-Largest organ

-Normal skin is dry, supple and ACIDIC

-Skin(Dermis and Epidermis) is 2mm thick

-OUTER LAYER OF SKIN

-20 CELL LAYERS THICK

-PROTECTS AND CONTAINS NERVE ENDINGS AND CAN REPRODUCE

BASAL LAYER-SINGLE LAYER OF REPRODUCING CELLS

MELANOCYTES-RESPONSIBLE FOR SKIN PIGMENT

RETE PEGS/RIDGES-PROTRUSIONS THAT INTERLOCK WITH DERMAL PAPILLAE

-INNERMOST LAYER

-NOURISHES EPIDERMIS AND PROVIDES STRENGTH AND ELASTICITY

-CONTAINS COLLAGEN, ELASTIN, VESSELS AND NERVES

-HAIR FOLLICLES, SWEAT GLANDS- cannot reproduce

-CONTAINS FIBROBLASTS AND MACROPHAGES

-NOT A SKIN LAYER

PROVIDES PADDING AND EVEN DISTRUBUTION OF PRESSURE

-CRITICAL TO PREVENTION OF SKIN BREAKDOWN

-CANNOT REPRODUCE OR REGENERATE

-HIGHLY VASCULAR

-HIGHEST METABOLIC RATE

-MOST VULNERABLE TO PROLONGED PRESSURE

-CANNOT REPRODUCE OR REGENERATE

PRIMARY- PROTECTION AGAINST PATHOGENS, IRRITANTS AND LOSS OF FLUID/ELECTROLYTES

SECONDARY- HEAT REGULATION, SENSORY PERCEPTION, EXCRETION, SYNTHESIS OF VITAMIN D

-SKIN LOSS STIMULATES MITOSIS

-'TURNOVER' TIME FOR YOUNG ADULT IS APPX 21 DAYS

-AGE 35 DOUBLES TO 42 DAYS

-STEROIDS INHIBIT EPIDERMAL MITOSIS

-USE CLEANSER/RINSE CLOSE TO NORMAL PH

EMOLLIENTS-SOFTEN AND REPLACE LIPDS(MINERAL OIL)

HUMECTANTS-ADDS WATER TO VERY DRY SKIN

-APPLY TO DAMP SKIN

*MACERATION STRETCHES CELLS IN THE SKIN INCREASING THE RISK OF DAMAGE

Partial thickness-  superficial, confined to skin layers

Full thickness-  extends beyond skin layers into bone, muscle or fat

PARTIAL THICKNESS

(SUPERFICIAL)

-DAMAGE OCCURS FROM THE TOP DOWN

REDNESS, MACERATION, FRICTION OR SHEAR MAY CAUSE SUPERFICIALINJURY

-CAUSED BY FRICTION, SHEAR OR TRAUMA

-MINIMIZE FURTHER DAMAGE,  AVOID ADHESIVES IF SKIN IS FRAGILE

-KEEP WOUND BED MOIST

SKIN TEAR WITH MIN LOSS-ROLL FLAP IF AVAILABLE.  SECURE WITH STERISTRIPS AND COVER WITH NONSTICK OR SILICONE DRESSING

SKIN TEAR WITH TISSUE LOSS-FOAM DRESSING WITH SILICONE ADHESIVE OR SILICONE CONTACT LAYER + GAUZE

-PADDING AND NONADHERENT DRESSING

PETROLATUM-EASY TO APPLY AND REMOVE

-LESS EFFECTIVE WITH LIQUID STOOL

ZINC OXIDE-HIGH PROTECTION AGAINST LIQUID STOOL

-DIFF TO APPLY/REMOVE UNLESS MIXED WITH PETROLATUM

DIMETHICONE-NON OCCLUSIVE, EASY APPLICATIONREMOVAL

-LESS PROTECTION AGAINST LIQUID STOOL

COPOLYMER FILM-LESS EXPENSIVE AND LESS FREQUENT APPLICATION

PRESSURE ULCER(PU) 

VS

INCONTINENCE ASSOCIATED DERMATITIS

LOCATION

PU-BONY PROMINENCE

IAD-PERINEUM

DEPTH

PU-DEEP

IAD-SUPERFICIAL

ASSCIATED FACTORS

PU-REDUCED MOBILITY

IAD-INCONTINENCE

FULL THICKNESS INJURY BEGINS AT THE MUSCLE AND GOES UP

-TURN Q2 HOURS IN BED

-TURN Q1 HOUR IN CHAIR

CHARACTERISTICS OF SHEAR DAMAGE

-UNDERMINING, TUNNELING, SINUS TRACTS

DEEP TISSUE INJURY

-BRUISING UNDER THE SKIN

-SMOKING(CAUSES VASOCONSRICTION)

