Pressure Ulcers of the Lower Limb



Fig. 20.1
Common locations of pressure or trophic ulcers of lower limb. Heel is the most common site of pressure or trophic ulcer (ac), as this portion is the most pressure bearing area of limb. It can be acute or chronic. The acute variety of heel ulcer is most commonly found in ICUs and any acute illness need to be bedridden, and commonly located in the posterior portion of heel (a) along with lower portion of tendo-achilis (b). If not protected well & early, they can turn very deep and leads to damage of deeper structures including tendo-achilis. The chronic variety is found in un-protected insensate heel (c). The other area may be any pressure points like lateral and medial malleoli (d) (especially by ill fitting shoes & prosthesis), base of 5th metatarsal (e), head of metatarsal (f), and dorsum of foot (g)



“Pressure sores” is the term used commonly in the United Kingdom, but again pressure injuries that are not open wounds (such as blisters and non-blanching erythema) are not true sores, but only “pressure damage,” and still belong to this family of pressure ulcers. “Pressure ulcers” is a term used widely in the United States and other countries and has been accepted as the Europe-wide term by the European Pressure Ulcer Advisory Panel (EPUAP).



20.2 Etiology (Mechanism of Ulcer Formation)


There are many factors that can contribute to the development of pressure ulcers, but the final common pathway to ulceration is tissue ischemia. The tissues are capable of sustaining pressure on the arterial side of around 30–32 mm Hg for only a small duration of time. But when pressure increases even slightly above capillary filling pressure, it causes microcirculatory occlusion, and this in turn initiates a downward spiral toward tissue ischemia and ulceration [2, 3].

Pressure ulcers can develop when a large amount of pressure is applied to an area of skin over a short period of time. They can also occur when less pressure is applied over a longer period of time. The extra pressure disrupts the flow of blood through the skin. Without a blood supply, the affected skin becomes starved of oxygen and nutrients and begins to break down, leading to ulcer formation.

The majority of people affected with pressure sores are those having health conditions (mental or physical) that encourage immobility, especially those who are confined to bed or chair for prolonged periods of time. Several other health conditions that influence blood supply and capillary perfusion, such as type 2 diabetes, can make a person more vulnerable to pressure ulcers. Age is also a factor that majority (approx two thirds) of pressure ulcers occur in old age people (60–80 years) [4]. To put it more simply, any individual, with or without a medical condition, who is incapable of avoiding prolonged periods of uninterrupted compression, is at a risk of pressure ulcers. Majority of patients affected with pressure ulcers frequently develop it over a bony prominence. Approximately 67 % of cases reported are affected over the area where skin covers the bones such as sacral, ischial, and trochanteric pressure ulcers [5], and in the lower extremities, these are seen in the malleolar, heel, patellar, and pretibial locations – account for approximately 25 % of all pressure sores [6]. Leg and foot ulcers have many causes that may further define their character (Fig. 20.2a–g). Table 20.1 describes the various direct and indirect causes of pressure ulcers of the lower extremity.

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Fig. 20.2
Various etiologic factors of pressure ulcer specific to lower extremity. Deformity of limb or foot that can change the pressure distribution (location or surface area) of limb may lead to pressure ulcer of limb/foot. The common causes are: Neurologically deformed limb (a1a3), Charcot’s foot (b), Post burn contracture and deformities (c), walking over the grafted or reconstructed heel or sole (d), pressure due to ill-fitting prosthesis (e), Diabetic foot associated trophic ulcer (f), and ulcers due to continuous pressure and friction by footwear over prominent metatarsal head (g)



Table 20.1
Causes of pressure ulcers of the lower extremities

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20.2.1 Direct Causes


Pressure ulcers develop when the soft tissues of the body are distorted and contorted in a fixed manner by the prolonged external force or pressure. This distortion occurs either because the soft tissues are compressed and/or sheared between the skeleton and a support, such as a bed or chair when the person is sitting or lying, or because something is pressing into the body, such as a shoe, a prosthesis, a surgical appliance, or clothing elastic. Blood vessels within the distorted tissue are compressed, angulated, or stretched out of their usual shape, and blood is unable to pass through them [7]. The tissues supplied by these blood vessels become ischemic. Besides occluding the blood flow, tissue distortion also obstructs lymphatic flow, which in turn leads to accumulation of metabolic waste products, proteins, and enzymes in the affected tissue. This too can compound the tissue damage.

