eMedicine Specialties > Plastic Surgery > Pressure Ulcers

Pressure Ulcers, Nonsurgical Treatment and Principles: Treatment & Medication

Author: Christian N Kirman, MD, Resident Physician, Department of Plastic and Reconstructive Surgery, Wake Forest University Baptist Medical Center
Coauthor(s): Joseph A Molnar, MD, PhD, FACS, Associate Director of Burn Unit, Associate Professor, Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine
Contributor Information and Disclosures

Updated: Jul 28, 2009

Treatment

Medical Care

With thorough and comprehensive medical management, many pressure ulcers may heal completely without the need for surgical intervention. Successful medical management of pressure ulcers relies on key principles, including pressure reduction, adequate debridement of necrotic and devitalized tissue, control of infection, and meticulous wound care.

  • Spasticity should be controlled pharmacologically with such medications as diazepam, baclofen, or dantrolene sodium. Patients with spasticity refractory to medication may be candidates for neurosurgical ablation. Flexion contractures may also be relieved surgically.
  • Nutritional status should be evaluated and optimized to ensure adequate intake of calories, proteins, and vitamins. Malnutrition is one of the few reversible contributing factors, and establishing adequate caloric intake has been shown to improve healing of pressure sores. Recently, 6 clinical studies were reviewed to examine the effect of oral nutritional supplementation (ONS) enriched with arginine, vitamin C, and zinc in pressure ulcer care. The reviewed practice-based studies show positive effects of this ONS on pressure ulcer healing as well as a potential reduction of the risk of developing pressure ulcers.13,14
  • Implementation of more invasive methods of nutrient delivery becomes an ethical issue and must be weighed against the complications of such delivery. Goals of nutritional support should include adequate protein intake and the establishment of a positive nitrogen balance, with 1.0-2.0 g/kg/day being recommended for patients with pressure ulcers.
  • Other important considerations include the cessation of smoking, adequate pain control, maintenance of adequate blood volume, and correction of anemia. These issues are directed at preventing vasoconstriction in the wound and optimizing the oxygen carrying capacity of the blood.

A system of assessing wound healing must be in place to facilitate continuity of care among the various health care providers involved in the care of the patient. This often includes serial photography, detailed descriptions of the wound, and measurement of wound dimensions.

Other treatment options of unproven efficacy are presently being studied. These include the use of hyperbaric oxygen, electrotherapy, and growth factors. Initial studies of electrotherapy seem promising, and topical application of the recombinant human growth factor becaplermin (Regranex) has been approved for use in patients with diabetic neuropathic ulcers of the lower extremity. However, not enough evidence is available to support their recommendation for use in treating pressure sores.

When medical management has been optimized, most of the signs of impending ulceration of stage I pressure sores resolve. Approximately 75% of stage II pressure sores also heal with conservative management. However, stage III and IV ulcers are much less likely to heal spontaneously and often require a surgical approach.15

Pressure Reduction

The first step in healing a pressure ulcer is determination of the cause, ie, pressure, friction, or shear. Turning and repositioning the patient remains the cornerstone of prevention and treatment through pressure relief. Repositioning should be performed every 2 hours, even in the presence of a specialty surface or bed. Patients who are bedbound should be positioned at a 30 degree angle when lying on their side to minimize pressure over the ischial tuberosity and greater trochanter. Efforts should be made to avoid sliding the patient over a surface to prevent shear forces and friction. Patients who develop a pressure sore while sitting should be placed on bed rest with frequent repositioning.

Pressure reduction may be achieved through the use of specialized support surfaces for bedding and wheelchairs that can maintain tissue pressures less than 30 mm Hg. In theory, reduction of tissue pressures below capillary filling pressures should allow for adequate tissue perfusion. These specialized surfaces include foam devices, air-filled devices, water-filled devices, gel-filled devices, low air-loss beds (eg, Flexicair, KinAir), and air-fluidized beds (eg, Clinitron, FluidAir). Low air-loss beds support the patient on multiple inflatable air-permeable pillows. Air-fluidized beds suspend the patient on an air-permeable mattress containing millions of uniformly sized silicone-coated beads.

These devices are often heavy, expensive, difficult to clean, and require ongoing maintenance to ensure proper function. Pressure reduction beds have been shown to reduce pressure sore incidence and severity when compared to conventional hospital mattresses. However, pressure sores may develop in patients using these devices, and the importance of turning and repositioning cannot be overemphasized. More than 75 companies sell pressure-reduction devices, with annual industry revenues in excess of 8 billion dollars. In addition, air-permeable devices may warm the patient considerably and lead to significant insensitive fluid losses. Special consideration should be given to temperature and hydration in these patients.

