integumentary system lecture

Post on 08-Apr-2015

349 Views

Category:

Documents

0 Downloads

Preview:

Click to see full reader

TRANSCRIPT

Integumentary System

NCM 104

CJ Cantos RN

The Skin

As the external covering of the body, the skin performs the vital function of protecting internal body structures from harmful microorganisms and substances.

Regions of the Skin

Epidermis

Dermis

Hypodermis

Epidermis

The epidermis is what type of tissue?? Keratinized stratified squamous epithelium

Thick skin has five layers

Thin skin has four layers

Stratum corneum

Stratum lucidum

Stratum granulosumStratum spinosumStratum

basale

Layers of the Epidermis

Stratum corneum Stratum lucidum Stratum granulosum

Keratinization Cells still alive

Stratum spinosum Epidermal dendritic cells

Stratum basale (germinativum) Melanocytes Tactile Cells

Cells of the Epidermis

Keratinocytes

Melanocytes

Epidermal Dendritic Cells (Langerhans Cells)

Tactile Cells (Merkel Cells)

A layer of squamous epithelial cells. Most of these cells produce a tough, fibrous

protein called keratin. The epidermis also produced specialized

cells called melanocytes. These produce melanin (skin pigment). Aggregations of melanocytes are nevi (moles and birthmarks).

Stratum corneum

Stratum lucidum

Stratum spinosum

Stratum granulosum

Stratum basale

Dermis

2 layers: Papillary (areolar) Reticular (dense

irregular)

Hypodermis (subcutaneous)

Areolar and adipose connective tissue

Anchors skin to underlying structures

Allows skin to slide freely

Larger in women than men

Epidermal Appendages

Glands Hair Nails

Exocrine Glands

Sebaceous (oil) glands Occur over entire body,

except palms and soles Produce sebum as lubricant

Sudoriferous (sweat) glands Merocrine glands – most

numerous, sweat or sensible perspiration

Apocrine glands – confined to axillary, nipple, anal and genital areas; viscous sweat

Merocrine

Apocrine

Sebaceous

Hair: Structure

Hair is composed of dead epidermal cells that begin to grow and divide in the base of the hair follicle.

As the cells are pushed toward the skin surface, they become keratinized and die.

Hair color is genetically determined.

Hair Growth and Replacement Scalp hair grows for 2 to 5 years. Approximately 50 hairs are lost each day. Sustained hair loss of more than 100 hairs

each day usually indicates that something is wrong.

Hair Growth

Rate of hair growth is about 2 mm/week

Growth cycles – active (2-5 years) and dormant phases (3-4 months)

Hair

Three types of hair: Lanugo Terminal Vellus

Hair Consists of root

and shaft Layers of the

hair: Medulla – central

core not found in all hair

Cortex – surrounds medulla

Cuticle – outermost layer

Location and Functions Hair can be found EVERYWHERE,

except for on the palms, soles, lips, sides of fingers and toes, parts of the external genitalia, nipples

Functions: Protects from the sun and sweat Senses touch Reduces heat loss Screens nasal passages

Male Pattern Baldness Genetic and hormonal

influences Genetic: 2 alleles, one

for uniform hair growth and one for baldness Baldness gene is

dominant in males Hormonal:

Testosterone causes terminal hair to be replaced by vellus hair

Nails Scale like

modification of epidermis

Contain hard keratin

Grows from the nail matrix

Nails:

- Produced by cells in the epidermis

- Nail plate (body): visible portion

- Nail root: located under cuticle

- Lunula: half moon crescent shaped

white portion under cuticle

- Nail bed: located under nail plate

- Hypoxia: decr. oxygen in blood, nail bed will turn blue- cyanosis

Integumentary System Functions

Protection (chemical, physical, and biological barriers)

Prevents loss of water Temperature regulation Metabolic regulation Immune defense Sensory receptors Excretion by means of secretion

Physiology:Protection

-Physical barrier that protects underlying tissues from injury, UV light and bacterial invasion.

Regulation of body temp.- high temp. pores open sweat comes to surface and is evaporated.

