Decubitus L89.x0

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 07.08.2021

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bedsores; Decubital ulcer; Pressure Sore; pressure sores; pressure ulcer

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Lesions that occur as a result of prolonged pressure on the tissue.

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Ulcer classification according to depth of infestation:
  • Grade I: epidermal
  • Grade II: subcutaneous
  • Grade III: subcutaneous with fascia and muscles
  • Grade IV: subcutaneous with tendons, bones, joints
  • Grade V: undermining, pockets, fistulas.

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Permanent pressure as well as friction and shear forces against a fixed resistance are discussed as the cause of compression and damage to supplying capillaries and nerves in skin, subcutis and muscles. This results in a consecutive reduced perfusion and malnutrition, whereby there seems to be a mutual relationship between pressure and time. Toxic metabolic products (lactic acid,CO2, pyruvates) are accumulated by the anaerobic metabolic situation. This is followed by edema formation and cellular infiltration due to increased capillary permeability and vascular dilatation of the arterioles and venules, which affect the nutritive circulation by way of shunt formation through steal effects. Ischemia and necrosis are the result.

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Patients with reduced mobility (paralysis, impaired consciousness, cachexia, old age, post-traumatic, postoperative) are at risk of pressure ulcers. Patients with reduced sensitivity due to polyneuropathy (e.g. diabetes mellitus) or a disease of the central nervous system (e.g. multiple sclerosis) are at increased risk.

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Hypo- or anaesthetic areas (especially on prominent bones: sacrum, trochanter, shoulder blade, heel).

Clinical features
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Ulcerations of varying size, deep, partly reaching to the underlying bones with necrotic inflammatory deposits and undermined pocket-shaped wound edges. Surrounding skin inflammationally irritated.

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First changes of the skin can be detected after only one hour at a pressure of 60 mm Hg. Fibrin deposits persist with hardly any fibrinolytic activity due to an oxygen diffusion barrier.

Differential diagnosis
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Ulcers of different genesis.

