ulcer

ulcer

 [ul´ser]

a local defect, or excavation of the surface of an organ or tissue, produced by sloughing of necrotic inflammatory tissue.

aphthous ulcer a small painful ulcer in the mouth, approximately 2 to 5 mm in diameter. It usually remains for five to seven days and heals within two weeks with no scarring.

chronic leg ulcer ulceration of the lower leg caused by peripheral vascular disease involving either arteries and arterioles or veins and venules of the affected limb. Arterial and venous ulcers are quite different and require different modes of treatment. Venous stasis ulcers occur as a result of venous insufficiency in the lower limb. The insufficiency is due to deep vein thrombosis and failure of the one-way valves that act during muscle contraction to prevent the backflow of blood. Chronic varicosities of the veins can also cause venous stasis.

Patient Care. Stasis ulcers are difficult to treat because impaired blood flow interferes with the normal healing process and prolongs repair. Patient care is concerned with preventing a superimposed infection in the ulcer, increasing blood flow in the deeper veins, and decreasing pressure within the superficial veins.

decubitus ulcer pressure ulcer.

duodenal ulcer an ulcer of the duodenum, one of the two most common types of peptic ulcer.

gastric ulcer an ulcer of the inner wall of the stomach, one of the two most common kinds of peptic ulcer.

Hunner's ulcer one involving all layers of the bladder wall, seen in interstitial cystitis.

hypertensive ischemic ulcer a manifestation of infarction of the skin due to arteriolar occlusion as part of a longstanding vascular disease, seen especially in women in late middle age, and presenting as a red painful plaque on the lower limb or ankle that later breaks down into a superficial ulcer surrounded by a zone of purpuric erythema.

marginal ulcer a peptic ulcer occurring at the margin of a surgical anastomosis of the stomach and small intestine or duodenum. Marginal ulcers are a frequent complication of surgical treatment for peptic ulcer; they are difficult to control medically and often require further surgery.

peptic ulcer see peptic ulcer.

perforating ulcer one that involves the entire thickness of an organ, creating an opening on both surfaces.

phagedenic ulcer

1. any of a group of conditions due to secondary bacterial invasion of a preexisting cutaneous lesion or the intact skin of an individual with impaired resistance as a result of a systemic disease, which is characterized by necrotic ulceration associated with prominent tissue destruction.

2. tropical phagedenic ulcer.

pressure ulcer see pressure ulcer.

rodent ulcer ulcerating basal cell carcinoma of the skin.

stasis ulcer ulceration on the ankle due to venous insufficiency and venous stasis.

stress ulcer a type of peptic ulcer, usually gastric, resulting from stress; possible predisposing factors include changes in the microcirculation of the gastric mucosa, increased permeability of the gastric mucosa barrier to H⁺, and impaired cell proliferation.

trophic ulcer one due to imperfect nutrition of the part.

tropical ulcer

1. a lesion of cutaneous leishmaniasis.

2. tropical phagedenic ulcer.

tropical phagedenic ulcer a chronic, painful phagedenic ulcer usually seen on the lower limbs of malnourished children in the tropics; the etiology is unknown, but spirochetes, fusiform bacilli, and other bacteria are often present in the developing lesion, and protein and vitamin deficiency with lowered resistance to infection may play a role in the etiology.

varicose ulcer an ulcer due to varicose veins.

venereal ulcer a nonspecific term referring to the formation of ulcers resembling chancre or chancroid about the external genitalia; there are both sexually transmitted and other types.

ul·cer

(ŭl'sĕr),

A lesion through the skin or a mucous membrane resulting from loss of tissue, usually with inflammation. See: erosion.

Synonym(s): ulcus

[L. ulcus (ulcer-), a sore, ulcer]

ulcer

/ul·cer/ (ul´ser) a local defect, or excavation of the surface, of an organ or tissue, produced by sloughing of necrotic inflammatory tissue.

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corneal ulcer  ulcerative keratitis.

decubital ulcer , decubitus ulcer bedsore; an ulceration due to an arterial occlusion or prolonged pressure, as when a patient is confined to a bed or a wheelchair.

duodenal ulcer  a peptic ulcer situated in the duodenum.

gastric ulcer  an ulcer of the gastric mucosa.

Hunner's ulcer  one involving all layers of the bladder wall, occurring in chronic interstitial cystitis.

jejunal ulcer  an ulcer of the jejunum; such an ulcer following surgery is called a secondary jejunal u.

marginal ulcer  a gastric ulcer in the jejunal mucosa near the site of a gastrojejunostomy.

peptic ulcer  an ulceration of the mucous membrane of the esophagus, stomach, or duodenum, due to action of the acid gastric juice.

perforating ulcer  one involving the entire thickness of an organ or of the wall of an organ creating an opening on both surfaces.

phagedenic ulcer 

1. a necrotic lesion associated with prominent tissue destruction, due to secondary bacterial invasion of an existing cutaneous lesion or of intact skin in a person with impaired resistance as the result of systemic disease.

2. tropical phagedenic u.

plantar ulcer  a deep neurotrophic ulcer of the sole of the foot, resulting from repeated injury because of lack of sensation in the part; seen with diseases such as diabetes mellitus and leprosy.

rodent ulcer  ulcerating basal cell carcinoma of the skin.

stercoraceous ulcer , stercoral ulcer one caused by pressure of impacted feces; also, a fistulous ulcer through which fecal matter escapes.

stress ulcer  peptic ulcer, usually gastric, resulting from stress.

trophic ulcer  one due to imperfect nutrition of the part.

tropical ulcer 

1. a lesion of cutaneous leishmaniasis.

2. tropical phagedenic u.

tropical phagedenic ulcer  a chronic, painful, phagedenic ulcer of unknown cause, usually on the lower limbs of malnourished children in the tropics.

varicose ulcer  an ulcer due to varicose veins.

venereal ulcer  a nonspecific term referring to the formation of ulcers resembling chancre or chancroid about the external genitalia.

ulcer

(ŭl′sər)

n.

1. A lesion of the skin or a mucous membrane such as the one lining the stomach or duodenum that is accompanied by formation of pus and necrosis of surrounding tissue, usually resulting from inflammation or ischemia.

2. A corrupting condition or influence.

ulcer

[ul′sər]

Etymology: L, ulcus, a sore

a circumscribed, craterlike lesion of the skin or mucous membrane resulting from necrosis that accompanies some inflammatory, infectious, or malignant processes. An ulcer may be shallow, involving only the epidermis, as in pemphigus, or deep, as in a rodent ulcer. Some kinds of ulcers are peptic ulcer, pressure ulcer, and serpent ulcer. ulcerate, v., ulcerative, adj.