Sensation:- nerve endings and receptors that detect pain, touch, pressure and temp.Pacinian corpuscles: pressureMeissner’s corpuscle: light touch

Excretion:- sweat removes water, salts, uric acid and ammonia from body surface.

Synthesis of Vit. D (calciferol):- UV light stimulates skin to make Vit. D.

Effects of Aging on the Skin Skin vascularity and the number of

sweat and sebaceous glands decrease, affecting thermoregulation.

Inflammatory response and pain perception diminish.

Thinning epidermis and prolonged wound healing make elderly more prone to injury and skin infections.

Skin cancer more common.

Assessment of Skin

Integrity. Color. Temperature

and moisture.

Texture. Turgor and

mobility. Sensation. Vascularity.

There are seven parameters that should be examined in performing physicalassessment of the skin:

Skin LesionsPrimary Lesions

1. Macule and Patch – Flat, nonpalpable skin color changeMacule - <1cm, circumscribed borderPatch - >1cm, may have irregular border2. Blisters – Circumscribed, elevated, palpable mass containing serous fluidVesicle - <.5cmBullae - >.5cm3. Papule and Plaque – Elevated, palpable, solid mass, circumscribed borderPapule - <.5cmPlaque - >.5cm, flattened lesion

4. Wheal – Elevated mass with transient borders, often irregular, with surrounding edema5. Nodule and tumor – Elevated, palpable solid mass, extends deeper into the dermis than a papuleNodule - .5 – 2cm circumscribedTumor - >1-2cm, don’t have always sharp borders6. Pustule – Pus – filled blisters or papules7. Cyst – Encapsulated fluid – filled or semisolid mass in the subq tissue or dermis

Secondary Lesions Scale- flaky accumulation of

excess keratin Crust- collection of inflammatory

cells and dried serum, blood or pus

Erosion – loss of superficial epidermis

Scar – skin mark left after healing of a wound or lesion

Fissure – crack in the epidermis usually extending into the dermis

Keloid – hypertrophied scar tissue, excessive collagen formation

Ulcer - deeper erosion, loss of epidermis and papillary dermis

Lichenification-thickening of skin secondary to chronic rubbing, irritation and scratching

Vesicular Lesions Petechia – small, 1-2mm round red or purple

macule Ecchymosis – round or irregular macular

lesion, larger than petechia Cherry angioma – papular and round,

normal age – related skin alteration Spider angioma – red arteriole lesion,

central body with radiating branches, noted of face, neck arms and trunk

Telangiectasia – spider-like or linear, bluish or red, noted on legs and anterior chest, secondary to superficial dilation of venous vessels and capillaries

Primary Lesions

Secondary Lesions

Vesicular Lesions

Common Diagnostic Tests for Integumentary Disorders Biopsy

1. Shave2. Punch3. Incision4. Excision

Patch Testing. Tzanck smear. Skin scrapings.

Wood’s light examination

Culture and sensitivity.

Diagnostic Tests

1) Skin Biopsy Punch, excisional, incisional & shave

Nursing Interventions

Preprocedure - Secure consent

- clean site

Postprocedure – place specimen in a clean container & send to pathology laboratory

– use aseptic technique for biopsy site dressing, assess site for bleeding & infection

– instruct px to keep dressing in place for 8hrs & clean site daily

Diagnostic Tests

2) Skin Culture Used for microbial study Viral culture is immediately placed on ice

3) Wood’s Light Examination Skin is viewed through a Wood’s glass under

UV

Nursing Interventions

Preprocedure – darken room

Postprocedure – assist px in adjusting to light

Diagnostic Test

4) Skin Testing Administration of an allergen by patch

or ID techniques

Nursing InterventionsPreprocedure – d/c systemic steroids or

antihistamines 48º prior, consent, ready resuscitation equipments

Postprocedure

– keep skin-patch area dry

– instruct to avoid activities which can increase sweating if doing a patch test

– record site, date, time of test, ff-up & reading

Wounds

A disruption in the integrity of the body. Three phases of healing:

Defensive (inflammatory) phase. Reconstructive (proliferative) phase. Maturation phase.

Wound Drainage: Types

Serous Exudate (composed primarily of serum, the clear portion of blood; watery in appearance).

