Background

This article discusses the management oI chronic wounds. This topic is naturally diverse and Iar-
reaching. Wound care in general and in terms oI speciIic etiologies is considered. The images
below depict a sacral pressure ulcer.
Image oI advanced sacral pressure ulcer shows the eIIects oI
pressure, shearing, and moisture. Sacral pressure ulcer beIore and
aIter Ilap closure.
Recent studies
In a prospective study, Campbell et al determined the incidence oI heel pressure ulcers in 150
orthopedic patients. The cohort consisted oI patients who were admitted to an acute care hospital
either Ior elective orthopedic surgery or Ior treatment oI a Iractured hip. The incidence oI heel
pressure ulcers in all patients was 13.3, with the incidence in patients with hip Iracture being
higher than that in the elective surgery patients (16 vs 13, respectively). However, patients
with hip Iracture in whom pillows and rolled sheets were used to relieve heel pressure had a
signiIicantly lower ulcer rate than did the other hip Iracture patients. When all patients in the
study were taken into account, the presence oI respiratory disease was the only Iactor
signiIicantly associated with pressure ulcer development.
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Epidemiology
Frequency
Pressure ulcers occur in approximately 9 oI hospitalized patients, usually during the Iirst 2
weeks oI hospitalization. A study Iound that even with the use oI a pressure-reducing bed and
early nutritional support, 3 oI patients in a surgical intensive care unit who were employed in
the study developed pressure ulcers.
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The annual risk oI pressure ulceration in patients with
neurologic impairment is 5-8, with a liIetime risk oI approximately 85 and a mortality rate oI
8.
The prevalence oI pressure ulcers among patients residing in long-term care Iacilities has been
reported as 2.3-28 and has been an increasingly common reason Ior litigation.
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The
presence oI a pressure ulcer increases a nurse's workload by 50 Ior the patient and adds
approximately $20,000 to the hospital bill. The treatment oI pressure ulcers in the United States
is estimated to cost more than $1 billion annually.
Venous ulcers make up 70 oI chronic lower extremity ulcers.
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The incidence oI venous ulcers
in the United States is approximately 600,000 cases annually. The recurrence rate is up to 90.
According to the National Institute oI Diabetes and Digestive and Kidney Diseases, an estimated
18 million Americans (6.3 oI the population) are known to have diabetes, and millions more
are considered to be at risk. OI those at risk, diabetes is undiagnosed in 5.2 million. Diabetic Ioot
lesions are responsible Ior more hospitalizations than any other complication oI diabetes. Among
patients with diabetes, 15 will develop a Ioot ulcer, and 12-24 oI those with a Ioot ulcer will
require amputation. Indeed, diabetes is the leading cause oI nontraumatic lower-extremity
amputations in the United States, accounting Ior 60 oI these amputations.
Every year approximately 5 oI persons with diabetes develop Ioot ulcers, and 1 require
amputation.
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Diabetic peripheral neuropathy conIers the greatest risk oI Ioot ulceration;
microvascular disease and suboptimal glycemic control contribute. Even with successIul
treatment resulting in ulcer healing, the recurrence rate in that patient population is 66, and the
amputation rate rises to 12.
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For excellent patient education resources, visit eMedicine's Diabetes Center. Also, see
eMedicine's patient education article Diabetic Foot Care.
Etiology
In general, Iactors that adversely aIIect wound healing can be remembered by using the
mnemonic device DIDN'T HEAL, as Iollows:
O D Diabetes: The long-term eIIects oI diabetes impair wound healing by diminishing
sensation and arterial inIlow. In addition, even acute loss oI diabetic control can aIIect
wound healing by causing diminished cardiac output, poor peripheral perIusion, and
impaired polymorphonuclear leukocyte phagocytosis.
O I InIection: InIection potentiates collagen lysis. Bacterial contamination is a necessary
condition but is not suIIicient Ior wound inIection. A susceptible host and wound
environment are also required. Foreign bodies (including sutures) potentiate wound
inIection.