Chronic ulcer of the palate

ulcer

Dermatology A defect in a mucocutaneous surface. See Bairnesdale ulcer, Buruli ulcer, Esophageal ulcer, Kissing ulcer, Pressure ulcer, Rodent ulcer ENT Mouth ulcer, see there. See Aphthous ulcer GI disease Duodenal ulcer, see there. See Cushing's ulcer, Dieulafoy ulcer, Peptic ulcer, Stercoral ulcer, Stress ulcer Ophthalmology A defect on the epithelium of the eye. See Corneal ulcer, Corneal neurotrophic ulcer, Geographic ulcer, Peptic ulcer, Serpiginous ulcer.

ul·cer

(ŭl'sĕr)

An erosive or penetrating lesion on a cutaneous or mucosal surface, usually with inflammation.
Compare: erosion
Synonym(s): ulcus.

[L. ulcus (ulcer-), a sore, ulcer]

ulcer

(ul'ser) [L. ulcus, sore, ulcer]

A lesion of the skin or mucous membranes marked by inflammation, necrosis, and sloughing of damaged tissues. A wide variety of insults may produce ulcers, including trauma, caustic chemicals, intense heat or cold, arterial or venous stasis, cancers, drugs (such as nonsteroidal anti-inflammatory drugs [NSAIDs]), and infectious agents such as Herpes simplex or Helicobacter pylori.

amputating ulcer

An ulcer that destroys tissue to the bone by encircling the part.

APHTHOUS ULCER

aphthous ulcer

An ulcer of the oral mucosa, usually less than 0.5 cm in diameter. If it persists for longer than 2 weeks, it should be biopsied to rule out cancer. Synonym: aphthous stomatitis; canker sore See: illustration

Etiology

Aphthous ulcers are found in stomatitis, Behçet syndrome, Crohn disease, acquired immunodeficiency syndrome, and some cancers.

Treatment

For patients with oral ulcers, application of a topical anesthetic or a protective paste provides symptomatic relief and makes it possible to eat without pain.

arterial ulcer

Ischemic ulcer.

atonic ulcer

A chronic ulcer with little tendency to heal.

Buruli ulcer

An infection of the skin and underlying tissues with Mycobacterium ulcerans. The infection, common in the tropics and subtropics, develops slowly from a painless or minimally painful nodule on the skin into underlying bone, which it gradually destroys. The spread of the disease may be prevented with bacille Calmette-Guérin (BCG) vaccine.

callous ulcer

A chronic, slowly healing ulcer with indurated, elevated edges but no granulation.

Cameron ulcer

See: Cameron ulcer

chiclero ulcer

A Central American term for cutaneous leishmaniasis.

chronic leg ulcer

Any long-standing, slowly healing ulcer of a lower extremity, esp. one caused by occlusive disease of the arteries or veins or by varicose veins.

Curling ulcer

See: Curling ulcer

Cushing ulcer

See: Cushing, Harvey

decubitus ulcer

Pressure ulcer

denture ulcer

An ulcer of the oral mucosa caused by irritation from wearing dentures.

Patient care

To prevent irritation and ulceration of the mucous membranes of the mouth, denture wearers should clean dentures daily and remove them while sleeping. Poorly fitting dentures should be reconstructed or padded by a denturist.

diabetic foot ulcer

Diabetic foot infection.

duodenal ulcer

An open sore on the mucosa of the first portion of the duodenum, most often the result of infection with Helicobacter pylori. It is the most common form of peptic ulcer.

See: peptic ulcer

follicular ulcer

A tiny ulcer originating in a lymph follicle and affecting a mucous membrane.

fungal ulcer

1. An ulcer in which the granulations protrude above the edges of the wound and bleed easily.

2. An ulcer caused by a fungus.

gastric ulcer

An ulcer of the gastric mucosa.

Etiology

Common causes are NSAIDs, use of alcohol or tobacco, and infection with H. pylori.

See: peptic ulcer

Hunner ulcer

Interstitial cystitis.

indolent ulcer

A nearly painless ulcer usually found on the leg, characterized by an indurated, elevated edge and a nongranulating base.

ischemic ulcer

An ulcer caused by diminished blood flow through an artery, esp. one that nourishes a finger or toe. These ulcers are usually found in patients with peripheral vascular disease. They may result in loss of digits as a result of gangrene.

Synonym: arterial ulcer

Marjolin ulcer

See: Marjolin ulcer

Meleney ulcer

See: Meleney ulcer

Mooren ulcer

See: Mooren ulcer

peptic ulcer

An ulcer in the lining of the duodenum, the lower end of the esophagus, or the stomach (usually along the lesser curvature). Peptic ulcer disease is a common illness, affecting about 10% of men and 5% of women during their lifetimes. Curling ulcer; Helicobacter pylori; stress ulcer; Zollinger-Ellison syndrome;

Etiology

Common causes of peptic ulcer are factors that increase gastric acid production or impair mucosal barrier protection, e.g., salicylates and NSAIDs, smoking, H. pylori infection of the upper gastrointestinal tract, pathological hypersecretory disorders, consumption of alcohol and coffee, and severe physiological stress. Ulcers occur in men and women and occur most frequently in patients over age 65, with about 1.6 million cases diagnosed annually in the U.S. The relationship between peptic ulcer and emotional stress is not completely understood.

Symptoms

Patients with peptic ulcers may be asymptomatic or have gnawing epigastric pain, esp. in the middle of the night or when no food has been eaten for several hours. At times, heartburn, nausea, vomiting, hematemesis, melena, or unexplained weight loss may signify peptic disease. Food intake often relieves the discomfort. Peptic ulcers that perforate the upper gastrointestinal tract may penetrate the pancreas, causing symptoms of pancreatitis (severe back pain) and chemical peritonitis followed by bacterial peritonitis or an acute abdomen as irritating gastrointestinal (GI) contents and bacteria enter the abdominal cavity. Bacterial peritonitis can lead to sepsis, shock, and death.

Diagnosis

Endoscopy (esophagogastroduodenoscopy) provides the single best test to diagnose peptic ulcers because it allows direct visualization of the mucosa and permits carbon–13 urea breath testing, cytological studies, and biopsy to diagnose H. pylori and rule out cancer. During endoscopy, tissue can be excised, vessels ligated, or sclerosants injected. Barium swallow or upper GI x-ray series may also be used to provide images for diagnosis or follow-up and may be the initial test for patients whose symptoms are not severe.

Treatment

H. pylori causes most peptic ulcers in the duodenum; antibiotics (clarithromycin and amoxicillin) are prescribed to treat H. pylori, and antisecretory (proton pump inhibitor) drugs like lansoprazole or omeprazole should be given to all patients with duodenal ulcers. Bismuth or other coating agents may be used as a barrier to protect the duodenal mucosa. Peptic ulceration of the stomach may be treated with the same medications if biopsies or breath tests reveal H. pylori. When patients have ulcers caused by the use of NSAIDs or tobacco, withholding these agents and treating with an H₂ blocker, e.g., ranitidine, provides an effective cure. The prostaglandin analogue misoprostol may also be used to suppress or prevent peptic ulcer caused by use of NSAIDs. GI bleeding is managed initially with passage of a nasogastric tube and iced saline lavage, possibly with norepinephrine added. Gastroscopy then allows visualization of the bleeding site and laser or cautery coagulation. When conservative medical treatment is ineffective, vagotomy and pyloroplasty may be used to reduce hydrochloric acid secretion and enlarge the pylorus to enhance gastric emptying. More extreme surgical therapy (including subtotal gastric resection) may be needed in rare instances of uncontrollable hemorrhage or perforation occurring as a result of peptic ulcer disease.