Purulent exudate (also called pus; may vary in color).

Hemorrhagic exudate (has a large component of RBCs; color depends on whether bleeding is old or fresh),

Factors Affecting Wound Healing Age. Oxygenation. Smoking Drug therapy. Diseases such as diabetes. Nutrition and diet.

Wound Care

3 types of wound dressings:1. Passive

2. Interactive

3. Active

5 Rules of Wound Care

1. Categorization

2. Selection

3. Change

4. Evolution

5. Practice

Categories of Dressings

1. Occlusive

2. Wet

3. Moisture – retentivea. Hydrogels

b. Hydrocolloids

c. Foam dressings

d. Calcium Alginates

INTEGUMENTARY

DISORDERS

Pruritus

Itch-scratch cycle

Interventions:- Antihistamines- Avoid hot environment

Hydradenitis Suppurativa

Chronic suppurative folliculitis of perianal, axillary and genital area or under breast

Commonly after puberty Unknown cause but genetics Abnormal blockage of sweat glands

causes recurrent inflammation then scarring occurs

Management

Hot compresses Antibiotics Isotretinoin I and D Surgery

Seborrheic Dermatoses Chronic increase production of sebum Etiology:

Genetic Hormones Nutritional status Infection Emotional stress

2 forms Oily Dry

Management

No cure for seborrhea Corticorsteriods Maximal aeration of skin folds Frequent shampooing Antiseborrheic shampoo

Acne Vulgaris

Inflammation of sebaceous glands and hair follicles

Etiology Unknown but related to:

Heredity Cosmetic use Drugs Bacteria

Assessment

Papule Pustule Nodule Comedones

Acne Vulgaris

Management: Topical- Benzoyl peroxide- Retinol Systemic- Tetracycline- Clindamycin

Eczematous Disorders

Atopic Dermatitis

Atopic DermatitisEtiology     Unknown occurs more frequently in children

When one or both parents have allergies like asthma, hay fever, or contact dermatitis

Infantile eczema - infant allergies Eczema in older children - allergies to dust

mites Intensified by dry skin, detergents,

constricting clothing, or perfumed soaps and lotions

Atopic Dermatitis

S/S:      Infancy: red papules (raised lesions)

usually appears first in the cheeks and then spread to the forehead, scalp, and down extensor surfaces of the arms and legs

Intense Pruritus Childhood eczema characterized by dry,

scaly, papular patches of skin on wrists, hands, ankles, antecubital and popliteal spaces

No laboratory diagnostic test for eczema

Nursing Interventions Bathe or shower daily with tepid water

using mild soap only on nonaffected areas

Pat, rather than rub, skin dry Immediately after bath, apply emollient

such as Eucerin or Lubriderm Avoid use of scented or perfumed

lotions Apply wet wraps to severely affected

skin after applying topical medications Use antibacterial soaps for hand

washing Avoid wool or constricting clothing

which can trap perspiration

Nursing InterventionsAdminister prescribed meds as

ordered1.  Topical steroids

(hydrocortisone 1% or triamcinolone 0.1%) are applied to lesions to reduce inflammation during flare ups

2. Antihistamines to control itching

3. Oral antibiotics for secondary infections

Nursing Interventions

Perform health teaching on:

1. Identify foods that exacerbate rash

2. Avoid suspected environmental allergens

Contact Dermatitis Skin reacts to external irritants

like: allergens (e.g. poison ivy or

cosmetics). harsh chemical substances

(detergents, insecticides). metals such as nickel. mechanical irritations from wool

or glass fibers. body substances like urine or

feces.

Contact Dermatitis

Assessment: a. Pruritusb. Burningc. Edemad. Erythemae. Vesicles with drainage

Contact Dermatitis

Treatment:1. Antihistamines2. Prophylactic antibiotics3. Topical steroids

Interventions: a. Elevate to reduce edemab. Cold compressc. Prevent scratchingd. Assist in skin testinge. Use hypoallergenic materialsf. Administer antibiotics,

antipruritics, steroids

Exfoliative Dermatitis Progressive inflammation of the

skin gradually worsens. The entire body is affected. Chills,

fever, and malaise set in. Severe reactions to drugs such as

penicillin may be causative. May also be due to underlying skin or systemic disease

Exfoliative dermatitis can be fatal.