As the living tissues are not static, the way they are distorted changes over time. When constant pressure is maintained, soft tissues mold themselves to accommodate the external shape. This is known as tissue creep [8]. This may reduce the external pressures but may also exaggerate internal distortions. The chances of atrophy of the skin with thinning of this protective barrier, making the skin more susceptible to minor compression, and internal conjugation of soft tissues are significantly high in paraplegic patients [9], and particularly in these susceptible patients, pressure ulcers can occur within 1 to 2 hours [10]. If ischemia persists for a sufficient length of time, necrosis takes place. This is usually the beginning of a pressure ulcer.


20.2.1.1 Pressure


Although pressure is the main cause of promoting ulcers, it is important to understand that the application of pressure in itself does not cause damage. Divers and soft-bodied sea organisms can operate at great depths of water with no risk of pressure damage. Although the external pressures can be extremely high, they do not cause tissue distortion because the pressure is uniformly spread. It is only when pressure becomes nonuniform and pressure gradients occur between adjacent areas of tissue that distortion occurs and the potential for pressure damage arises. The damage only occurs when the pressure becomes nonidentically scaled and evokes the pressure distortion.

Areas particularly susceptible to pressure damage include bony prominences [5] which have a thin covering of soft tissue, such as the posterior heel, malleoli, trochanters, and elbows. When the body is supported on these pressure points, large compressive force is accumulated on to a small surface area, and there is little padding to disperse this pressure. The height of the available tissue cover over the bony prominence is not the only determining factor for developing pressure sores. Although the soles of the feet have a thin covering of soft tissue, they have a vasculature that is particularly well adapted to withstand considerable distorting forces. On the sacrum and ischial tuberosity on the other hand, although there is a relatively thick covering of soft tissue and a wide supporting surface, the blood vessels are not adapted for weight bearing, which means that even with fairly light compression, pressure ischemia can develop rapidly. Hence, soles of feet do not develop pressure sores even after prolong weight bearing in ambulatory patients unless there are underlying causes, making them insensate and more prone to pressure damage.

When compression occurs, pressure is applied from at least two sides – the boney prominence inside and the unyielding support outside (Fig. 20.3a). This is the reason why pressure damage can present in two distinct clinical patterns. Tissue distortion and superficial damage occur with pressure on the skin surface, particularly if the supporting surface is uneven. If this is maintained for a prolonged period, it may still result in extensive damage as successive layers of tissues are destroyed. Superficial pressure ulcers caused by compression with minimal shearing tend to have a characteristic regular outline and can often be matched easily to the shape of the underlying bony prominence (Fig. 20.3b) or the object that caused the ulcer.

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Fig. 20.3
(ad) Severity or grading of pressure ulcers

The most serious pressure damage usually occurs as a result of the deformation in the deep tissues much closer to the underlying bony prominences. Because the pressures can be much higher than at the skin/support interface and because larger blood vessels are more likely to be affected, necrosis of a large volume of tissue often takes place. When the supporting structures of the skin have been destroyed, more extensive parts of the skin become nonviable and die subsequent to the primary deep tissue destruction. As the nonviable skin breaks down, a cavity filled with necrotic tissue is revealed or large areas of undermining under viable skin are encountered (Fig 20.3c, d).


20.2.1.2 Shear


When external forces that move in different directions are applied to the same tissue mass, shearing occurs. The bony structure of the body tends to move toward the feet if someone is sitting up in bed, because the gravitational force drags the upper part of the body downward. However, at the skin/support interface, frictional forces resist the movement of the body. The tissues between the skin and the skeleton are therefore distorted, and any blood vessels running through the area become sheared along with the rest of the tissue. Shearing occludes flow more easily than compression (e.g., it is easier to cut off flow in a water hose by bending than by pinching it), so shear can be considered to be even more significant than pressure in the causation of pressure ulcers [11]. Areas of the body particularly susceptible to shearing include ischial tuberosities, heels, shoulder blades, and elbows. These are areas on which the body is frequently supported when in a position (such as sitting or lying semi-recumbent) which allows forward slide. Superficial pressure ulcers caused by shearing tend to have uneven appearance.


20.2.1.3 Friction


Friction, along with pressure and shear, is also frequently cited as a cause of pressure ulcers [12]. Friction can cause pressure ulcers both indirectly and directly. In the indirect sense friction is necessary to generate the shearing forces. However, it is often directly responsible for tissue damage, as when blisters are caused by a patient being dragged up a bed with a rough sheet, or ill-fitting footwear causing blister formation. However, this type of injury is an acute mechanical and heat trauma, and the etiology is quite different to that of pressure ulcers. Friction is not, therefore, a direct cause of pressure ulcers, although it is clearly possible that skin weakened by pressure ischemia may be more susceptible to friction, and the two will act together to hasten skin breakdown.