Patient care

The ambulatory patient is educated about agents that increase the risk for peptic ulceration and given specific instructions to avoid them. Instruction should include the importance of adhering to prescription drug therapies, adverse reactions to H₂-receptor antagonists and omeprazole (dizziness, fatigue, rash, diarrhea), and the need for follow-up examination and care.

For the hospitalized patient with ulcer-related bleeding, careful monitoring of vital signs, fluid balance, hemoglobin levels, and blood losses may enhance early recognition of worsening disease. Intravenous (IV) access is established, and IV opiates are administered as prescribed for pain control. The patient is kept nil per os (NPO). Electrolytes and fluids are replaced as needed. Endoscopic or other diagnostic and treatment procedures are explained to the patient, and the effects of prescribed therapies or transfusions are carefully assessed. All patient care concerns apply after major surgery. The patient is assessed for possible complications: hemorrhage, shock, malabsorption problems (iron, folate, or vitamin B₁₂ deficiency anemias), and dumping syndrome. To avoid these problems, the patient is advised to drink fluids between meals rather than with meals, eat 4 to 6 small, high-protein, low-carbohydrate meals daily, and lie down after eating. Before and after discharge, health care professionals should help the patient to develop coping mechanisms to relieve anxiety. Patients are taught to recognize signs and symptoms of disease recurrence (e.g., coffee-ground emesis, the passage of black or tarry stools, or epigastric pain). Patients who use antacids and have a history of cardiac disease or whose sodium intake is restricted for any reason are warned to take only those antacids that have low amounts of sodium. The need for ongoing medical care is stressed.

perforating ulcer

An ulcer that erodes through an organ, e.g., the stomach or duodenum.

phagedenic ulcer

Tropical ulcer.

postpolypectomy ulcer

An erosion through the lining of the gastrointestinal tract resulting from endoscopic removal of a tumor.

PRESSURE UCLER

pressure ulcer

Damage to the skin or underlying structures from compression of tissue and inadequate perfusion. Pressure ulcers typically occur in patients who are bedridden or chair bound. Patients with sensory and mobility deficits (such as patients with spinal cord injury, stroke, or coma); malnourished patients; patients with peripheral vascular disease; hospitalized elderly patients; and nursing home residents are all at risk. Some evidence also suggests that incontinence is a risk factor. Synonym: bed soredecubitus ulcerpressure sore See: Norton scale for table.

The most common sites of skin breakdown are over bony prominences (the sacrum and the trochanters, the heels, the lateral malleoli and also the shoulder blades, ischial tuberosities, occiput, ear lobes, elbows, and iliac crests). The combination of pressure, shearing forces, friction, and moisture leads to tissue injury and occasionally necrosis. If the ulcer is not treated vigorously, it will progress from a simple red patch of skin to erosion into the subcutaneous tissues, eventually extending to muscle or bone. Deep ulcers often become infected with bacteria and develop gangrene. See: illustration

Treatment and Prevention

The most important principle is to prevent the initial skin damage that promotes ulceration. In patients at risk, aggressive nursing practices, such as frequent turning of immobile patients and the application of skin protection to bony body parts, are frequently effective. Gel flotation pads, alternating pressure mattresses, convoluted foam mattresses and sheepskins or imitation sheepskins may be employed. Specialized air-fluid beds, waterbeds, or beds with polystyrene beads provide expensive but effective prophylaxis. If the patient develops an ulcer, topical treatments with occlusive hydrocolloid dressings, polyurethane films, absorbable gelatin sponges, collagen dressings, wound-filter dressings, water-vapor permeable dressings, and antibiotic ointments aid the healing of partial-thickness sores. Deeper lesions may need surgical débridement. Skin-damaging agents such as harsh alkaline soaps, alcohol-based products, tincture of benzoin, hexachlorophene, and petroleum gauze should be avoided. Consultation with a wound care specialist is advantageous.

Patient care

The skin is thoroughly cleansed, rinsed, and dried, and emollients are gently applied by minimizing the force and friction used, esp. over bony prominences. Patients who are not able to position themselves are repositioned every 1–2 hr to prevent tissue hypoxia resulting from compression. A turning sheet or pad is used to turn patients with minimal skin friction. Care providers should avoid elevating the head of the bed higher than 30° (except for short periods) to reduce shearing forces on the skin and subcutaneous tissues overlying the sacrum. Range-of-motion exercises are provided, early ambulation is encouraged, and nutritious high-protein meals are offered. Low-pressure mattresses and special beds are kept in proper working order. Doughnut-type cushions should not be used because they decrease blood flow to tissues resting in the center of the doughnut.

Ulcers are cleansed and débrided, and other therapeutic measures are instituted according to institutional protocol or prescription. Consultation with a nutritionist may be needed to assess and optimize the patient's nutritional status, and to provide high-protein meals with added vitamin C to promote healing, protein and calorie-rich supplements, or enteral feedings. Weak or debilitated patients should be assisted to eat, with care taken to prevent swallowing difficulties.

RODENT ULCER: on the ear

rodent ulcer

A basal cell carcinoma that has caused extensive local invasion and tissue destruction, esp. on the face. The usual sites are the outer angle of the eye, near the side and on the tip of the nose, and at the hairline.

Synonym: Jacob ulcer See: illustration

Saemisch ulcer

See: Saemisch ulcer

serpiginous ulcer

A creeping ulcer that heals in one part and extends to another. See: Mooren ulcer

shield ulcer

A corneal ulcer found in some patients with vernal conjunctivitis. The ulcer is sometimes associated with corneal plaques that may permanently impair vision.

simple ulcer

A local ulcer with no severe inflammation or pain.

specific ulcer

An ulcer caused by a specific disease, e.g., syphilis or lupus erythematosus.

stercoral ulcer

A rarely occurring ulcer of the colon caused by pressure from impacted feces. Perforation through the walls of the colon may cause peritonitis, sepsis, and sometimes death.

stress ulcers

Multiple small, shallow ulcers that form in the mucosa of the stomach or, occasionally, in the duodenum in response to extreme physiological stressors. See: Curling ulcer; Cushing ulcer under Cushing, Harvey; peptic ulcer

traumatic ulcer

An ulcer due to injury of the oral mucosa. Its causes include biting, denture irritation, toothbrush injury, and sharp edges of teeth or restorations.

trophic ulcer

An ulcer caused by the failure to supply nutrients to a part.

tropical ulcer

1. An indolent ulcer, usually of a lower extremity, that occurs in those living in hot, humid areas. The cause may or may not be known; it may be caused by a combination of bacterial, environmental, and nutritional factors. Synonym: phagedenic ulcer

2. The tropical sore caused by leishmaniasis.

varicose ulcer

An ulcer, esp. of the lower extremity, associated with varicose veins.

venereal ulcer

An ulcer caused by a sexually transmitted disease, i.e., chancre or chancroid.