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  • Wound cleansing (see wound treatment below)
    :The depth of the dead tissue is decisive for the procedure of debridement. Removal of epidermal and dermal necroses. Débridement can be performed autolytically, mechanically or enzymatically.
    Mechanical: Thorough, while preserving the healthy tissue. The debridement is performed with a scalpel.
    The wound is rinsed with tap water through a hand shower/whirlpool, with saline or Ringer's solution.
    The antiseptics used are polyvidon iodine, octenidine and polihexanide.
  • Moist wound treatment (see below wound treatment)
    :Interactive wound dressings are medical devices which are free of active ingredients and can maintain a moist wound environment without causing tissue maceration of the surrounding skin. The highly resorptive polymers absorb the exudate and interactively regulate the moisture conditions in the wound. Interactive wound dressings include alginate, hydrogel, hydrocolloid, soft foam and foil dressings as well as activated carbon dressings. The moist wound conditions allow the fresh epithelial cells to "migrate" easily in comparison with the open, drying wound. The thermal insulation has a positive effect on cell growth. In addition, the desired hypoxia in the area of the wound surface caused by the moist wound conditions promotes angiogenesis.
    Self-adhesive dressings should extend 2-3 cm beyond the wound edges. Non-self-adhesive dressings are adapted to the wound so that they fill it loosely. Deeper wound cavities can be filled, for example, with a hydrogel or a drapable calcium alginate or soft foam dressing. Closing wound dressing. In problem areas or non-self-adhesive dressings, the fixation can also be supported with a protective skin film. In any case, the dressing should lie against the wound surface.
  • Dressing change during the exudation phase
    :The dressing is changed so often that the absorption capacity of the dressing is not exceeded. In hydrocolloid dressings, a fluid bubble forms as a sign of the need for dressing change; after exposure of the wound, it is filled with a yellowish gel, the nature and odour of which are putrid; this is not wound secretion, but components of the dressing in conjunction with absorbed exudate. In hydrogel, alginate and soft foam dressings, the exudate is absorbed without gel formation. Removal of the wound dressing is usually atraumatic and painless for the patient. If a dressing does adhere to the wound, it can be removed by a short shower with saline or Ringer's solution while rinsing with tap water.
    Enzymatic debridement: In fibrin-covered ulcers, enzymatic wound removal can be performed.
  • Granulation
    :The increasing formation of granulation tissueis called the
    proliferative phase. Exudates during granulation are easily removed by wound irrigation. It is now sufficient to change the interactive wound dressing on average three times a week, e.g. twice at home, once in the practice where debridement can be performed. Hypergranulations do not require any inhibitory therapy.
  • Epithelisation
    :The retention of an interactive wound dressing can be increased to up to seven days during the epithelisation phase. There is then hardly any exudation, on the other hand the freshly formed epithelium is protected in a moist environment and does not dry out.
  • Interface doctor/nursing staff/relatives
    :At the beginning daily presentation to the treating doctor for debridement and infection control. The further therapy is carried out by the home nursing staff. It is important that the doctor, professional and lay nursing staff work together smoothly. However, the realization of a complete transfer during care in the outpatient area requires one or more physically strong caregivers who can constantly take care of the patient.
  • Systemic therapy
    :Septic and aseptic ulcer:
    Accumulations of wound secretions and pus can be hidden under closed necrosis caps, which, due to the occlusive effect, create ideal conditions for the development, spread and generalisation of infections.
    Antibiogram and resistance determination from wound swabs and blood must be carried out at any time for treatment as part of the status assessment of a given local and systemic infection symptomatology, as well as regularly in immunocompromised patients. If sepsis is suspected, blood cultures must be taken during a fever attack.
    Complete debridement of necrotic material, guarantee of sufficient secretion drainage and pressure relief are, in addition to specific systemic antibiotics, the cornerstones of ulcer treatment in cases of extensive infection.
    The so-called normal flora, but also pathogenic microorganisms, colonise skin and mucous membranes without penetrating the tissue or causing a reaction of the macroorganism. In all open wounds there is secondary colonisation by bacteria and possibly fungi. However, it is not possible (and not necessary) to create completely germ-free wound conditions by local or systemic antibiotics. The local instillation of antibiotic active substances is not recommended because of the many times higher risk of sensitisation or development of resistance in chronic wounds and the rapid inactivation of these substances!
    Systemic, germ-specific antibiotics are the therapy of choice in addition to mechanical debridement in both local and systemic infection. Until the antibiogram is obtained, therapy can be initiated with a broad spectrum antibiotic. After opening abscesses or mechanical debridements, only a rinsing with saline or Ringer's solution should be performed locally. The use of antiseptics has no further advantages!
    In the presence of a wound infection, alginate dressings/tamponades and odour and bacteria-absorbing activated carbon dressings with elemental silver should be used.
  • Nutritional therapy
    : Four rules apply:
    • Ensure adequate food supply
    • Survey nutritional status
    • Instructions for increased nutrient intake or supplementation
    • Identify and compensate for vitamin, mineral and trace element deficits.
  • Pain with guiding and warning function
    :With grade I and II decubitus ulcers, the pain is usually easy to localise and must be regarded as a useful warning signal. The patient can end the pain himself if he changes his position. Because the change of position is an adequate reaction, the pain must not be attenuated by analgesics or tranquilizers, provided that it can be sufficiently suppressed by changing position alone.
    Attenuated or missing pain sensation in neuropathy is possible, in spinal processes (e.g. paraplegic syndrome) the rule. Drug treatment of acute and chronic pain is based on the WHO's "analgesic dosing ladder" concept. According to this scheme, non-opiatal analgesics are to be used first and then increasingly stronger medications (opiates), if necessary with the use of additional medication.
    The implantation of a morphine pump and spinal cord stimulation are further procedures for the treatment of unmanageable chronic pain or the failure of other methods.