O D Drugs: Steroids and antimetabolites impede proliIeration oI Iibroblasts and collagen
synthesis.
O N Nutritional problems: Protein-calorie malnutrition and deIiciencies oI vitamins A, C,
and zinc impair normal wound-healing mechanisms.
O T Tissue necrosis, resulting Irom local or systemic ischemia or radiation injury, impairs
wound healing. Wounds in characteristically well-perIused areas, such the Iace and neck,
may heal surprisingly well despite unIavorable circumstances. Conversely, even a minor
wound involving the Ioot, which has a borderline blood supply, may mark the onset oI a
long-term, nonhealing ulcer. Hypoxia and excessive tension on the wound edges also
interIere with wound healing because oI local oxygen deIicits. See, Ior example, the
pressure ulcers shown in the image below. Pressure ulcers
oI the lateral aspect oI the right Ioot.
O H Hypoxia: Inadequate tissue oxygenation due to local vasoconstriction resulting Irom
sympathetic overactivity may occur because oI blood volume deIicit, unrelieved pain, or
hypothermia, especially involving the distal extent oI the extremities.
O E Excessive tension on wound edges: This leads to local tissue ischemia and necrosis.
O A Another wound: Competition between several healing areas Ior the substrates
required Ior wound healing impairs wound healing at all sites.
O L Low temperature: The relatively low tissue temperature in the distal aspects oI the
upper and lower extremities (a reduction oI 1-1.5C |2-3F| Irom normal core body
temperature) is responsible Ior slower healing oI wounds at these sites.
$pecific etiologies
Arterial insufficiency
See InIrainguinal Occlusive Disease.
Jenous insufficiency
Patients with varicose veins or nonIunctional venous valves aIter deep vein thrombosis develop
ambulatory venous hypertension, that is, distal venous pressure remains elevated despite
ambulation. This constant venous hypertension seems to cause white cell and Iibrin buildup,
which impairs capillary blood Ilow or traps growth Iactors. Macromolecules pass into the dermis
and eventually cause the hemosiderin deposition and brawny induration in the distal leg (gaiter
area) characteristic oI chronic venous insuIIiciency.
Lymphedema
Although not typically a cause oI ulceration, extremity ulcers may Iail to heal because oI
untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate
adjuncts to the treatment oI recalcitrant wounds in edematous extremities. For advanced and
nonresponsive lymphedema, complex decongestive physiotherapy is a useIul treatment option.
Neuropathy
Sensory neuropathy involving the Ieet may lead to unrecognized episodes oI trauma caused by
ill-Iitting shoes. This is compounded by motor neuropathy causing intrinsic muscle weakness
and spaying oI the Ioot on weight bearing. The result is a convex Ioot with a rocker-bottom
appearance. Multiple Iractures go unnoticed, until bone and joint deIormities become marked.
This is termed a Charcot Ioot (ie, neuropathic osteoarthropathy) and is observed most commonly
in people with diabetes mellitus, aIIecting approximately 2 oI persons with diabetes.
!ressure (decubitus) ulcers
Pressure (decubitus) ulcers occur because oI prolonged ischemia-producing external pressure,
usually to a soIt tissue region overlying a bony prominence. Tissue ischemia results when
external pressure exceeds capillary closing pressure (ie, 25-32 mm Hg in healthy individuals),
the minimum pressure that causes collapse oI the capillary when applied to a capillary bed.
Shearing Iorces, exposure to constant moisture, and heat buildup also are major contributing
Iactors. For example, the stratum corneum, the outer layer oI skin, becomes 25 times more
Iragile at a relative humidity oI 100 than at a relative humidity oI 25 and becomes 4 times
more Iragile at 95F (35C) than at 86F (30C).
Neoplasms
Neoplasms strongly suggest malignancy in any chronic nonhealing wound, particularly iI the
wound appears to have occurred spontaneously.