VENOUS STASIS ULCER: On lateral malleolus

venous stasis ulcer

A poorly and slowly healing ulcer, usually located on the lower extremity above the medial malleolus. Typically it is edematous, pigmented, and scarred. The skin is extremely fragile and easily injured. In the U.S. about 3.5% of people over 65 have venous stasis ulcers. Women are three times more likely than men to be affected. See: illustration

Patient care

Assessment includes a detailed medical and surgical history and physical examination. When the lower extremities are examined, characteristic markers of venous ulceration include ankle flare (distention of small veins on the medial aspect of the foot due to chronic venous hypertension); dermatitis; pigmentation changes on the skin surface, usually appearing as brown discolorations affecting the medial part of the leg; woody induration of the leg; and varicosities. The health care professional should examine the leg for lesions superior to the medial malleolus and should carefully measure the size, shape, and margins of wounds; drainage or exudates; surrounding skin; and pain or tenderness. The patient should be advised to elevate the legs 7 in (18 cm) above the heart for 2 to 4 hr during the day and at night. Compression devices (such as graduated pressure stockings, Unna boot) are used to help reduce edema, improve venous blood flow, and aid healing. Before applying any compression device or wrap, the health care professional should measure the patient’s leg circumference at the wound and the wound size of the ulcer. The wound should be cleansed regularly, and aggressive debridement employed as needed. Wounds with light to moderate drainage benefit from a moisture-retentive dressing (such as hydrocolloid, transparent film, some foams), whereas wounds with moderate to heavy drainage do better with an absorbent dressing (such as foams, alginates, special absorptive dressings). Underlying problems such as obesity, deep venous thrombosis, diabetes, and cardiovascular disease must be assessed and managed as part of the wound care protocol.

ulcer

A local loss of surface covering (EPITHELIUM).and sometimes deeper tissue in skin or MUCOUS MEMBRANE. An open sore. Loss of surface leads to infection and further tissue damage. Ulcers may be caused by physical or chemical damage, by loss of blood supply or by local infection. Ulcers of the STOMACH or DUODENUM are called peptic ulcers. See also BEDSORES, VARICOSE ULCERS and TROPICAL ULCERS.

Ulcer

A site of damage to the skin or mucous membrane that is characterized by the formation of pus, death of tissue, and is frequently accompanied by an inflammatory reaction.

Mentioned in: Birthmarks, Canker Sores, Dermatitis, Diabetic Foot Infections, Gastritis, Genital Herpes, H-2 Blockers, Impetigo, Nasal Packing, Yaws

ulcer

non-healing, chronic wound showing concomitant tissue repair and tissue breakdown, chronic inflammation and deposition of fibrous tissue in surrounding/underlying soft tissues, and threat of secondary infection; caused by loss of/breakdown/infection of epidermal/dermal tissues, with subcuticular tissue and deeper structure involvement; characterized by pain (unless in neuropathic tissues), chronic inflammation, fibrosis of underlying and local peripheral tissue, fluid exudation and proneness to infection predisposing factors include arterial, venous, lymphatic, neurological and immune compromise (see Table 1); presence of foreign body (including necrotic material) within the wound, repeated microtrauma, and concurrent systemic disease and drug regimes contribute to non-healing; normal healing events (i.e. healing by secondary intention [inflammation, epithelialization, wound contraction, connective tissue maturation]) are prolonged, disrupted and often non-sequential (Table 2); healing is promoted by addressing the cause of tissue breakdown and concomitant factors that interrupt normal healing, together with measures to promote systemic wellness (Table 3; see Table 4), including rest (e.g. use of a full contact cast to allow non-weight-bearing ambulation), regular wound care (and dressings appropriate to phase of healing to optimize wound environment; see Table 5 and Box 1), antibiotics (to control infection Table 6), pressure bandaging and/or diuretics (to control or reduce foot/limb oedema), vascular surgery (to improve arterial supply/venous return) and tight glycaemic control (see Table 7, Table 8 and Table 9 and Box 2)

• complicated ulcer secondarily infected chronic wound penetrating to and involving deeper structures; possibly complicated by osteomyelitis

• decubitus ulcer; pressure sore ulcer formation at pressure point (e.g. posterior/plantar margin of heels, sacrum, elbows) in bed-bound patients, caused by compromised local blood supply and reduced tissue viability, relative immobility and general patient debility

• gastric ulcer erosion of gastric mucosa due to chronic ingestion of non-steroidal anti-inflammatory drugs or infection with Helicobacter pylori

• Marjolin's ulcer neoplastic deterioration of pre-existing long-standing ulcer

• mixed-pathology ulcer chronic wound caused by mixed pathology, e.g. secondary bone infection within a neuroischaemic ulcer

• neuroischaemic ulcer ulcer development in neuropathic ischaemic tissue

• neuropathic ulcer plantar ulcer induced by relatively minor trauma, in an insensitive foot (see trophic ulcer)

• perforating ulcer ulcer whose base penetrates to involve subcuticular structures, e.g. tendon/bone (which may be visible within the lesion base)

• rodent ulcer see basal cell carcinoma

• trophic ulcer deep plantar ulcer (prone to both aerobic and anaerobic infections) induced by relatively minor trauma and/or tissue stress (e.g. pressure/friction) in a neuropathic (anaesthetic) foot, e.g. in diabetes or leprosy; skin surrounding the ulcer tends to exuberant callous formation (see Box 3 and Table 10)

• varicose ulcer; venous ulcer wide, shallow ulcer most commonly found at lower medial one-third of leg in association with poor and prolonged compromised venous return and/or venous stasis; develops within area of oedematous tissue characterized by signs of compromised venous function (e.g. varicose eczema, haemosiderosis, woody tissue fibrosis, scars of healed earlier ulceration, atrophy blanche and varicose veins)

Table 1: Phases in the progression of an ulcer to healing

Ulcer phase	Characteristics	Comment
Active phase	Wound dimensions increase (undermined wound edges) Exudation Formation of slough Periwound oedema and induration of edges	Dissolution and degradation of devitalized tissue ± infection Macrophage and enzyme activity Accumulation of degraded tissue and dead macrophages Chronic, non-resolving inflammation ± collagen deposition
Proliferative phase	Wound begins to infill (wound dimensions reduce) Epithelialization (saucerization) of margins	Formation of granulation tissue Recruitment of fibroblasts; collagen formation Epidermal cells at margins mitose and spread out to begin to close wound
Maturation phase	Wound contraction Wound closure Scar formation	Myofibrils within fibroblasts contract Epithelialization is complete Devascularization of fibrotic tissue that forms scar