General therapy
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Relieve the pressure to restore the blood supply.
Regular rearrangement. This can be done with simple aids, such as a pillow or a rolled up towel. In the case of superficial ulcers, a normal mattress can be used first.The
patient's independence must be promoted by the positioning, as much body surface as possible must lie on the mattress and a correct hip bendmust be

For local decubitus prophylaxis of subcutaneous ulcers, the use of therapeutic positioning systems is appropriate, e.g. lying aids for treatment and aftercare such as foam mattresses for relief of the sacral area, alternating pressure mattresses or static and dynamic airflow mattresses.

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In particular, mistakes in decubitus prophylaxis (according to Diem) should be avoided:
  • Too long repositioning intervals
  • Incorrect storage technology
  • Use of non-breathable bearing materials (e.g. rubber ring)
  • Use of pressure-loaded bearing arrangement aids (e.g. air ring)
  • Incorrect personal hygiene (e.g. drying Franzbranntwein)
  • Application of powders or occlusive dressings
  • Bed rest prescribed for too long
  • Lack of physical therapy.

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Staging and therapy of the decubitus ulcer



Grade I

Skin redness that disappears at the touch of a finger. No pain. Heals in a short time when pressure is relieved.

Prophylaxis is crucial! Mobilisation as quickly as possible, physiotherapy, adequate positioning as well as frequent and regular repositioning (at least every 2 hours) of bedridden patients (repositioning plan!), measures to promote circulation. Relieve pressure, if necessary by positioning aids: water pillows, special mattresses, beds for decubitus (changing pressure gradients), heel ring.

Grade II

Blistering, bluish livid skin discoloration, severe pain (epidermis and dermis affected).

Pressure relief like grade I! Also: In case of weeping changes with blistering, moist compresses with antiseptic additives such as potassium permanganate (light pink).

Grade III

Transformation into necrosis, oedema and inflammation of the peripheral region; regressive pain symptoms (skin defect to periosteum).

In addition: removal of necroses and cleansing, granulation-promoting external agents (e.g. fibrolane), hydrocolloid foils (e.g. Varihesive extra thin), covering of the surrounding area with hard zinc paste. If necessary, zinc sprays (e.g. Desitin ointment spray). Avoidance of secondary infections and regular swabs (see also ulcer therapy).

Grade IV

Open decubitus ulcer (all layers including periosteum and possibly bones involved).

Removal of the necroses, cleaning of the wound see Pressure relief and repositioning see grade I. Antibiosis after antibiogram. Surgical consultation, if necessary surgical reconstruction, consecutive VAC therapy and defect coverage. Clarification of bone involvement.

Grade V

undermining, pockets, fistulas

Evaluation and documentation of the decubital ulcer

Medical consultation:

Assessment of the severity of the disease by the patient

previous illnesses, family, personal

ulcer age

under 2 weeks □

more than 2 weeks □

Recurrence Vulcus □

1st ulcer year: □

Previous treatment

Previous diagnostics

Ulcer Classification




Grade I

Grade II

Grade III

Grade IV

Grade V

epidermal dermal


subcutaneously with fascia and muscles

subcutaneously with tendons, bones, joints

hypodermination, bags, fistulas

Ulcer size

Largest vertical Ø in cm

Ulcer localization

Occipital bone Shoulder blade


sacrum and coccyx



Heel Ear


Gr. Mound


Blood pressure ( mm Hg)

Infection status









Wound swab

Germs and resistances

Findings on pain

Acute, non-cyclical

Acute, cyclical


Blood sugar fasting


Blood sugar postprandial


Urine status

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  1. Baumgarten M et al (2003) Pressure ulcers and the transition to long-term care. Adv Skin Wound Care 16: 299-304
  2. Brem H et al (2003) Wound-healing protocols for diabetic foot and pressure ulcers. Surg Technol Int 11: 85-92
  3. Diem D (1992) Decubitus prophylaxis and therapy. dermatologist 43: 461
  4. Gillitzer R (2002) Modern wound management. dermatologist 53: 130-45
  5. Schoeller T et al (2003) Coverage of pressure sores with free flaps. Surgeon 74: 671-676
  6. SeilerWo (1987) Rational decubitus therapy. Dtsch med Wochenschr 112: 889-890


Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 07.08.2021