Manifestations Generalized erythema Fever and GI symptoms Skin color turning dark red Scaling after a week High output heart failure Hyperuricemia

Management

Comfortable room temperature Fluid and Electrolyte balance Antibiotics Oral/Parenteral Steroids Provide symptomatic relief

Scaling DisordersPsoriasis

A chronic inflammatory disease marked by epidermal proliferation High incidence among Caucasian/European Most common in 15 – 35 yrs old

Etiology: Unknown but related to heredity/genetics Exacerbating factors:

Local trauma, Overexposure to sun, Infection and Illness

Psoriasis Manifestations

Profuse, erythematous silvery scales or plaques.

Often covering large areas of the body

Pruritus, accompanied with pain Psoriatic arthritis Guttate psoriasis Palmar – pustular psoriasis Erythrodermic psoriasis

Psoriasis

Psoriasis

Psoriasis

Nursing Management Gentle removal of scales

Coal tar therapy/Oil baths Topical corticosteroid

Discuss the administration of additional medical treatments Topical nonsteroidal – Calcipotreine and Tazarotene Intralesional therapy Systemic cytotoxic medication1. Methotrexate2. Hydroxyurea3. Cyclosporine4. Oral retinoids Photochemotherapy

Nursing Management

Photochemotherapy Binds with DNA and decrease cell

proliferation Oral psoralens, phototherapy of UV A light

(PUVA) or (PUVB)

Pyodermas

Impetigo

Impetigo A highly contagious, superficial skin

infection caused by staphylococci or streptococci or both

Impetigo

Etiology:  Acquired through contact with

infected person who share toys, books, towels, or toiletries

GABH Streptococci Bullous impetigo always caused

by S. aureus

ImpetigoManifestations Painful, burning sensation over lesions Pruritus may be present Nonbullous impetigo begins as a single

erythematous macule that rapidly progresses to a vesicle or pustule.

Pustule ruptures leaving a honey-colored crust over the superficial erosion

Mild regional lymphadenopathy may occur

Nursing Management

Soak crusts in warm water Gently wash with

antibacterial soap and remove crusts

Good hand washing Do not touch or pick at

lesions Keep fingernails short and

clean to prevent spread of infection

Nursing Management

Administer meds as ordered Topical antibiotic Systemic antibiotic for:1. Non bullous – Oral penicillin2. Bullous – Cloxacillin,

Dicloxacillin3. Penicillin allergy -

Erthyromycin

Erysipelas & CellulitisErysipelas

– inflammation, acute, superficial, rapidly spreading caused by B-hemolytic Streptococcus

Cellulitis – inflammation/infection of deeper dermis usually caused by Streptococcus pyogenes

Erysipelas & Cellulitis

Assessment:- Swelling or edema- Redness- Pain or tenderness- Fever- Pruritus

Erysipelas & Cellulitis

Treatment:- IV antibiotics (Penicillin,

Cloxacillin)- Antipyretics- Elevate affected area- Warm compress for 2x a day

Folliculitis, Furuncle, Carbuncle Folliculitis

- infection of hair follicle Furuncle

- deep in 1 or more hair follicles and spread in surrounding dermis

Carbuncle - abscess of the skin and subcutaneous

tissues; extension of a furuncle, large and deep - seated

Folliculitis, Furuncle, Carbuncle Assessment:- Papule, pustule, nodule, node, cyst- Fever- Pain and tenderness

Folliculitis, Furuncle, CarbuncleManagement- Don’t destroy wall of induration- Never squeeze or prick, specially if

in the face- Oral antibiotics- Bed rest- I and D- Warm, moist compress- Wear gloves

Fungal InfectionsTinea

Etiology:- Dermatophytes, yeasts

1. Tinea Pedis- Prevalent on communal showers and pools- Potassium permanganate - Topical antifungal agents - Keep feet dry as possible

