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A pressure ulcer is an ischaemic necrosis of the skin and subcutaneous tissue caused by unrelieved and prolonged vascular compression on a specific area of the body, usually between a bony prominences and a supporting item such as a bed or chair.

This external pressure is transmitted through the support (bed, armchair) and affects the parts of the body bearing the support. The extent and seriousness of the pressure ulcer depends on several factors, particularly the intensity of the pressure, the duration, the resistance of the tissue to pressure and the general condition of the patient.

Locally, tissue damage is the result of three forces:

Aetiology

Several factors contribute to the development of pressure ulcers. A distinction is made between:

• factors independent of the patient (extrinsic risk factors)

• factors dependent on the patient's condition.

EXTRINSIC RISK FACTORS (INDEPENDENT OF THE PATIENT)

• Pressure

Pressure is perpendicular force applied to a specific area of living tissue. This pressure is applied particularly on bony prominences.. Where soft tissues between the bone relief and the underlying support are compressed. These forces correspond to the distribution of the body weight over the contact surface area.

• Friction

These are forces applied between two surfaces in contact with each other and moving relative to each other. These forces are often responsible for the initial skin abrasion.

• Shear

These are forces that cause slip and torsion of the subcutaneous layers. They exist especially in an unstable semi-seated position in which subcutaneous layers are subject to a kneading type force.

INTRINSIC RISK FACTORS (DEPENDENT ON THE PATIENT'S CONDITION)

Age

• If the patient is more than 10 years old, this is a risk factor.

Poor skin condition

• Skin resistance is reduced by age, long term corticosteroid treatment and deficiency conditions.

Conditions that reduce sensitivity

• Impaired sensitivity and motor control
• Anaesthesia, hypoesthesia
• Spinal and neurological conditions
• Neurological disorders which prevent pain signals associated with excessive weight-bearing and reflex actions leading to a position change.

Concomitant diseases

• Hypoxia due to arterial disease and/or venous return anomalies, diabetes
• Cancer, infection, anaemia and hyperthermia are all risk factors.

Incontinence

• Maceration due to both urinary and faecal incontinence may causeskin abrasions.

Nutritional status

• Malnutrition appears to be a major risk factor in the development of pressure ulcers. All pressure ulcer treatment must be accompanied by appropriate dietary management.

Localisation

80% of pressure ulcers are on the sacrum (tailbone) or heels. Another possible location is the trochanter (hip bone).

AT-RISK PATIENT IN A SITUATION CONDUCIVE TO THE DEVELOPMENT OF PRESSURE ULCERS

An orthopaedic or neurological disorder combined with a deterioration in the general condition of the patient causes immobility which will increase bearing pressures (for example a surgical operation, prolonged immobilisation, age, etc.).

This risk is demonstrated by a local red area that might be reversible and which disappears under pressure. This stage in the formation of pressure ulcers can be avoided by the application of appropriate treatment and preventive measures.

Stages

Pressure ulcers can be broken down into four stages. It is important to consider the four stages as being four manifestations of the pressure ulcer, and not four phases that necessarily follow each other. In some patients, a pressure ulcer can begin with a phlyctena (blister) or a superficial wound, or even a deep lesion (for example a black necrotic patch on the heel). A pressure ulcer can sometimes develop into a black necrosed spot (deep pressure ulcer).

STAGE 0: REVERSIBLE RED AREA

An at-risk patient with no formed lesion may have a stage 0 pressure ulcer.
The sub-clinical stage (no lesion, skin intact) can also be manifested by a red area but a red area that is reversible, in other words this red area will turn white under pressure (see photo).
This stage 0 is a warning stage.

STAGE 1: PERSISTENT RED AREA

This is a red patch, an oedema, an induration that is sometimes hot and often painful.
This red area (hyperthermia) does not turn white under pressure.
This persistent erythema is a manifestation that the epidermis or even the dermis is affected.
Special care is necessary at this stage. Massaging the area is not recommended as it could exacerbate the situation.
The skin is not broken at this point.

STAGE 2: IRREVERSIBLE RED AREA WITH SUPERFICIAL DERMAL-EPIDERMAL ULCER

This stage results in:

• either a phlyctena leading to separation of the epidermis
• or epidermal and then dermal-epidermal erosion

STAGE 3: TISSUE NECROSIS

The epidermis, dermis and hypodermis are affected, without the muscle fascia being damaged. The photo shows a pressure ulcer covered with a dry blackish necrotic plaque adjacent to healthy tissue. This is a definitive sign of devitalisation of the underlying tissues.
The external appearance is deceptive and does not provide any indication to the extent of of the depth of the lesions.