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Basal cell carcinoma appears smooth, pearly, and elevated above the skin surIace, as illustrated
in the image below, whereas squamous cell cancer is oIten somewhat erythematous and scaly
and almost always occurs on sun-exposed areas. Particularly pertinent in wound care is the so-
called Marjolin ulcer, a squamous cell carcinoma originating in a chronic wound, such as a burn
scar or sinus tract.
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This implies that even a wound that is decades old is not necessarily
benign. Patients with Kaposi sarcoma typically present with multiIocal violaceous lower
extremity lesions. Patients with cutaneous lymphoma present with a single nodule or a group oI
papules Irom one to several centimeters in diameter, and these almost always occurs above the
waist.
Basal cell cancer maniIesting as a chronic leg ulcer.
PerIorm a biopsy oI every wound suggestive oI neoplasm, but remember that biopsy Iindings are
diagnostic only iI an adequate representative specimen is obtained.
#adiation damage
The adverse eIIects oI prolonged or excessive electromagnetic radiation vary with the
wavelength. Wavelengths oI electromagnetic radiation are as Iollows:
O amma rays - Less than 0.01 nm
O -rays - 0.01-10 nm
O Ultraviolet C - 10-280 nm
O Ultraviolet B - 280-320 nm
O Ultraviolet A - 320-400 nm
O Visible light - 400-760 nm
O InIrared - 760 nm to 1 mm
O Microwave - 1 mm to 30 cm
O #adio waves - Centimeters to meters
amma radiation and x-ray exposure cause a zone oI stasis, in which local blood supply is
impaired by coagulative necrosis due to thrombotic occlusion oI smaller arteries. amma and x-
ray radiation also spawn ionized oxygen that adversely aIIects DNA. The long-term result is
inhibition oI regeneration oI skin cells Irom dividing basal cells. This may cause recalcitrant
painIul skin ulcers. The surrounding skin is atrophic, with atrophy oI hair Iollicles and a paucity
subcutaneous Iat.
Ultraviolet radiation exposure, particularly ultraviolet B, causes sunburn initially and
subsequently conveys a continuing risk oI skin malignancy (eg, basal cell carcinoma, squamous
cell carcinoma, melanoma).
Excessive exposure to inIrared radiation, which induces repeated or persistent skin hyperthermia
oI 43-47C, may cause erythema ab igne. Patients with this skin condition present with
telangiectasia, erythematous patches, and hyperpigmentation.
Atheroembolism syndrome
Patchy areas oI ischemia involving the Ieet, especially in the presence oI palpable pedal pulses,
suggest the possibility oI atheroembolism oI plaque Iragments Irom ulcerated, although
nonocclusive, proximal atherosclerotic plaques or Irom thrombi lining the wall oI an inIrarenal
aortic aneurysm.
!yoderma gangrenosum
Pyoderma gangrenosum usually starts as a small painIul papule or nodule, which is oIten
erroneously presumed to be the result oI an insect bite. The lesion enlarges, becomes ulcerated,
and develops overhanging, violaceous borders, as shown in the image below.
Chronic ulcer oI medial aspect oI right leg due to pyoderma
gangrenosum.
The histologic Iindings oIten are nonspeciIic. Associated underlying systemic problems, which
occur in one halI oI patients with pyoderma gangrenosum, are oIten the best clues to the
diagnosis. Examples oI such systemic diseases include various arthritides, inIlammatory bowel
disease, hepatitis, myeloproliIerative disorders, myeloma, primary biliary cirrhosis, systemic
lupus erythematosus, and Sjgren syndrome. An important clue is a paradoxical response in
which debridement exacerbates the wound, particularly near the areas debrided. When
myoIascial and osseous tissues become involved, the only choice may be surgical debridement to
try to save the extremity.