Tinea2. Tinea Corporis

- ringed lesions on face, neck, trunk and extremities

- animal contact (pets)- topical antifungal - use clean towel daily

3. Tinea Capitis- hair shafts- red scaling patches- classic sign: “black dots”, temporary

hair loss- Griseofulvin; topical has no effect- shampoo 2-3x a week with Nizoral

Tinea4. Tinea Cruris

- “itch jock”- young, joggers, obese and tight clothing- topical antifungal- avoid excessive heat- avoid synthetic clothing and wet bathing

suit5. Tinea Ungum

- onychomycosis- nails become thickened and friable and

lusterless- antifungal therapy 6 weeks for

fingernails and 12 weeks for toenails

Candidal Intertrigo

Predisposing factors: Obesity DM Recent antibiotic therapy Warm, moist environment

Candidal Intertrigo

Hx and Assessment: Pruritus Pain Well-demarcated, beefy-red,

erythematous patches surrounded by satellite pustules

Restricted to intertriginous areas In infants- diaper rash

Candidal Intertrigo

Treatment: Topical antifungal Reduce moisture Reduce friction through weight loss

Parasitic Infections

Pediculosis Capitis

Infestation of the hair and scalp with lice

Highly communicable parasite Spread through direct or

indirect contact

Pediculosis Capitis

Etiology:  Lice live and reproduce only in

humans Incubation period 8 to 10 days Lice can survive for up to 48 hours

from human host Nits can survive for 8 to 10 days away

from human host Lice bites release saliva into dermis

which causes itching

Pediculosis CapitisManifestations Look for nits – silvery, glistening oval

bodies Commonly found in back of neck and

ears Pruritus Erythema, scaling, and skin

excoriation

Nursing Management Apply about 2 oz of pediculicide; agent onto

wet hair and add additional water to lather Rinse hair thoroughly Remove nits from damp hair Delouse environment by washing all of

child’s daily clothes and linens in hot water and detergent and drying fro 20 minutes in a hot dryer

Stuffed toys and items that cannot be washed should be sealed in a plastic bag for 2 weeks to make sure nits are dead

Nursing Management

Administer meds as ordered:Permethrin (Nix), Pyrethrum (Rid), Lindane (Kwell)

After initial treatment, one additional treatment may be needed no sooner than 7 days

Scabies Contagious skin condition

caused by the human mite sarcoptes scabiei

May affect anyone

ScabiesAssessment: Lesions appear as linear, grayish

burrows 1 to 10 cm long ending in a pinpoint vesicle, papule, or nodule

Lesions - @ webs of the fingers, body creases, axilla, waistline, and near genitalia

Secondary lesions (crust, vesicles, nodules & excoriations)

Intense pruritus that worsens at night

Scabies

Diagnosis Scraped skin from the burrows placed

on a slide and examined through a microscope

Nursing Management Warm soap and water bath Apply scabidal lotion to cool, dry skin

over the entire body Leave on for 12 to 24 hours before

washing off Treat all contacts Clothing, bedding, and towels should be

changed daily Vacuum floors, carpets, and furniture Items that cannot be washed should be

bagged for 4 days before use

Nursing Management Administer meds as ordered:1. Crotamiton (Eurax),

Permethrin 5% cream (Elimite), and Lindane (Kwell, Scavene).

2. Oral antihistamines3. Soothing creams or lotions4. Antibiotics for secondary

infection if present

Autoimmune disordersPemphigus

Group of serious skin disease characterized by appearance of bullae on normal skin and mucous membranes

Genetics, Jewish or Mediterranean Middle and late adulthood Also associated with the use of

penicillins, captopril and myasthenia gravis

Pemphigus Clinical manifestations

Oral lesions – painful, bleed easily and heal slowly

Skin bullae rupture and leave painful eroded areas that are oozing and weeping

Offensive odor Nikolsky’s sign Complications:

Secondary bacterial infections Fluid and electrolyte imbalances Hypoalbuminemia

Pemphigus

Nursing management Corticosteroids in High doses Immunosuppresants Plasmapheresis

TEN and Stevens Johnson Syndrome a life-threatening condition affecting

the skin, in which due to cell death the epidermis separates from the dermis.