It is delimited by a groove which, as it progresses, will cause separation of the entire plaque. This dry necrosis tends to become wet and subsequently Fibrinonecrotic.

STAGE 4: DEEP PRESSURE ULCER

Tissue damage goes beyond subcutaneous tissues and affects underlying structures (muscle fascia, tendons and/or joints).

A leg ulcer is the loss of skin tissue with a chronic progression, usually originating from an arterial or venous circulatory disorder, which together cause 95% of cases.
A venous aetiology is the most common (70% of all ulcers).

90% of leg ulcers are of vascular origin including those of venous / mixed and arterial origins. Other causes such as diabetic ulcers, angio-necrotic ulcers, blood diseases or cancers, are more unusual.

• The prevalence of leg ulcers is estimated to be 1% of the general population and increases with age, reaching 3% of the population aged 65 years or more.
• The proportion of ulcers with a mixed arterial-venous origin has increased during the past few decades, as a result of the ageing of patients suffering from these diseases.
• Ulceration does not tend to heal spontaneously.
• It is a genuine scourge due to its incapacitating nature and its cost for society.
• It can also lead to the complication of infection.

A distinction is made between ulcers of venous and arterial origin

LEG ULCER OF VENOUS / MIXED ORIGIN

The most common type of venous leg ulcer is one with a venous aetiology and there are two main indications with venous ulcers: varicose ulcers and post-phlebitic ulcers.

• Venous ulcer

This is the most common type of vascular ulcer. It can be the result of sequelae occurring at an earlier or later stage following a deep vein thrombosis or a varicose disease with incontinent leaky perforating veins.
The main biological characteristics are:
Lack of pain, the location around the malleolus, a wet appearance and the co-existence of skin disorders caused by chronic venous insufficiency (pigmented purpuric dermatitis, sclerous hypodermitis, atrophie blanche, etc.).
Some signs are important; lack of necrosis, non-deepening nature, presence of peripheral pulse.

• Mixed ulcer = Caused by a combination of both arterial c and venous insufficiency.

An arterial ulcer is the consequence of arterial circulatory insufficiency, causing peripheral ischemia.

• Post-phlebitic ulcer

30 to 50% of all venous ulcers are post-thrombotic. Deep venous trunks are affected, unlike the varicose ulcer. Post-thrombotic syndrome develops gradually and will continue to deteriorate if serious treatment is not actioned.

These ulcers are becoming less frequent due to improved good prevention of phlebitis over the last 15 years.

However, venous ulcers are becoming increasingly complicated due to arterial involvement and to an increase in the average age of patients suffering from them. For this reason, an arteriograph should be performed immediately without hesitation in on people suffering from an ulcer which does not respond to well-managed treatment (compression stockings, appropriate dressings).

LEG ULCER OF ARTERIAL ORIGIN

Arterial leg ulcers are less common. Their main biological characteristics are their painful nature, exacerbated by raising the limb to a horizontal position, the distal or “suspended” location away from the malleolus, the necrotic and deep appearance, the exposure of underlying structures, the atonic base, the sharp edges of the wound and the coexistence of signs of arterial insufficiency.

PERIPHERAL ARTERIAL DISEASE OR ARTERITIS

The origin of the development of a thrombosis is an atheromatous plaque.
Arterial disease occurs mainly in male smokers over the age of 50 years old.
A replacement collateral circulation develops when the main arteries are affected, however, this circulation is not always sufficient to satisfy the oxygen requirements of the active muscles in action.

The development of the condition has 4 stages:

The basic treatment for peripheral arterial disease is to surgically restore arterial circulation. Surgery may involve unblocking the arterial lumen or bypassing the blockage.

Diagnosis of an arterial ulcer and a venous ulcer

Clinical characteristics:

• The Location

Venous ulcers are usually located on the lower limb above or in the vicinity of the malleolus.
An ulcer with arterial origin is mostly located on the foot.

• The size, shape, depth and appearance of the base and the edges of the ulcer

• The appearance of the skin around the ulcer

Oedema can sometimes affect the entire leg, combined with skin inflammation. Examination of the ulcer must be accompanied by an examination of the leg and a holistic examination, concentrating specifically on the cardiovascular system, nutritional status and the patient's mobility.