When employing a pressure relief surface, these devices must be used properly. The patient's head and shoulders should be only minimally elevated on one pillow or a foam wedge to reduce shear forces and prevent the patient from "bottoming out" or having the sacrum or ischial tuberosities resting on the bed frame. In a recent comparative study, 2 different cushions to prevent heel pressure ulcers were investigated: a wedge-shaped, bedwide, viscoelastic foam cushion and an ordinary pillow. The patients using the wedge-shaped cushion had a decreased incidence of heel pressure ulcers, and the probability to remain pressure ulcer-free remained higher.16

  • The wound must be kept clean and free of urine and feces. The surrounding intact skin must be kept clean and dry. This should be done through frequent inspection and cleansing. The appropriate evaluation of urinary or fecal incontinence is complex but must be performed thoroughly. Potentially reversible causes should be identified and treated. Urinary incontinence secondary to urinary tract infection should be treated with antibiotics. Fecal incontinence secondary to diarrhea may be related to an infectious cause such as C difficile pseudomembranous colitis, which resolves with appropriate antibiotics.
  • Manual disimpaction and the addition of stool bulking agents to the diet may relieve overflow fecal incontinence. Urinary or fecal incontinence with no treatable cause may be minimized through the establishment of a bowel and bladder regimen. Constipating agents and a low residue diet also may be helpful. Diapers and incontinence pads may be helpful by absorbing moisture away from the surface of the skin if they are checked regularly and changed when soiled. If used inappropriately, these products may actually aggravate maceration and result in dermatitis. A bladder catheter or condom catheter in males may be used to control urinary incontinence. In the most severe cases involving chronic stool contamination, surgical diversion should be considered.
  • Bacterial contamination must be assessed and treated appropriately. Differentiation of infection from simple contamination through tissue biopsy guides the judicious use of antibiotics only in the former situation and hopefully avoids the development of resistant species. Antibiotics also are indicated when accompanying osteomyelitis, cellulitis, bacteremia, or sepsis is present.

Wound Dressings

Wound dressings vary with the state of the wound, and the goal is to achieve a clean, healing wound with granulation tissue. A stage I lesion may not require dressing. For more advanced ulcers, various dressing options are available, depending on the state of the wound.

  • Hydrocolloid dressings (eg, DuoDerm) form an occlusive barrier over the ulcer while maintaining a moist wound environment and preventing bacterial contamination. A gel is formed when wound exudate comes in contact with the dressing. Hydrocolloids help prevent friction and shear, and may be used in stage I, II, III, and some stage IV ulcers with minimal exudate.
  • Transparent adhesive dressings (eg, OpSite, Tegaderm) also provide a moist wound setting and prevent bacterial entry while promoting epithelialization. They minimize friction and shear, and may be used in shallow stage I, II, and III ulcers.
  • Alginate dressings (eg, SilvaSorb, Sorbsan) are fibrous products derived from brown seaweed and are available in nonwoven sheets and ropes. Alginate forms a gel when it comes into contact with wound drainage, and may be used in light to heavily draining stage II, III, and IV ulcers. It may be used in both infected and noninfected wounds; however, it should not be applied to dry or minimally draining wounds, as it can cause dehydration and delay wound healing.
Wounds with surface debris or fibrinous exudate may be mechanically debrided with wet-to-dry dressings incorporating normal saline or enzymatically debrided with collagenase (Santyl). Wounds with a high level of bacterial contamination may benefit from an antibiotic cream such as silver sulfadiazine (Silvadene), which is bactericidal to many gram-positive and gram-negative organisms as well as being effective against yeast.

Sulfamylon, bacteriostatic to many gram-positive and gram-negative organisms including Pseudomonas aeruginosa, can penetrate an eschar and promote autolytic softening of the eschar prior to debridement. Vacuum-assisted closure (VAC) sponges conform to the wound surface by suction and stimulate wound contracture while removing exudate and edema. Daily whirlpool therapy or pulse lavage therapy may be used to irrigate and mechanically debride the wound.

The choice of dressings is not as important as their appropriate application. These dressings are not a substitute for sharp debridement in the presence of eschar or other necrotic material. Trained individuals should apply dressings. Care should be taken to keep the wound dressing within the boundaries of the wound to prevent maceration of the surrounding skin. A hydrocolloid pad or skin sealant can be used to protect the surrounding skin and serve as a surface to which tape may be applied to hold dressings in place. Tubular mesh gauze, often used in burn patients, is another alternative to hold dressings in place in patients with extremely fragile skin.

A consensus statement was issued in October 2007 about dressings for acute and chronic wound management.

Wound Debridement

Even with optimal medical management, many patients require operative debridement, diversion of urinary or fecal stream, release of flexion contractures, neurosurgical ablation of spasticity, amputation, or reconstruction. For more information, please see Pressure Ulcers, Surgical Treatment and Principles.