Etiology: hypersensitivity complex affecting

the skin and the mucous membranes idiopathic possible medications infections

TEN and Stevens Johnson Syndrome Infections

herpes simplex virus, influenza, mumps, histoplasmosis, Epstein-Barr virus

Allergic reactions to drugs (Dicloflex, Fluconazole, Valdecoxib,

Penicillins, Barbiturates, Sulfas, Phenytoin, Modafinil, Ibuprofen

Idiopathic factors (up to 50% of the time) Malignancy (carcinomas and lymphomas) Herbal supplements containing ginseng. SJS

may also be caused by cocaine usage

TEN and Stevens Johnson Syndrome Clinical manifestations

Skin cracks Blisters on the lips and mouth Fever and red patches on the skin Burning sensation of the skin with

extensive blistering and ulceration May be localized to one part of the body

or systemic from head to toe Mucosal involvement Scalded – skin syndrome

TEN and Stevens Johnson Syndrome

TEN and Stevens Johnson Syndrome

TEN and Stevens Johnson Syndrome Steroids like prednisone Antipyretics Analgesics Offending drug must be removed at once!

IV Ig

Nursing Management

Administer meds as ordered Assess for s/s of infection Maintain hydration status of the pt Apply petroleum jelly over the skin

lesions to prevent excessive dryness WOF s/s of bleeding/ hypotension/

shock Prepare to administer Potassium

Permanganate

Nursing Management

Potassium per Manganate Dilute in 1 L of sterile water Enough to make it light pink to

prevent burns Let it drip over open lesions to

promote healing and dryness Psychosocial support

Burn Injury an alteration in skin integrity resulting in tissue loss or injury caused by heat, chemicals, electricity or radiation.

Burn InjuryCauses: Thermal

results from dry heat (flames) or moist heat(steam or hot liquids). It is the most common type.

Chemical caused by direct contact with either

acidic or basic agents. It destroys tissue perfusion leading to necrosis

Burn Injury Electrical

severity depends on type and duration of current and amount of voltage.

It follows the path of least resistance (muscles, bone, blood vessels and nerves).

Includes direct current, alternating current and lightning.

Radiation usually associated with sunburn or radiation

treatment for cancer. It is usually superficial. Extensive exposure to radiation may lead to tissue damage and multisystem damage.

Classification of burn according to depth:Superficial/partial thickness burn (1st degree)

Deep partial thickness burn

Full thickness burn (3rd degree)

Area involved epidermis Epidermis and part of dermis Epidermis, dermis hypodermis.

Appearance

Clinical findings Very painful, tingling and hyperesthesia, erythema, blanching, minimal or no edema.

Severe pain, sensitivity to cold air, blistering, edema

Painless, dry, pale white or charred, shock, hematuria and hemolysis.

Causes Sunburn, flash of flame Scalding, prolonged contact Fire, prolonged exposure

Treatment cooling Grafting Grafting scarring, escharotomy

Classification of burns based on extent

1. Minor Burn Injury- 2nd degree burn of <15% total body surface area (TBSA) in adults or <10% TBSA in children- 3rd degree burn of <2% TBSA not involving special care areas- Excludes all patients with electrical injury, inhalation injury or concurrent trauma and all poor-risk patients

2. Moderate, Uncomplicated Burn Injury- 2nd degree burns of 15-25% TBSA in adults or 10-20%

in children- 3rd degree burns of <10% TBSA not involving special

care areas- Excludes all patients with electrical injury, inhalation

injury or concurrent trauma and all poor-risk patients

3. Major Burn Injury- 2nd degree burns >25% TBSA in adults or >20% in children- All 3rd degree burns >10% TBSA- All burns involving special care areas- All Inhalation injury, electrical injury or concurrent trauma and poor risk patients

Burn InjuryAssessment Extent of burn using body surface area and cause. Head and both upper ext., 9% each; front and back

of trunk, 18% each, lower ext., 18%; perineum 1% Cardiac status/BP, dehydration and shock Respiratory status-airway patency Pain management requirements Increased nutritional needs Mobility deficits Past medical history which may require more

intense observation (e.g DM, CVD, etc)

Physiologic Changes Following Burns

Hypovolemic phase Changes Diuretic phase

-vascular to interstitial

hemoconcentration

Extracellular fluid shift -interstitial to vascular

hemodilution

- renal flow from BP & C.O.

oliguria

Renal function - renal flow from blood v.

diuresis

-Na reabsorption by kidneys but Na lost in exudate and trapped in edema fluid.