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$ickle cell
Patients with sickle cellassociated leg ulcers typically present with painIul small ulcers that start
as crusting nodules in the distal one third oI the leg, oIten near the malleoli. The surrounding
skin demonstrates absence oI hair Iollicles, hyperpigmentation, and atrophy oI subcutaneous Iat.
#adiograph Iindings may reveal periosteal thickening oI underlying bone; true osteomyelitis is
rare. Sickle cell ulcers are more common in males than in Iemales and occur predominantly in
persons aged 10-50 years. Patients with sickle cell anemia can also develop leg ulcers because oI
other etiologies; the physical examination should exclude arterial and venous insuIIiciency.
Calciphylaxis
Calciphylaxis is an unusual and oIten Iatal syndrome oI cutaneous necrosis that tends to develop
in patients with chronic renal Iailure, particularly those with diabetes. The average time oI onset
is 3 years aIter the start oI dialysis. The Iemale-to-male ratio is 3:1. The initial Iinding oI
calciphylaxis may be that oI livedo reticularis, Iollowed by painIul erythematous areas oI
thickening oI the skin and subcutaneous tissues. The most common site is the thigh, though the
condition may also occur in the legs or the upper extremities.
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Panniculitis signaling the onset oI calciphylaxis may be precipitated by trauma, such as the site
oI an injection. Proximal painIul myopathy, muscle weakness, and elevated serum creatine
kinase (CK) levels may occur. Laboratory testing may demonstrate a high serum phosphate level
and an elevated parathyroid hormone level. Skin biopsy reveals calciIication oI the arterial media
and luminal stricture oI small-to-medium blood vessels in the subcutaneous Iat. Muscle biopsy
shows patchy necrosis and atrophy.
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Necrobiosis lipoidica
Necrobiosis lipoidica usually involves the anterior tibial areas, though it can also occur in the
Iace, arms, and chest. Patients present with well-circumscribed, shiny, reddish-brown, oval,
painless nodules or papules that have a thick shiny surIace. Over several months or a year, the
lesions may gradually expand and develop a waxy yellow color. Trauma may lead to inIected
ulcerations, and involvement oI adjacent cutaneous nerves may precipitate considerable pain.
Necrobiosis lipoidica is more common in women and in persons with diabetes than in others, but
it may also occur in persons without diabetes and beIore the diagnosis oI diabetes.
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Long-
standing necrobiosis lipoidica may harbor a squamous cell carcinoma.
Jasculitic wounds
Vasculitic wounds tend to occur throughout the lower legs as multiple, small, painIul,
erythematous nodules. Scars resulting Irom previous vasculitic lesions may be a useIul clue. Any
oI the disparate systemic maniIestations oI the diseases oI cellular immunity associated with
atypical skin lesions, including unexplained Ievers, jaw claudication, malaise, #aynaud
phenomenon, myalgias, neurologic abnormalities, and cranioIacial pain syndromes, suggest the
possibility oI vasculitis. These lesions are rare.
The diIIerential diagnosis oI wounds with these Ieatures includes other uncommon problems,
such as anticoagulant-induced skin necrosis, atheroembolism syndrome (ie, trash Ioot), and
Buerger disease. Leukocytoclastic vasculitides represent a disparate group oI acquired
connective tissue problems; patients present with palpable purpuric skin lesions, petechiae, and
ecchymoses, usually involving the lower extremities. These syndromes include Wegener
granulomatosis, Sjgren syndrome, cryoglobulinemia, systemic lupus erythematosus, rheumatoid
arthritis, dermatomyositis, and hepatitis B. The common Iactor among these syndromes is a
hypersensitivity angiitis.
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Skin biopsy demonstrates cuIIing oI the dermal microcirculation by granulocytes, which are
Iound in diverse stages oI viability, including complete cellular disintegration (ie, nuclear dust).