  • Debridement is aimed at removing all devitalized tissue that serves as a reservoir for ongoing bacterial contamination and possible infection. Extensive debridement should be performed in the operating room, but minor debridement is commonly performed at the bedside. Although many of these patients are insensate, others are unable to communicate pain sensation because of cognitive dysfunction. Adequate pain control should be provided prior to any debridement, and vital signs often are a good indicator of pain perception. Great care should be taken during bedside debridement, as significant bleeding may occur.
  • Urinary or fecal diversion to prevent frequent bathing of the wound with urine or feces may be necessary in difficult instances where incontinence or fistulas do not resolve with medical therapy.
  • Release of flexion contractures or neurosurgical ablation of spasticity may assist with positioning problems and make tissues over the involved joint less susceptible to further injury.
  • Amputation may be necessary for a nonhealing extremity wound in a patient who is not a candidate for reconstructive surgery.
  • The goals of pressure sore reconstruction are improvement of patient hygiene and appearance, prevention or resolution of osteomyelitis or infection, reduction of fluid and protein loss through the wound, and prevention of future malignancy (Marjolin ulcer). Reconstructive options vary with the anatomic site of the ulcer, previous scars or surgeries, and surgeon preference. All reconstructions initially must begin with adequate debridement, including the removal of the entire bursal sac and any involved bone or heterotopic calcifications.

Wound closure then may be achieved in various ways. Few pressure sores can or should be closed primarily because of unacceptably high complication rates, primarily wound dehiscence resulting from excess tension on suture lines. A well-vascularized pad of tissue should be placed in the wound to eliminate dead space, enhance perfusion, decrease tension on the wound closure, and provide a new source of padding over the bony prominence. This tissue is typically a musculocutaneous or fasciocutaneous flap transposed or rotated on a pedicle containing its own blood supply, although more complex or recurrent wounds may require the use of a free flap with microvascular anastomosis. Prior to wound closure, drains should be placed in the bed of the wound. This allows external drainage of any fluid that may accumulate beneath the flap and hopefully avoids wound complications such as hematoma or seroma.

For information on specific flap surgery, see the Flaps section of eMedicine’s Plastic Surgery journal.

Surgical Care

For information on the surgical care of pressure sores, please refer to the eMedicine article Pressure Ulcers, Surgical Treatment and Principles.

Consultations

A multidisciplinary approach can lead to maximum benefit for the patient. Neurosurgery, urology, plastic surgery, orthopaedic surgery, and general surgery consultations all may be indicated in a particular patient. Rehabilitation medicine specialists, social workers, and psychologists or psychiatrists may work together with geriatricians and internists to improve the patient's health, attitude, support structure, and living environment. Plastic surgeons perform most pressure sore reconstructions, and consulting a plastic surgeon is appropriate with any complex or chronic wound.

Activity

Following successful wound closure, ambulatory patients should be out of bed with assistance as soon as possible. More strenuous physical activity should be delayed for approximately 6 weeks. In patients with ischial tuberosity ulceration, sitting may be resumed 6 weeks after a healed wound is achieved. Sitting may be gradually reintroduced over several weeks, and detailed guidelines have been published. Because of the extremely high pressures generated over the ischial tuberosities during sitting, wheelchair patients should lift themselves out of their seat or rock back in the chair every 15 minutes. These recommendations regarding the resumption of activity vary according to the clinical situation and are at the discretion of the treating physician.

Medication

The relief of spasticity when present is essential in the treatment and prevention of pressure ulceration. The most commonly employed medications are presented here.

Skeletal muscle relaxants (centrally acting)

Centrally acting skeletal muscle relaxants inhibit reflexes at the spinal level.


Baclofen (Lioresal)

May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at the spinal level.

Adult

5 mg PO tid initially; may increase to a maximum 20 mg PO tid/qid; not to exceed 80 mg/d
300-800 mcg/d intrathecal bolus or continuous infusion via implantable pump

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Opiate analgesics, benzodiazepines, alcohol, tricyclic antidepressants, guanabenz, MAO inhibitors, clindamycin, and hypertensive agents may increase baclofen effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May lower seizure threshold in epileptics; dose reduction may be required in the presence of renal impairment; elderly have an increased susceptibility to CNS depression; abrupt withdrawal has led to hallucinations and seizures


Diazepam (Valium)

Depresses all levels of the CNS, including the limbic and reticular formation, possibly by increasing GABA activity, which is a major inhibitory neurotransmitter. Individualize dosage and increase it cautiously to avoid adverse effects.