Na deficit

Na level -Na loss with diuresis, becomes normal in 1 week.

Na deficit

-released by tissue and RBC injury, decreased excretion from decreased renal function.

hyperkalemia

K level -K moves back into cells, lost by diuresis.

hypokalemia

Loss into tissues through increased capillary permeability

hypoproteinemia

CHON level -loss during continued catabolism

hypoproteinemia

-Tissue catabolism; CHON loss in tissue; more nitrogen loss that take in

negative nitrogen balance

Nitrogen balance -tissue catabolism, CHON loss immobility

negative nitrogen balance

-Anaerobic metabolism from decreased tissue perfusion; increased acid and products decreased renal output (this leads to retention of acids end products) loss of NaHCO3

metabolic acidosis

Acid-base balance

-occurs because of trauma

decreased renal flow

Stress response Occurs because of prolonged nature of injury or psychological threat to self

stress ulcers

Burn Injury

Diagnostic and lab test findings CBC-elevated HCT and decrease HGB due to

fluid shifts. UO indicated adequacy of renal status Electrolytes-decrease sodium and increase

potassium due to fluid shift BUN and creatinine-elevated due to

dehydration ABG’s and pulse oximetry-assess

respiratory failure. CVP - hydration status

Burn Injury

Goal of care Maintain fluid balance Prevent and manage infection Preserve mobility Decrease pain

Phases of Burn Management

1. Emergent/ Shock Phase2. Acute/ Diuretic Phase3. Rehabilitative Phase

Emergent/Resuscitative/ Shock Stage

Lasts from the onset of injury through successful fluid resuscitation

Fluid shifting from IVC - ITC

Emergent/Resuscitative/Shock Stage

Diagnostic and lab test findings- Elevated hematocrit and

decreased hemoglobin due to fluid shift

*Decreased sodium and increased potassium due to fluid shift

Elevated BUN and creatinine due to dehydration

Emergent/Resuscitative/Shock Stage

Fluid resuscitationConsensus formula 2-4mL/kg/%TBSA burn

½ given first 8 hrs. ½ next 16

Parkland (Baxter) 4 ml/kg/%BSA burn for 24 hour

pd. ½ first 8 hrs ½ next 16 hrs

Nursing Interventions remove jewelry and clothing to

decrease constriction of affected area,

flush burn with water, evaluate extent and depth of

burn, cover burn with clean cloth, arrange transfer to emergencyfacility maintain airway clearance.

Nursing Interventions

Medication Therapy Pain therapy Tetanus prophylaxis Topical antimicrobial as well as

systemic antibiotics

Emergent/Resuscitative Stage

High Priority Nursing Diagnoses

Fluid volume deficit Ineffective airway Altered nutrition requirements

Acute/ Diuretic Stage

Begins with the start of diuresis and ends with closure of the burn wound

Movement of fluid from ITC-IVT

S/s of hypervolemia, CHF Needs proper regulation of

fluid intake

Nursing Interventions Wound care management Nutritional therapies Infection control Pain management Psychosocial support Physical therapy Hydrotherapy Maintain fluid/hydration

status Maintain heated

environment.

Nursing interventions

Medication Therapy Antibiotic therapy-topical and systemic

Narcotic pain control usually required

IV fluid administration

Autograftingcare of graft site

a. Elevate & immobilizeb. Keep free from pressurec. Check for infectiond. Instruct client to protect

affected area from sunlighte. Use splints & support

garment

Rehabilitative Stage Begins with wound closure

and ends when the client returns to the highest level of health restoration.

Nursing Interventions Psychosocial evaluation, Support and management-

arrange counseling if necessary,

Prevention of immobility contractures-exercises or ongoing physical therapy

Assist in resumption to work, family and social life.

Preventative measures for scar formation

Assess home environment for needs and accessibility

top related