Table 2: Examples of ulcer classification systems

Classification system	Details	Comments
Wagner	Grade 0: local deformity or callosity but no open lesions Grade 1: partial or full skin thickness, superficial ulcer Grade 2: deep ulcer without osteomyelitis, but extending to ligament, tendon, bone, joint capsule or deep fascia Grade 3: deep ulcer with associated cellulitis, abscess formation and/or osteomyelitis and/or joint sepsis Grade 4: gangrene localized to the forefoot or heel Grade 5: extensive gangrene	Widely recognized and used system Rather generalist and non-specific Ignores neuropathy and lesion size, and thus their effects of choice of treatment/lesion management
S SAD	S = size of lesion (area; depth) S = sepsis (presence/absence) A = arteriopathy (ischaemia) D = denervation (sensory/autonomic/motor neuropathy)	Builds on from the Wagner system (above), introducing additional categories, each awarded 0 (normal), 1 (mild change), 2 (moderate change), 3 (severe change) subclassification
RYB	R = red wound (pale pink–beefy red ulcer base, proliferating/inflammatory ulcer) Y = yellow wound (moist, exudating ivory/ green/brownish sloughy wound) B = black wound (dry wound with black/ brown/tan hard eschar)	Wound assigned colour grading A limited classification that focuses solely on wound appearance and ignores other factors (e.g. distal sensory neuropathy, peripheral ischaemia, cellulitis, size/depth of lesion, phase of progression of lesion)
PEDIS	P = perfusion of limb/foot E = extent of wound (size of lesion) D = depth of lesion/tissue loss I = infection S = sensation (perception of light touch, vibration, contact of 10g monofilament, hot/cold discrimination)	Each subcategory is graded 1–4, where 1 = normal/absence and 4 = severe Useful research tool allowing indepth assessment of lesion progression over time, and comparison of lesions subjected to varying treatment modalities
DEPA	D = depth of lesion E = extent of bacterial colonization P = phase of ulcer (Table 11) A = associated aetiology (e.g. trauma, neuropathy, ischaemia, infection, diabetes mellitus) DEPA <6 = low-grade wound (i.e. local debridement, oral antibiosis as necessary, glycaemic control measures) DEPA 7–9 = moderate-grade wound (i.e. debridement, parenteral antibiosis, insulin therapy, wound-healing promotion agents, pressure relief) DEPA 10–12 = high-grade wounds (i.e. parenteral antibiosis, insulin therapy, wound-healing promotion agents, vascular reconstruction)	Each subcategorization is graded 1–3 to reflect increasing levels of severity Validated system Score 6 = wound likely to heal in time Score 10: great difficulty in healing Score 11–12 (especially heel wounds): prognostic of lower-limb amputation
University of Texas system	Tier 1 Wound graded 0–3 according to wound depth/tissue involvement: 0 = pre-/postulcer with intact epithelium 1 = superficial ulcer not involving bone/tendon 2 = ulcer penetrates to tendon/joint capsule 3 = ulcer penetrates to bone/joint Tier 2 Wound graded A–D according to wound burden/tissue status A = non-infected/non-ischaemic B = infected/non-ischaemic C = non-infected/ischaemic D = infected/ischaemic	Multisite validated system Two-tier wound classification (tier 1 = ulcer; tier 2 = wound burden/tissue status, e.g. 1C = no current ulcer; ischaemic foot) gives risk assessment Useful wound management ‘road map’ Should be used in conjunction with other markers of limb status (e.g. degree of sensory neuropathy, autonomic function; ankle–brachial pressure index, Buerger's test, presence of critical ischaemia, skin condition, local foot/toes deformity, subtalar joint range of motion)

Table 3: Phases in the progression of an ulcer to healing

Ulcer phase	Characteristics	Comment
Active phase	Wound dimensions increase (undermined wound edges) Exudation Formation of slough Periwound oedema and induration of edges	Dissolution and degradation of devitalized tissue ± infection Macrophage and enzyme activity Accumulation of degraded tissue and dead macrophages Chronic, non-resolving inflammation ± collagen deposition
Proliferative phase	Wound begins to infill (wound dimensions reduce) Epithelialization (saucerization) of margins	Formation of granulation tissue Recruitment of fibroblasts; collagen formation Epidermal cells at margins mitose and spread out to begin to close wound
Maturation phase	Wound contraction Wound closure Scar formation	Myofibrils within fibroblasts contract Epithelialization is complete Devascularization of fibrotic tissue that forms scar

Table 4: Features of chronic wounds (ulcers) as an aid to diagnosis

Feature	Neuropathic	Ischaemic	Infected	Healing
Base	Sloughy	Adherent slough	Deep and sloughy	Granulation and epithelialization
Walls	Undermined	Vertical	Undermined	Saucerized
Depth	Deep	Relatively shallow	Deep and penetrating	Shallow
Exudate	Moderate/copious thick	Moderate serous	Heavy, pus-y, bloody, malodorous	Scant, serous
Surrounding tissues	Heavy callosity	Cold, cyanotic	Cellulitic	Mild inflammation
Prognosis	Extending	Static, non-healing	Extending and spreading	Reducing

Table 5: Examination of chronic wounds (ulcers): appearance of the wound

Point of note	Features to be recorded
Site	The exact anatomical location of the wound
Size	The dimensions of the wound, in millimetres: • Width (medial–lateral distance) • Length (longitudinal distance) • Depth
Appearance	The appearance of the wound and the surrounding tissues: • Callosity • Maceration • Signs of local infection • Signs of spread of infection (cellulitis, lymphangitis, lymphadenitis)
Sides	The orientation of the walls of the wound in relation to the skin surface: • Undermined (extending wound) • Vertical (static wound) • Saucer-shaped (healing wound)
Base	The nature of the wound floor: • Sloughy (infected, non-healing) • Granulating (healing) • Hypergranulating (non-healing or traumatized wound) • Deep structures, such as joint capsule/tendon/bone, visible through wound base (extending wound)
Discharge	A deep swab of the discharge should be sent for pathology laboratory culture and sensitivity The amount and type of discharge should be noted (the amount can be inferred by the state of the dressing in relation to how long it has been in situ): • Colour – yellow/green (extending wound or infection); red/brown (blood or infection); turquoise green (Pseudomonas infection); clear (joint fluid or healing wound) • Texture – thick (staphylococcal infection or extending wound); thin (streptococcal infection or healing wound) • Amount – copious (infection); plentiful (extending or non-healing wound); scarce (healing wound) • Odour – very smelly (necrotic, infected); sweet (healing)

