-of-motion e
F. Weighing the client daily at the same time and in
clothes.
Nurse K is caring for Black Adam, a 22-year-old clien
term facility. Which nursing intervention would be a
when identifying nursing interventions aimed at pro
preventing contractures? Select all that apply.
A. Clustering activities to allow uninterrupted perio
B. Maintaining correct body alignment at all times.
C. Monitoring intake and output, using a urometer i
D. Using a footboard or pillows to keep feet in the c
position.
Correct Answers: B, D, & E
Correct body alignment, preventing foot drop, and r
motion exercises will help prevent contractures. Clu
activities will help promote adequate rest. Monitorin
output and weighing the client will help maintain flu
electrolyte balance.
Option A: Provide the patient with rest periods in be
activities. Consider energy-saving techniques. Rest p
essential to conserve energy. The patient must learn
his/her limitations.
Option B: Help the patient develop sitting bala
standing balance. This helps out in retraining n
pathways, promoting proprioception and mot
Keep limbs in functional alignment with one o
following: pillows, sandbags, wedges, or prefa
splints.
Option C: Assess input and output record and n
pattern. Pressure ulcers build up more rapidly
with nutritional insufficiency. Encourage a diet
and liquid intake of 2000 to 3000 ml per day un
contraindicated.
.
Option D: Use a footboard or pillows to keep the fee
correct position. This avoids foot drop and too much
flexion or tightness. Maintain feet in a dorsiflexed po
Option E: Assess the strength to perform ROM to al
assessment provides data on the extent of any phys
and guides therapy. Testing by a physical therapist m
needed. Execute passive or active assistive ROM exe
extremities.
ACID-BASE
IMBALANCES
 ACID-
BASE
BALANCE
RESPIRATORY ACIDOSIS
RESPIRATORY ACIDOSIS
pH < 7.35
pCO2 > 45 mm Hg (excess carbon dioxide in the blood)
Respiratory system impaired and retaining CO2; causing
acidosis

Common Stimuli
a. Acute respiratory failure from airway obstruction
b. Over-sedation from anesthesia or narcotics
c. Some neuromuscular diseases that affect ability to use chest
muscles
d. Chronic respiratory problems, such as Chronic Obstructive
Lung Disease
RESPIRATORY ACIDOSIS
Signs and Symptoms
Compensation: kidneys respond by generating
and reabsorbing bicarbonate ions, so HCO3
>26 mm Hg
Respiratory: hypoventilation, slow or shallow
respirations
Neuro: headache, blurred vision, irritability,
confusion
Respiratory collapse leads to
unconsciousness and cardiovascular collapse
RESPIRATORY
ACIDOSIS
RESPIRATORY ACIDOSIS
RESPIRATORY ACIDOSIS
Collaborative Management
1. Early recognition of respiratory status and treat cause
2. Restore ventilation and gas exchange; CPR for respiratory failure
with oxygen supplementation; intubation and ventilator support if
indicated
3. Treatment of respiratory infections with bronchodilators, antibiotic
therapy
4. Reverse excess anesthetics and narcotics with medications such as
naloxone (Narcan)
5. Chronic respiratory conditions
Breathe in response to low oxygen levels
Adjusted to high carbon dioxide level through metabolic
compensation
(therefore, high CO2 not a breathing trigger)
Cannot receive high levels of oxygen, or will have no trigger to breathe;
will develop carbon dioxide narcosis
Treat with no higher than 2 liters O2 per cannula
RESPIRATORY ALKALOSIS
pH < 7.35
pCO2 < 35 mm Hg.
Carbon dioxide deficit, secondary to
hyperventilation

Common Stimuli
a.Hyperventilation with anxiety from uncontrolled
fear, pain, stress (e.g. women in labor, trauma
victims)
b. High fever
RESPIRATORY ALKALOSIS
 RESPIRATORY ALKALOSIS
Signs and Symptoms
Compensation: kidneys compensate by eliminating
bicarbonate ions; decrease in bicarbonate HCO3 < 22
mm Hg.
Respiratory: hyperventilating: shallow, rapid
breathing
Neuro: panicked, light-headed, tremors, may develop
tetany, numb hands and feet (related to symptoms of
hypocalcemia; with elevated Ph more Ca ions are bound
to serum albumin and less ionized “active” calcium
available for nerve and muscle conduction)
May progress to seizures, loss of consciousness
(when normal breathing pattern returns)
Cardiac: palpitations, sensation of chest tightness
RESPIRATORY ALKALOSIS
Collaborative Management
1.Treatment: encourage client to breathe slowly in
a paper bag to rebreathe CO2
2.Breathe with the patient; provide emotional
support and reassurance, anti-anxiety agents,
sedation
3.On ventilator, adjustment of ventilation settings
(decrease rate and tidal volume)
4.Prevention: pre-procedure teaching, preventative
emotional support, monitor blood gases as
 METABOLIC ACIDOSIS