-DIABETES

-HYPERLIPIDEMIA

-HTN

-OVER 66 Y/O

-OBESITY

-CRI

Midsized vessels- tibial & peroneal

-can be bypassed

Small vessels (arterioles)

-cannot be bypassed

INTERMITENT CLAUDICATION

-PAIN IN CALF, THIGH, BUTTOCK BROUGHT ON BY ACTIVITY ANDRELIEVED WITH APPX 10 MIN REST (50% OCCLUSION)

-Pain progressing to nocturnal pain and rest pain = 90% occluded

LEAD(Ischemia)

vs

NEUROPATHIC PAIN

ISCHEMIC PAIN WORSENS WITH ACTIVITY AND ELEVATION

-IMPROVES WITH REST AND DEPENDENCY

NEUROPATHIC PAIN IMPROVES WITH ACTIVITY

6 P'S

PAIN, PULSENESS, PALLOR, PARASTHESIA, PARALYSIS, POLOR

ACUTE LIMB ISCHEMIA!!!!

-INDICATES EMBOLUS AND NEEDS URGENT CARE

-hair loss, ridging of nails, thin shiny skin, pallor or ashen skin

-ELEVATIONAL PALLOR

-DEPENDENT RUBOR

TEMP CHANGES- COLDNESS, PROXIMAL TO DISTAL

PROLONGED VENOUS FILLING TIME

-RAISE LEG TIL VEINS COLLAPSE

-PLACE LEG IN DEPENDENT POSITION AND COUNTSECONDS TIL VEINS REFILL    >20 INDICATES LEAD

CAPILLARY REFILL-  >3 SECONDS INDICATES LEAD

-NOT AS VALID AS VENOUS FILLING

ABI

-1.0 is normal ABI

ABI < 0.9 indicates LEAD

Test

Rest for 10-15 minutes

Obtain brachial valies for each arm

Obtain DP and PT in BLE

Divide the higher of the foot values by the higher brachial value

                 ________

Brachial / Feet 

1.0           NORMAL

< 0.9         LEAD

<0.6-0.8   BORDERLINE PERFUSION

<0.5          SEVERE ISCHEMIA

<0.4          CRITICAL ISCHEMIA (Limb threatened)

> 1.3         ELEVATED(Calcification, non compressible arteries

-occurs in diabetes, arthritis, CRI

Refer to MD if ABI < 0.8 and no response to conservative care

LOCATED ON DISTAL FEET AND TOES

ULCER BED IS PALE OR NECROTIC FROM POOR PERFUSION

TYPICAL 'PUNCHED OUT' APPEARANCE

LOW TO MINIMAL EXUDATE

*INFECITON COMMON BUT S/SX ARE MUTED BC OF DIMMINISHED BLOOD FLOW

-FAINT 'HALO' OF ERYTHEMA CAN INDICATE INFECTION

1st Priority- IMPROVE PERFUSION

-SCD'S

-SMOKING CESSATION

-REVASCULARIZATION

-MEDS (CILOSTAZOL, STATINS)

-HYPERBARIC OXYGEN TREATMENTS

2ND Priority- PREVENT FURTHER INJURY

-AGGRESSIVE EDUCATION

-AVOID CONSTRICTING CLOTHES/FOOTWEAR

-PROFESSIONAL NAIL CARE

-DIABETES CONTROL

MANAGMENT OF ARTERIAL ULCERS

OPEN WOUNDS

-manage exudate

-maintain moist wound surface

-consider silver dressings to reduce bacterial load

-caution with occlusion

MANAGEMENT OF ARTERIAL ULCERS

closed wounds

-covered with eschar, uninfected and poorly perfused

Goal-  Maintain closed wound

-Paint with iodine

-leave open or cover with dry non occlusive dressing

MANAGMENT OF ARTERIAL ULCERS

Infected Wounds

-even if closed/covered with eschar

-AGGRESSIVE TREATMENT OF INFECTION

-NO TOPICAL ANTIBIOTIC TREATMENTS-USE SYSTEMIC

DEBRIDEMENT, REVASCULARIZATION, HBOT

MAY REQUIRE AMPUATION IF NO RESPONSE TO TREATMENT

VENOUS ULCERS

-MOST COMMON TYPE OF LEG ULCER

-CAUSED BY VENOUS INSUFFICIENCY.COMPROMISED VENOUS RETURN

-VENOUS CONGESTION CAUSES BACKPRESSURE RESULTING IN LEAKAGE OF FLUIDS, WBC'S AND PROTEIN INTO TISSUE

RESULTS IN:

FIBROSIS, INFLAMMATION, AND EDEMA

-DVT

-OBESITY

-PREGNANCY

-SEDENTARY LIFESTYLE

-VARICOSE VEINS

-AGING