Table 6: Types of wound dressings and indications for their use

Dressing Type	Features	Indicated Use
Primary Wound-Dressing Films
Semi-permeable adhesive film	Non-absorbent Non-adherent to wound surface Gas and water vapour permeable, but impermeable to water Non-shedding Transparent, allowing observation of wound	Low exudating wounds
Perforated film, absorbent	Low adherence (absorbent pad covered by perforated film)	Low exudating wounds
Low-adherent Wound Contact Layers
Unmedicated viscose	Non-absorbent; non-shedding	Non-adherent primary dressing
Medicated tulle	Low-adherent polyethylene glycol or paraffin impregnated tulle incorporating an antiseptic (e.g.: chlorhexidine gluconate; iodine)	Topical antisepsis
Semi-permeable hydrogels	Hydrophilic polymers in either sheet or amorphous formulations Highly absorbent Gas permeable, but impermeable to water Dressing surface may dry out, and thus requires rehydration with saline	Removal of slough Rehydration of dry, necrotic tissue to allow its later sharp debridement Absorption of heavy exudation Carrier of topical antimicrobials (e.g.: metronidazole)
Hydrocolloids	Interactive (form a gel when in contact with wound surface) Usually formulated with an occlusive, water-repellent backing Promote an acidic and hypoxic wound environment, and facilitates neoangiogenesis	Not suitable for infected wounds Maintain a moist, temperature controlled wound environment
Alginates	Seaweed derivatives which form a hydrophilic gel in contact with the wound surface Require irrigation to remove from wound surface	Absorption of exudation Moisten with saline before application
Polyurethane foams	Smooth low-adherent wound contact layer backed with hydrophobic foam Highly gas-permeable Maintain a moist wound environment and good thermal insulation	Absorption of moderate exudation Outer layer prevents ‘strike through’
Silver agents	Silver ions impregnated into dressing Antibacterial action	Topical antisepsis, including resistant forms

• Removal and absorption of exudate to prevent maceration of tissues and growth of wound contaminants and microorganisms, and prevent ‘strike-through’

• Maintenance of correct levels of humidity at the wound surface in order to encourage keratinocyte migration across the wound surface

• Gaseous permeability to allow correct oxygen levels within the wound; high oxygen levels promote keratinocyte function; relative hypoxia promotes neoangiogenesis and macrophage function, and reduces pain

• Impermeable to microorganisms, by the prevention of ‘strike-through’

• Maintenance of the correct tissue pH; oxygen dissociates from haemoglobin, and neoangiogenesis is stimulated at acidic (i.e. <7.4) pH levels

• Maintenance of the correct temperature, in order to promote fibroblast and keratinocyte division, and thereby promote healing; the wound takes up to 3 hours to regain its pre-dressing rate of cell mitosis, and a 10°C fall in wound temperature reduces oxygen dissociation from oxyhaemoglobin

• Low adherence, so that newly formed tissues are not disrupted during dressing changes; ‘wet to dry’ dressings cause considerable tissue damage when the dressing is changed

• Non-contaminating, in order to prevent shedding of the dressing fibres into the wound; shed fibres can cause foreign-body and toxic reactions

• Ease of application

• Comfortable in situ, and well conforming to the wound site

Table 7: Indicative antibiotic/antimicrobial regimes

Infection site	Indicative antibiotic regime
Skin
Impetigo	Localized infection: topical fusidic acid (or mupirocin if MRSA+ve); dicloxacillin; azithromycin Widespread infection: oral flucloxacillin or erythromycin (if penicillin-sensitive)
Erysipelas	Phenoxymethylpenicillin or erythromycin
Cellulitis	Benzylpenicillin and flucloxacillin (or erythromycin if penicillin-sensitive); co-amoxiclav
Infected ulcer	Topical antibiotics: mupirocin, fusidic acid Topical antiseptics: povidone-iodine
Infected burns (e.g. caustic burns)	Silver sulfadiazine
Animal/human bites	Co-amoxiclav (doxycyline + metronidazole if penicillin-sensitive)
Osteomyelitis	Flucloxacillin (clindamycin if penicillin-sensitive) Vancomycin if MRSA+ve or Staphylococcus epidermidis -+ve Sodium fusidate (has good bone penetration)
Septic arthritis	Flucloxacillin + fusidic acid (clindamycin if penicillin-sensitive) Vancomycin if MRSA+ve or Staphylococcus epidermidis -+ve
Prevention of infection in orthopaedic surgery	Single dose of intravenous cefuroxime or intravenous flucloxacillin
Staphylococcus species	Systemic flucloxacillin; fusidic acid (erythromycin if penicillin-sensitive)
Streptococcus species	Systemic penicillin, erythromycin, clindamycin, phenyloxymethylpenicillin
Beta-haemolytic streptococci	Systemic phenyloxymethylpenicillin
Pseudomonas aeruginosa	Systemic ciprofloxacin; ticarcillin + clavulanic acid; azlocillin; piperacillin
Anaerobic infection	Systemic metronidazole (also as topical beads in the treatment of anaerobe-infected ulcers)
Note: Swab of the wound/exudate is taken to ensure the most effective antibiotic is prescribed; the patient is started on a broad-spectrum antimicrobial and the medication modified as necessary once the laboratory results confirm the regime of choice. MRSA, meticillin-resistant Staphylococcus aureus .

Table 8: Examination of chronic wounds (ulcers): history of the wound

Points of note	Questions that should be asked
Duration	How long has the wound been present?
Size	Has the wound changed (got bigger/smaller; altered its appearance)?
Number	Is there an increase/decrease in the number of wounds?
Previous wounds	Have similar wounds occurred in the past? If so, when?
Sensory changes	Has the patient noted any changes of sensation in the affected foot (increased sensitivity; decreased sensitivity; paraesthesia)?
Tissue changes	Have the surrounding tissues altered in appearance (swelling; limb/foot oedema; colour changes; dryness of skin)?
Cause	What does the patient think caused the wound in the first place?

