ulcer

(ŭl′sĕr)

(ŭl′sĕr-ă)
pl. ulcera [L. ulcus, stem ulcer-, sore, ulcer]
An open sore that forms on an epithelial surface, e.g., the skin, the mucous membranes, or the lining of the gastrointestinal tract, 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

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.
SYN: SEE: aphthous stomatitis; SEE: canker sore

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APHTHOUS ULCER

CAUSES
Aphthous ulcers are found in stomatitis, Behçet syndrome, Crohn disease, AIDS, 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

SEE: Ischemic ulcer.

atonic ulcer

A chronic ulcer with little tendency to heal.

Buruli ulcer

An ulcer of the skin and underlying tissues caused by infection 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

SEE: 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

A breakdown of the skin in the foot of someone with diabetes. This often occurs in patients with neuropathy. If prompt care is not given, it may result in infection or amputation.

duodenal ulcer

ABBR: DU An open ulcer 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 Helicobacter pylori.

SEE: peptic ulcer

Hunner ulcer

SEE: 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.
SYN: SEE: 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).
SEE: Curling ulcer; SEE: Helicobacter pylori; SEE: stress ulcer; SEE: Zollinger-Ellison syndrome

INCIDENCE
Peptic ulcer disease is a common illness, affecting about 10% of men and 5% of women during their lifetimes.

CAUSES
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 AND SIGNS
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 intermittent infusions of proton pump inhibiting drugs. 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 four to six 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

SEE: Tropical ulcer.

postpolypectomy ulcer

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

pressure ulcer

Damage to the skin or underlying structures from compression of tissue and inadequate perfusion.

INCIDENCE
The incidence and prevalence of pressure ulcers is highest in nursing home residents and patients in Intensive Care Units (ICUs). In ICUs, prevalences as high as 30% to 40% have been identified.

CAUSES
Pressure ulcers typically occur in patients who are bedridden or wheelchair bound. Patients with sensory and mobility deficits (such as spinal cord injury, stroke, or coma); malnourished patients; patients with peripheral vascular disease; hospitalized older patients; and nursing home patients are at risk.

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

DIAGNOSIS
Diagnosis is made from inspection of the wound and daily measurements of its size. Cultures are sometimes taken to try to identify wound contamination or infection.

PREVENTION
Most important is the prevention of 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.

TREATMENT
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 to 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-shaped 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.
SYN: SEE: bedsore; SEE: decubitus ulcer; SEE: pressure sore; SEE: sloughing phagedena
SEE: Norton scale for table.

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PRESSURE UCLER

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.
SYN: SEE: Jacob ulcer

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RODENT ULCER On the ear

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; SEE: Cushing ulcer under Cushing, Harvey; SEE: 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.
SYN: SEE: 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

A poorly and slowly healing ulcer, usually located on the lower extremity above the medial malleolus.

INCIDENCE
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.

SYMPTOMS AND SIGNS
Affected skin is fragile, easily injured, typically edematous, pigmented, and scarred.

DIAGNOSIS
Diagnosis of venous stasis ulcer is made by inspection of the skin. Characteristics 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 brown discoloration 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 integrity; and pain or tenderness.

TREATMENT
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 night. Ankle flexion and extension, and slow walking also help manage ulcers. Compression devices, (such as graduated pressure stockings or Unna boots) are used to reduce swelling, improve venous return, and aid healing. Before applying compression devices the health care professional should assess the leg for evidence of active infection (cellulitis). Cellulitis is a contraindication to leg compression. Skin grafts may be employed for wounds that fail to heal with compression. Ablation or surgical reconstruction of veins in the leg may also help patients who have been adherent with care and continue to suffer with ulcerations that do not heal.

PATIENT CARE
The wound should be cleansed regularly to remove adherent scaling skin or crusting exudates, and aggressive debridement employed as needed. Wounds benefit equally well from moisture-retentive dressings, silver-impregnated dressings, or absorbent dressings. Before placing a compressive stocking or device, and each time such a device is replaced, the circumference of the leg and the size of the ulcer should be carefully recorded. Underlying problems, such as obesity, deep venous thrombosis, diabetes mellitus, and cardiovascular disease should be assessed and managed as part of all wound care protocols.

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VENOUS STASIS ULCER On lateral malleolus