METABOLI Diagnostic test

C findings:
ACIDOSIS 1. ABG: pH <
pH <7.35 7.35,
Deficit of HCO3 < 22
bicarbonate in the 2.Electrolytes: Serum
blood NaHCO3 <22 K+ >5.0 mEq/L
mEq/L 3.
mg/dLSerum Ca+2 >
Caused by an 10.0
excess of acid, or
loss of bicarbonate 4.Serum Mg+2 < 1.6
 METABOLIC ACIDOSIS
Common Stimuli
a. Acute lactic acidosis from tissue hypoxia (lactic acid produced
from anaerobic metabolism with shock, cardiac arrest)
b. Ketoacidosis (fatty acids are released and converted to
ketones when fat is used to supply glucose needs as in
uncontrolled Type 1 diabetes or starvation)
c. Acute or chronic renal failure (kidneys unable to regulate
electrolytes)
d. Excessive bicarbonate loss (severe diarrhea, intestinal
suction, bowel fistulas)
e. Usually results from some other disease and is often accompanied
by electrolyte and fluid imbalances
f. Hyperkalemia often occurs as the hydrogen ions enter cells to
lower the pH displacing the intracellular potassium; hypercalcemia
and hypomagnesemia may occur
METABOLIC ACIDOSIS
 METABOLIC ACIDOSIS
Signs and Symptoms
Compensation: respiratory system begins to compensate by
increasing the depth and rate of respiration in an effort to lower
the CO2 in the blood; this causes a decreased level of carbon
dioxide: Pco2 <35 mm HG.
Neuro changes: headache, weakness, fatigue progressing to
confusion, stupor, and coma
Cardiac: dysrhythmias and possibly cardiac arrest from
hyperkalemia
GI: anorexia, nausea, vomiting
Skin: warm and flushed
Respiratory: tries to compensate by hyperventilation:
deep and
 METABOLIC ACIDOSIS
Signs and Symptoms
Compensation: respiratory system begins to compensate
by increasing the depth and rate of respiration in an effort to
lower the CO2 in the blood; this causes a decreased level
of carbon dioxide: Pco2 <35 mm HG.
Neuro changes: headache, weakness, fatigue progressing
to confusion, stupor, and coma
Cardiac: dysrhythmias and possibly cardiac arrest from
hyperkalemia
GI: anorexia, nausea, vomiting
Skin: warm and flushed
 METABOLIC ACIDOSIS
Collaborative Management
1. MEDICATIONS: Correcting underlying cause will often
improve acidosis.
2. Restore fluid balance, prevent dehydration with IV
fluids
3. Correct electrolyte imbalances
4. Administer Sodium Bicarbonate IV, if acidosis is severe
and does not respond rapidly enough to treatment of
primary cause. (Oral bicarbonate is sometimes given to
clients with chronic metabolic acidosis) Be careful not to
overtreat and put client into alkalosis.
5. As acidosis improves, hydrogen ions shifts out of the cells
and potassium moves intracellularly. Hyperkalemia may
become hypokalemia and potassium replacement will be
needed.
 METABOLIC ALKALOSIS

METABOLIC COMMON STIMULI

ALKALOSI Loss of hydrogen
S and chloride ions
through excessive
pH >7.45 vomiting, gastric
NaHCO3 >26 suctioning, or
mEq/L excessive diuretic
therapy.
Caused by an Excessive ingestion of
excess of acid, or bicarbonate rich
loss of bicarbonate antacids or excessive
from the body treatent of acidosis
with sodium
METABOLIC ALKALOSIS
 METABOLIC ALKALOSIS
Signs and Symptoms Diagnostic test findings
Compensation: Lungs 1. ABG‟s: pH> 7.45,
respond by decreasing the
depth and rate of respiration HCO3 >26
in effort to retain carbon 2.Electrolytes: Serum
dioxide and lower pH
K+ < 3.5 mEq/L
Neuro: altered mental
status, numbness and 3.Electrocardiogram:
tingling around mouth, as with hypokalemia
fingers, toes, dizziness,
muscle spasms (similar to
hypocalcemia due to less
ionized calcium levels)
Respiratory: shallow, slow
breathing
 METABOLIC ACIDOSIS
Collaborative Management
1.Correcting underlying cause will often improve
alkalosis
2.Restore fluid volume and correct electrolyte
imbalances (usually IV NaCl with KCL).
3.With severe cases, acidifying solution may be
administered.
4.Assessment: Vital signs, Neuro,
cardiac, respiratory assessment
5. Repeat arterial blood gases and
electrolytes
ABG INTERPRETATION
REMINDER:

PRACTICE ABG
INTERPRETATION.
 TIP: Do some exercises in
https://abg.ninja/abg and be an
expert in ABG interpretation.
END