Table 9: Examination of chronic wounds (ulcers): appearance of the wound

Point of note	Features to be recorded
Site	The exact anatomical location of the wound
Size	The dimensions of the wound, in millimetres: • Width (medial–lateral distance) • Length (longitudinal distance) • Depth
Appearance	The appearance of the wound and the surrounding tissues: • Callosity • Maceration • Signs of local infection • Signs of spread of infection (cellulitis, lymphangitis, lymphadenitis)
Sides	The orientation of the walls of the wound in relation to the skin surface: • Undermined (extending wound) • Vertical (static wound) • Saucer-shaped (healing wound)
Base	The nature of the wound floor: • Sloughy (infected, non-healing) • Granulating (healing) • Hypergranulating (non-healing or traumatized wound) • Deep structures, such as joint capsule/tendon/bone, visible through wound base (extending wound)
Discharge	A deep swab of the discharge should be sent for pathology laboratory culture and sensitivity The amount and type of discharge should be noted (the amount can be inferred by the state of the dressing in relation to how long it has been in situ): • Colour – yellow/green (extending wound or infection); red/brown (blood or infection); turquoise green (Pseudomonas infection); clear (joint fluid or healing wound) • Texture – thick (staphylococcal infection or extending wound); thin (streptococcal infection or healing wound) • Amount – copious (infection); plentiful (extending or non-healing wound); scarce (healing wound) • Odour – very smelly (necrotic, infected); sweet (healing)

Table 10: Antibiotic regimes for the treatment of infection in plantar neuropathic ulceration

Identified microorganism	Example of antimicrobial drug
Streptococci	Oral amoxicillin 500mg tds (or IV amoxicillin 500mg 8-hourly)
Staphylococci	Oral flucloxacillin 500mg qds (or IV flucloxacillin 500mg 6-hourly)
Anaerobes	Oral metronidazole 400mg tds (or IV metronidazole 500mg 8-hourly)
Gram-negatives	Oral ciprofloxacin 500mg bd (or IV ceftazidime 1g 6-hourly)
IV, intravenous.

• Debride the skin surrounding and overlying ulcer of all callosity

• Take a deep bacteriological swab of the ulcer base

• Initiate broad-spectrum antibiotic therapy if infection is suspected (tailor the antibiotic once the swab has been cultured and the microorganism sensitivity identified; severe infections/cellulitis may require treatment as an inpatient with intravenous antibiotic drugs)

• Cut back all unsupported tissue at the periphery of the ulcer and necrotic tissue to healthy bleeding tissue (if an entire digit is necrotic, a ray excision amputation may be required)

• Cleanse the ulcer using normal saline (Normasol) at 37°C delivered under pressure from a disposable needleless syringe

• Dry the ulcer area with non-shedding sterile gauze

• Dress the ulcer (exudating wounds require absorbent dressings that wick the exudates away and prevent tissue maceration)

• Reduce plantar pressures (with padding, triple-layer bespoke insoles in bespoke shoes, removable or full-contact casts)

• Review weekly; maintain antibiosis and non-weight-bearing regime until the ulcer has healed

• Debride the skin surrounding and overlying ulcer of all callosity

• Take a deep bacteriological swab of the ulcer base

• Initiate broad-spectrum antibiotic therapy if infection is suspected (tailor the antibiotic once the swab has been cultured and the microorganism sensitivity identified; severe infections/cellulitis may require treatment as an inpatient with intravenous antibiotic drugs)

• Cut back all unsupported tissue at the periphery of the ulcer and necrotic tissue to healthy bleeding tissue (if an entire digit is necrotic, a ray excision amputation may be required)

• Cleanse the ulcer using normal saline (Normasol) at 37°C delivered under pressure from a disposable needleless syringe

• Dry the ulcer area with non-shedding sterile gauze

• Dress the ulcer (exudating wounds require absorbent dressings that wick the exudates away and prevent tissue maceration)

• Reduce plantar pressures (with padding, triple-layer bespoke insoles in bespoke shoes, removable or full-contact casts)

• Review weekly; maintain antibiosis and non-weight-bearing regime until the ulcer has healed

Table 11: Antibiotic regimes for the treatment of infection in plantar neuropathic ulceration

Identified microorganism	Example of antimicrobial drug
Streptococci	Oral amoxicillin 500mg tds (or IV amoxicillin 500mg 8-hourly)
Staphylococci	Oral flucloxacillin 500mg qds (or IV flucloxacillin 500mg 6-hourly)
Anaerobes	Oral metronidazole 400mg tds (or IV metronidazole 500mg 8-hourly)
Gram-negatives	Oral ciprofloxacin 500mg bd (or IV ceftazidime 1g 6-hourly)
IV, intravenous.

ulcer 

A localized lesion of the skin or of a mucous layer in which the superficial epithelium is destroyed and deeper tissues are exposed. See abscess.
corneal ulcer A superficial loss of corneal tissue as a result of infection that has led to necrosis. It may be caused by a bacterium (e.g. Pseudomonas aeruginosa, Streptococcus pneumoniae), by a virus (e.g. herpesvirus), or by a fungus (e.g. Candida, Aspergillus, Penicillium). It causes pain and usually reduced visual acuity, especially if the ulcer occurs in the centre of the cornea. Corneal ulcers usually look dirty grey or white and are opaque areas of various sizes and a mucopurulent discharge may be present. If induced by contact lenses, especially extended wear lenses, patients must cease wearing their lenses immediately, and the appropriate therapy instituted: antibacterial, antifungal or antiviral agent. See corneal facet; herpes simplex keratitis; hypopyon keratitis; rosacea keratitis; ulcerative keratitis; keratocele; keratomycosis; leukoma.
dendritic ulcer See herpes simplex keratitis.
von Hippel's internal ulcer A depression noted in the posterior surface of the cornea. This lesion resembles posterior lenticonus, except that it is thought to be due to an infection or inflammation. The lesion can be differentiated from Peter's anomaly by the presence of endothelium and Descemet's membrane in the former. Due to its posterior location, the lesion does not usually disturb visual function. See Peter's anomaly.
marginal corneal ulcer Benign condition due to a hypersensitivity reaction to bacterial conjunctivitis, particularly staphylococcal blepharoconjunctivitis. It is characterized by infiltration of the peripheral cornea by white cells and by ocular irritation. The condition is usually self-limiting but painful. Treatment includes frequent cleaning of the eyelid margin with a cotton-tipped applicator or face cloth or cotton ball with baby shampoo, warm compresses, antibiotic ointment and occasionally topical corticosteroids.
Mooren's ulcer A rare, superficial ulcer of the cornea of unknown origin. It starts near the limbus as an overhanging advancing edge that in severe cases spreads over the entire cornea and may even invade the sclera. The patient complains of pain and blurred vision. There are two types: a self-limiting form, usually unilateral, affecting old people, and a progressive form, bilateral, affecting young people. The condition is difficult to treat and this may include topical and systemic steroids, immunosuppressants, or conjunctival excision. See peripheral ulcerative keratitis.
serpiginous ulcer See hypopyon keratitis.
shield ulcer A localized corneal ulcer noted in severe cases of vernal conjunctivitis. The lesion is usually oval or pentagonal resembling a warrior's shield. It is located in the upper portion of the cornea as a result of irritation from the large papillae on the palpebral surface of the overlying eyelid.

ul·cer

(ŭl'sĕr)

Lesion through skin or mucous membrane resulting from loss of tissue, usually with inflammation.
See: erosion

[L. ulcus (ulcer-), a sore, ulcer]

ulcer (ul´sur),

n a loss of covering epithelium from the skin or mucous membranes, causing gradual disintegration and necrosis of the tissues.