Adult

2-10 mg PO bid/qid or 15-30 mg extended release PO qd; 5-10 mg IV/IM q2-4h

Pediatric

<6 months: Not established
>6 months: Not to exceed 0.25 mg/kg PO divided tid/qid

Additive CNS depression with other CNS depressants; cimetidine, oral contraceptives, disulfiram, fluoxetine, isoniazid, ketoconazole, metoprolol, propoxyphene, propranolol, or valproic acid may decrease metabolism of diazepam, enhancing its actions; may decrease the efficacy of levodopa; rifampin and barbiturates may increase metabolism of diazepam and decrease its effectiveness

Documented hypersensitivity; narrow-angle glaucoma; hypothyroidism

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Addictive; use cautiously in the presence of hepatic or renal impairment; dosage reduction is required in the elderly

Skeletal muscle relaxants (direct acting)

Direct-acting skeletal muscle relaxants inhibit muscle contraction by decreasing calcium release from the sarcoplasmic reticulum in muscle cells.


Dantrolene (Dantrium)

Stimulates muscle relaxation by modulating the skeletal muscle contractions at a site beyond the myoneural junction and by acting directly on the muscle itself. Most patients respond to a dose of 400 mg/d or less.

Adult

25 mg PO qd initially; may increase to a maximum 100 mg PO bid/qid; not to exceed 400 mg/d

Pediatric

<5 years: Not established
>5 years: 0.5 mg/kg PO initially; may increase to maximum 3 mg/kg PO bid/qid; not to exceed 400 mg/d

Additive CNS depression with other CNS depressants; increased risk of hepatotoxicity in women older than 35 y receiving concomitant estrogen therapy; increased risk of arrhythmias when used concomitantly with verapamil

Documented hypersensitivity; active hepatic disease such as hepatitis or cirrhosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In cardiac or pulmonary disease

More on Pressure Ulcers, Nonsurgical Treatment and Principles

Overview: Pressure Ulcers, Nonsurgical Treatment and Principles
Differential Diagnoses & Workup: Pressure Ulcers, Nonsurgical Treatment and Principles
Treatment & Medication: Pressure Ulcers, Nonsurgical Treatment and Principles
Follow-up: Pressure Ulcers, Nonsurgical Treatment and Principles
Multimedia: Pressure Ulcers, Nonsurgical Treatment and Principles
References
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Further Reading

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Keywords

decubitus ulcers, pressure sores, ulcerations, pressure ulcers, surgical and nonsurgical treatment, decubitus, ischial tuberosity ulcer, ischemia, tissue necrosis, capillary filling pressure, shear forces, friction sores, maceration, microcirculatory occlusion, tissue anoxia, Shea classification, National Pressure Ulcer Advisory Panel, pressure reduction, tissue perfusion, sacrum ulcer, operative debridement, skeletal muscle relaxants, repositioning

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Contributor Information and Disclosures

Author

Christian N Kirman, MD, Resident Physician, Department of Plastic and Reconstructive Surgery, Wake Forest University Baptist Medical Center
Christian N Kirman, MD is a member of the following medical societies: North Carolina Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph A Molnar, MD, PhD, FACS, Associate Director of Burn Unit, Associate Professor, Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine
Joseph A Molnar, MD, PhD, FACS is a member of the following medical societies: American Association of Plastic Surgeons, American Burn Association, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, American Society of Plastic Surgeons, North Carolina Medical Society, Peripheral Nerve Society, and Wound Healing Society
Disclosure: KCI, Inc.  Honoraria Speaking and teaching; Integra Life Sciences Honoraria Speaking and teaching; Clincal Cell Culture Grant/research funds Co-investigator; KCI, Inc Wake Forest University receives royalties Other

Medical Editor

Albert E Cram, MD, FACS, Professor Emeritus, Departments of Surgery, Otolaryngology Head & Neck Surgery and Orthopedic Surgery, University of Iowa College of Medicine; Consulting Staff, Iowa City Plastic Surgery
Albert E Cram, MD, FACS is a member of the following medical societies: American Association of Tissue Banks, American Burn Association, American College of Surgeons, American Heart Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons
Disclosure: ethicon Grant/research funds Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Wayne Stadelmann, MD, Stadelmann Plastic Surgery, PC
Wayne Stadelmann, MD is a member of the following medical societies: Alpha Omega Alpha, New Hampshire Medical Society, Northeastern Society of Plastic Surgeons, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Nicolas (Nick) G Slenkovich, MD, Director, Colorado Plastic Surgery Center
Nicolas (Nick) G Slenkovich, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Society of Aesthetic Plastic Surgery, American Society of Plastic Surgeons, and Colorado Medical Society
Disclosure: Nothing to disclose.

Chief Editor

Lars M Vistnes, MD, FRCSC, FACS, Professor of Surgery, Emeritus, Stanford University Medical Center
Lars M Vistnes, MD, FRCSC, FACS is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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