The various disorders in this group are diIIerentiated by clinical and serologic criteria. The
presence oI asymptomatic palpable purpura without thrombocytopenia suggests a drug adverse
eIIect, such as those caused by iodides, penicillin, aspirin, chlorothiazides, oxytetracycline,
isoniazid, or benzoic acid.
Anticoagulant-induced skin necrosis
Anticoagulant-induced skin necrosis is an unusual complication oI anticoagulant therapy.
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It
may occur with heparin or warIarin, though it is more common with warIarin. WarIarin-induced
skin necrosis maniIests as painIul hemorrhagic skin lesions, usually in an area having abundant
adipose tissue, such as the thighs, abdomen, or breasts. The Iemale-to-male ratio is 4:1.
This complication is oIten attributable to hereditary coagulation abnormalities. WarIarin
(Coumadin) depletes vitamin Kdependent coagulation Iactors, such as protein C. ThereIore,
during the Iirst several days oI warIarin therapy, a period oI transient hypercoagulability may
occur, particularly in patients with hereditary coagulation abnormalities, such as protein C
deIiciency or protein S deIiciency, antithrombin 3 deIiciency, or activated protein C
resistance.
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Actinomycosis
Actinomyces israelii is a Iastidious anaerobic bacterium that is relatively common and usually
nonpathogenic. In rare individuals, particularly hosts who are immunocompromised, the
bacterium can become pathogenic and cause chronic, draining, painless skin ulcers and sinuses,
usually in the head and neck. False-negative tissue cultures are common because the organism is
oIten diIIicult to culture in vitro. However, microscopic examination oI wound exudates may
demonstrate characteristic sulIur granules. Actinomycosis is responsive to penicillin but requires
long-term therapy.
Yaws
Yaws is a treponematosis caused by Treponema pertenue, which is endemic in humid regions
near the equator. Approximately 3-4 weeks aIter exposure, a pruritic sore that resembles a
raspberry (the mother yaw) develops at the site where the spirochete enters the skin. This lesion
eventually opens to Iorm an ulcer. Scratching spreads the organism and results in multiple
tubercles and ulcerations elsewhere, including the hands, Ieet, and genitals. These ulcers may
have a caseous crust. #esults oI serologic testing Ior syphilis may be positive.
Treatment is with a single large dose oI penicillin. Untreated yaws can erode to bone and joints
and can become deIorming and crippling.
The lesions oI pinta, caused by Treponema carateum, are similar to those oI yaws, but, unlike
yaws, no ulceration is present. Pinta typically begins as a papule on the dorsum oI the Ioot or leg.
The papule enlarges and becomes a pruritic plaque, which changes Irom a copper to gray to
bluish color over time. #egional lymphadenopathy may occur. Pinta is also responsive to
penicillin.
Mucormycosis
Mucormycosis is an acute and sometimes rapidly progressive, even Iatal, Iungal inIection that
may occur in patients who are immunocompromised, especially Iollowing a burn. The primary
lesions are plaques, ulcerations and abscesses, or painIul ecchymotic nodules, which may
ulcerate and then become necrotic and Iorm eschars. The diagnosis is conIirmed by
demonstrating Iungal elements oI the black discharge in KOH preparations and by culturing on
standard laboratory media.
Cutaneous anthrax
Cutaneous anthrax results Irom skin exposure to Bacillus anthracis, a gram-positive bacillus.
Cutaneous anthrax evolves Irom a pruritic papule to an ulcerated wound in 1 or 2 days and then
into a black eschar over the next week or so. Associated regional lymphadenopathy may be
present. Findings on special stains and cultures oI the wound exudate are diagnostic.
Anthrax is transmissible Irom specimens; thereIore, so laboratory personnel should be warned in
the event oI clinical suspicion oI this disease. OI course, appropriate public health authorities
must be notiIied. See Anthrax Ior details.