“Ugly duckling” stage of mixed dentition.

ulcer, aphthous

n an open, shallow lesion in the oral cavity that causes pain; commonly known as a
canker sore. The cause is unknown, and treatment is limited to alleviating the symptoms.

ulcer, aphthous, recurrent (RAU)

n periodic episodes of aphthous lesions on nonkeratinized oral tissues lasting from 1 week to several months. Trauma and immunologic factors are involved in the etiology. The single or multiple discrete or confluent ulcers have a well-defined marginal erythema and a central area of necrosis with sloughing. Also called
canker sore and
recurrent aphthae.

ulcer, autochthonous

n See chancre.

ulcer, decubitus

n 1. a bedsore.
2. older term for a traumatic ulcer of the oral mucosa. More commonly called
traumatic ulcer.

Decubitus ulcer.

ulcer, diabetic

n an ulcer, usually of the lower extremities, associated with diabetes mellitus.

ulcer, herpetic

n an ulcer on keratinized orofacial tissues that is secondary to the vesicle of herpes simplex after the intact surface is broken by trauma to the lesion; a shallow ulcer with an irregular, erythematous border and a yellow-gray base. Contagious through all stages of lesion. Can be treated by topical acyclovir. Also called a
cold sore.

ulcer, Mikulicz's

n.pr See periadenitis mucosa necrotica recurrens.

ulcer, pemphigoid aphthous,

n a lesion located on the gingiva or mucous membranes due to a chronic disease of the autoimmune system. It is indicated by a wound with a thick wall that ruptures within 24 to 48 hours and leaves an eroded and painful surface area. It heals through the formation of a scar.

ulcer, peptic

n an ulcer of the stomach or duodenum. Most ulcers are associated with
H. pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach. They can also be caused or worsened by drugs such as aspirin and other NSAIDs.

ulcer, pterygoid

n See aphtha, Bednar's.

ulcer, rodent,

n See carcinoma, basal cell.

ulcer, traumatic,

n an ulcer that is caused by trauma. It can be due to faulty oral hygiene, rough foods, oral habits, poor-fitting dentures, or inadvertent mastication or biting of oral tissues. The offending cause may need to be removed by the patient or clinician. After this treatment, it must heal within a 2-week period to rule out any oral cancer concerns. The older term in dentistry is
decubitus ulcer.

ulcer

a local defect, or excavation of the surface of an organ or tissue, produced by sloughing of necrotic inflammatory tissue. They occur in all organs and tissues and are to be found under those headings, e.g. abomasal, corneal, gastric.

---

button ulcer

see button ulcer.

callous ulcer

see set-fast (2).

collagenase ulcer

a rapidly expanding, erosive ('melting') corneal ulcer, seen particularly in brachycephalic breeds of dogs.

Curling's ulcer

acute ulceration of the stomach or duodenum seen after severe burns of the body in humans.

decubitus ulcer

see decubitus ulcer.

dendritic ulcer

linear, branching pattern of ulceration on the cornea; characteristic of herpesvirus infections. See also herpetic keratitis.

eosinophilic ulcer

see eosinophilic ulcer.

gastroduodenal ulcer

common in foals 1-3 months old. Many are asymptomatic. Clinical cases manifest by mild, intermittent colic. See also gastric ulcer, duodenal ulcer.

geographic ulcer

a large, superficial, irregularly shaped corneal ulcer, typically formed by the coalescence of several dendritic ulcers.

indolent ulcer

see eosinophilic ulcer, refractory ulcer (below).

infectious dermal ulcer

a systemic, fatal bacteremia of snakes manifested by multiple, small cutaneous ulcers. Called also scale rot.

intestinal ulcer

is rare in all species. When they do occur, intestinal ulcers usually cause signs of chronic enteritis. It is a common lesion in adenocarcinoma of the intestine. See also peptic ulcer.

lip ulcer

see eosinophilic ulcer.

lip and leg ulcer

see ulcerative dermatosis.

melting ulcer

see collagenase ulcer (above).

ulcer mound

a gastric ulcer viewed tangentially radiographically creates a mound in the otherwise smooth outline of radiopaque material in the stomach.

necrotic ulcer of swine

see ulcerative granuloma of swine.

perforating ulcer

one that involves the entire thickness of an organ, creating an opening on both surfaces. See also ulcer perforation.

phagedenic ulcer

a necrotizing lesion in which tissue destruction is prominent.

refractory ulcer

a chronic, superficial corneal ulceration in dogs, particularly common in Boxers, that extends into the superficial stroma, often undermining epithelium at the edges. The cause is unknown but abnormalities of the basal epithelial cells and anterior stroma have been noted. Response to the usual methods of treatment for corneal ulceration is characteristically very slow; superficial keratectomy is the treatment of choice. Called also superficial corneal erosion syndrome, Boxer ulcer.

rodent ulcer

see eosinophilic ulcer.

stress ulcer

superficial ulcerations or erosions of mucosa in the stomach, duodenum or colon. The possible predisposing factors include changes in the microcirculation of the gastric mucosa, increased permeability of the gastric mucosa barrier to H+, and impaired cell proliferation.

stromal ulcer

a corneal ulcer involving the stroma.

trophic ulcer

one due to imperfect nutrition of the part. In dogs, may develop in digital and metatarsal pads in association with tibial nerve injury.

Patient discussion about ulcer

Q. Is it an ulcer? I am worried! Hi friend, I'm 35 year old male and recently I started to suffer from some strange symptoms I have never experienced. The first symptom was sharp pain in my upper abdomen that starts two of three hours after eating. In the beginning I thought it could be connected with some food intolerance but then I started to get this pain early in the morning, before any eating what so ever and all this was accompanied with nausea, frequent burping and weight loss. I have read some stuff about stomach ulcer and I could say that I poses almost every major symptom. Is there any way for me to be sure that I have developed disease of ulcer?

A. There is nothing you could do to check do you have ulcer or not by your self. Anyone who thinks he may have an ulcer needs to see a doctor because over time, untreated ulcers grow larger and deeper and can lead to other problems. So go now to the doctor.
http://www.youtube.com/watch?v=YrcrG-dcIXA

Q. What are the symptoms of Ulcerative Colitis? I am 40 years old and suffer from a lot of stomach aches and diarrhea. Do I have Ulcerative Colitis? What are its symptoms?

A. Here's a pretty good article that covers symptoms of UC:

http://www.wearecrohns.org/ucers/articles/319

Q. What is the difference between duodenal ulcer and stomach ulcer? I was diagnosed recently with duodenal ulcer. I heard the term stomach ulcer but not duodenal. What causes duodenal and what cause stomach ulcer? And how do they treat duodenal ulcer?

A. The duodenum is right after the stomach. They are both (as published a few years back) caused 90% of the time from a bacteria named helicobacter pylori. Hence the treatment for it is probably antibiotics. But I guess that should be your doctor’s call. Good luck!