Additional tests

Assessment of the condition of the vascular system will give information about blood perfusion in the lower limbs and concerns the narrow arterial, venous and micro-circulation component. These examinations provide additional essential information complementary to the clinical examination.

This condition develops in diabetic patients due to vascular, neurological and metabolic disorders.

This wound may necessitate amputation if left untreated :

Diabetes

Diabetes is a state of hyperglycaemia (high blood glucose) resulting from both genetic and environmental factors.

DEFINITION OF GLYCEMIA

Glycaemia: level of glucose in the blood.
Normal glycaemia in a healthy subject, on an empty stomach, is between 0.7 and 1.1 g/l.
Hypoglycaemia: below 0.7 g/l.
Hyperglycaemia : above 1.1 g/l.
Diabetes: above 1.26 g/l.

TWO TYPES OF DIABETES

There are two main types of diabetes:

• IDD or Type I Insulin Dependent Diabetes (10% of diabetics) This form of diabetes is characterised by the complete or almost complete disappearance of insulin secretion by the pancreas. This lack of insulin is responsible for serious hyperglycaemia and will have a fatal outcome if not treated.
• NIDD or Type II Non-Insulin Dependent Diabetes (90% of cases) Type II diabetes is characterised by insulin resistance, frequently accompanied with obesity. This type of diabetes is defined by its development over the age of 35 years and there is no need for insulin treatment during the first year after its discovery.

In both types of diabetes, chronic hyperglycaemia is responsible for long-term complications which is why the disease is so serious.

COMPLICATIONS

• 15% of diabetic patients have or have had a wound on their feet.
• The risk of amputation is 15 to 20 times higher in the diabetic population than it is in the general population.
• 5% to 10% of diabetics will at some stage undergo amputation (toe/leg).
• In 30% to 50% of cases, there is a risk of contralateral amputation within 5 years.
• The mortality rate is 50% after amputation within 5 years.
• The extent of this human and financial problem should prompt improvements in preventive care.
• One amputation represents the annual full-time salary of 2 nurses.
• Amputation is the most financially expensive complication of diabetes.

Perforating diabetic foot ulcer

This condition develops in diabetic patients due to vascular, neurological and metabolic disorders. This wound can frequently lead to an amputation.

Definition

Chronic, painless and clean ulceration, usually located under the head of the 2nd or 3rd metatarsal bone in the foot or on any other point of normal or abnormal pressure on the underside of the foot. It is usually secondary to a reduction or disappearance in sensitivity, within the context of a diabetic angiopathy and neuropathy or deformation of the foot posture. It is readily complicated by infections, abscesses or osteitis.

• Incidence/ Prevalence: 2.2 million* diabetics in France in 2006 (glycaemia > 1.26 g/l). Every year, 6% of diabetics suffer from a Malum Perforans Pedis (MPP) or perforating diabetic foot ulcer. 5 to 24% of patients will require amputation.
• 50% mortality within 5 years after the amputation.

• Origin: This is a complex response to a sensory and neurovegetative disorder that causes muscular weakness leading to deformation of the foot structure (collapse of the arch of the foot) and reduction or loss of skin sensitivity to pain or friction. All these factors, combined with weakness of the skin and lack of attention by patients, is the starting point for this ulcer called a diabetic Malum Perforans Pedis (MPP) or perforating diabetic foot ulcer.

• Characteristics: The MPP is originates as small ulcer and is a complication of the erosion of an initial callus by hyperpressure. It takes the form of a wound with well-defined keratinous and sharp edges. It is atonic and is frequently torpid. Secondary infection often occurs in the form of remote purulent fistulae and underlying osteoarthritis.

• Prevention: Check the sensitivity of the foot (cold, heat, foreign body, reflexes, etc.). Pay special attention to shoes, toenails, hard skin, fungal infection between the toes, foreign bodies. Careful hygiene is essential.

• Aetiology: slight trauma, blister on weight-bearing callus
• blister, erosive cracking
• ulceration, gateway for infection
• swelling in surrounding integuments and establishment of infection, risk of underlying osteoarthritis,
• complete destruction of metatarsal bones by progressive osteolysis and risk of spread in separation areas (infectious cellulitis)
• diabetic gangrene
• if Peripheral Arterial Occlusive Disease: risk of amputation.