!athophysiology
The phases oI normal wound healing can be described as Iollows:
Hemostatic or inflammatory phase
This phase starts immediately and lasts 2-5 days. Tissue damage releases chemical mediators
called cytokines (eg, transIorming growth Iactor |TF|-beta |interleukin-1beta|), which initiate a
complex interrelated process that causes hemostasis and begins the healing process. Platelets
aggregate to stem bleeding. They also release serotonin and other vasoconstrictors and activate
the coagulation cascade. The result is conversion oI Iibrinogen into Iibrin, which stabilizes the
platelet plug. At that point, prostaglandins and activated complement cause vasodilation and
increase capillary permeability. This allows plasma to leak into the tissue surrounding the
wounded area. This is the inIlammatory exudate.
Monocytes and neutrophils are attracted to the site oI injury. Neutrophils trap and kill bacteria
immediately, while monocytes become activated macrophages, which produce growth Iactors
and cytokines and scavenge nonviable tissue and bacteria. Angiogenic growth Iactors stimulate
neovascularization oI the wound bed.
!roliferative phase
This phase lasts Irom 2 days to 3 weeks. Macrophages recruit Iibroblasts. These cells create a
network oI collagen Iibers. When adequate oxygen and vitamin C are present, granulation tissue
Iorms. Oxygen is incorporated by 2 amino acids, proline and lysine, which are both required Ior
collagen chain synthesis. Vitamin C is required Ior the hydroxylation oI proline to
hydroxyproline, an amino acid Iound in collagen.
During granulation, Iibroblasts create a collagen bed to Iill the deIect and grow new capillaries.
During contraction, myoIibroblasts pull the wound edges closer together to decrease the size oI
the wound. During epithelialization, new epithelium migrates Irom the intact epidermis around
the wound and can grow up to 3 cm over the granulation tissue. This process requires a moist
surIace.
Remodeling phase
This phase lasts Irom 3 weeks to 2 years.
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An organized Iorm oI collagen gradually replaces
the immature, soIt, gelatinous collagen. The eIIect is to increase the tensile strength oI the healed
wound, but it is less than 80 as strong as the original tissue.
Types of wound healing
First intention, also termed primary healing, is the healing that occurs when a clean laceration or
a surgical incision is closed primarily with sutures, Steri-Strips, or skin adhesive.
Second intention, also termed secondary healing, is the healing that occurs when a wound is leIt
open to heal by granulation, contraction, and epithelialization.
Delayed primary closure is a combination oI the other 2 types oI wound healing. It is oIten
intentionally applied to lacerations that are not considered clean enough Ior primary closure. The
wound is leIt open Ior 5-10 days; then, it is sutured closed to decrease the risk oI wound
inIection.
For excellent patient education resources, visit eMedicine's Procedures Center. Also, see
eMedicine's patient education article Suture Care.
!resentation
See Etiology.
Indications
All chronic wounds require assessment.
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Many heal with topical wound care; some require
surgical intervention. The details vary widely with the nature oI the wound. This article provides
inIormation regarding wound care in general and speciIic wound etiologies in particular.
Relevant Anatomy
LiIe is a constant battle against entropy (ie, disorder). The skin provides the primary barrier
between the human protoplasm and the entropy oI the external environment. Histologically, the
skin is divided into the epidermis and the dermis.
The epidermis consists oI 5 histologic strata. From superIicial to deep these layers are the (1)
stratum corneum, (2) stratum lucidum, (3) stratum granulosum, (4) stratum spinosum, and (5)
stratum germinativum. The keratinocyte, the preponderant epidermal cell, is generated in the
stratum germinativum and eventually desquamates (sloughs) when it reaches the stratum
corneum.
The dermis underlies the epidermis. A dermal vascular network Iunctions in thermoregulation
and provides metabolic support Ior the avascular epidermis. Fibroblasts synthesize supportive
and structural polymers, including ground substance, collagen, and elastin.
Skin appendages include sebaceous glands, hair Iollicles, and sweat glands.
Contraindications
See Treatment.