20.2.1.4 Immobility


Immobility is not a primary cause of pressure ulcers, but in the presence of additional factors, it can initiate them. Even small bodily movements such as leaning forward or readjusting are usually sufficient to give adequate pressure relief. Patients with ill-fitting plaster casts do not have this choice as they cannot move away from the pressure which is causing distortion of their tissues. Patients with profound immobility but intact sensation rarely develop pressure ulcers when they can still communicate. The pain of tissue ischemia ensures that these patients frequently ask for their position to be changed. Patients with orthopedic casts should be encouraged to report any discomfort and pain in order to prevent iatrogenic pressure ulcers.


20.2.1.5 Loss of Sensation


This is probably the most common cause of pressure ulceration. The person affected cannot feel the discomfort and pain normally caused by prolonged tissue distortion, does not have reflex protective responses to this type of stimulation, and is not stimulated to make protective movements by discomfort or pain.

The problem may arise in one of two ways:

1.

Damage or severance of the nervous system. This damage may be:

(i)

Congenital (e.g., spina bifida)

 

(ii)

Traumatic (e.g., spinal injury)

 

(iii)

A disease process (e.g., ischemic damage to the spine following rupture of an aortic aneurysm, metastatic disease, peripheral neuropathy secondary to diabetes or leprosy, and neurological diseases)

 

(iv)

Iatrogenic causes (e.g., spinal anesthesia and local nerve block)

 

 

2.

Causes in central nervous system: This may be due to unconsciousness or brain damage as in head injuries or brain diseases such as Alzheimer’s disease or long-term treatment for psychiatric conditions such as depression or schizophrenia. Although there is apparently adequate sensation, circulation, and mobility to prevent pressure ulcers, the brain seems to suppress protective reflexes and disregards sensory warnings of tissue ischemia. These patients may or may not feel ischemic pain, but even if they do, they do not make appropriate movements to relieve pressure.

 

With neuropathy being the underlying cause of ulceration (neurotrophic ulcers), many patients complain of burning, tingling, or numbness of the feet on presentation. The ulcer is usually on the plantar aspect of the foot, most commonly heel, under the great toe, or first metatarsal head (Fig. 20.1c, f). Because of pressure, it is often surrounded by a rim of hyperkeratotic tissue, which may even cover the ulcer and give the illusion that the ulcer has healed, when it in fact has not. Infected ulcers may be associated with cellulitis, lymphangitis, adenopathy, calor, edema, foul odor, and purulent drainage. Systemic signs such as fever and chills may be related, but are often absent, even in the presence of severe infection. There may be foot deformity or prominent areas of pressure associated with the ulcer (Fig. 20.2a–c). Neuropathy is the gateway to the development of foot ulceration in diabetic patients.


20.2.1.6 Combined Pathology


When the reactive hyperemia cycle ceases to function adequately, a pressure ulcer will almost certainly develop unless preventive action is taken. There are three potential causes of pressure ulcers:



  • Loss of movement


  • Failure of reactive hyperemia


  • Loss of sensation

The creation of a pressure ulcer can involve one or a combination of these factors. The diabetic patient with neuropathy of the feet is likely to have abnormal circulatory function in the involved area. On the other hand, the paralyzed patient with a spinal injury looses sensation and the ability to move the affected areas, and the ventilated patient doesn’t feel able or move due to anesthesia while the peripheral circulation may be compromised by the administration of inotropes (Fig. 20.1a).


20.2.1.7 Failure of Reactive Hyperemia Cycle


It is a known fact that tissue distortion causes ischemia that in turn stimulates protective movements to relieve pressure and circulatory activity to restore normal blood flow in the affected areas. These protective movements are often reflexes as the person is unaware of making them. However, if these prompt actions prove insufficient to relieve ischemia, the central nervous system is stimulated by constant signals of discomfort and pain to make sure that pressure is relieved before any permanent damage occurs. Once the pressure is relieved and the circulation restored, local capillaries begin to dilate and increased blood flow takes place, referred to as reactive hyperemia. As a result, a bright pink transitory patch appears on the skin, often called blanching erythema because it blanches on pressure unlike the dull red non-blanching erythema that indicates tissue damage (Fig. 20.1a) [13]. Reactive hyperemia ensures a rapid restoration of oxygen and carbon dioxide balance; it also flushes out waste products. Erythema subsides as soon as tissues are restored to their resting state.

Patients who fail to produce reactive hyperemia cannot recover from the pressure-induced ischemic episodes resulting in permanent damage to the tissues. Failure of reactive hyperemia can occur in very sick and dying patients in whom there is insufficient peripheral blood pressure to refill capillary beds emptied by compression. Clinically, this presents as white patches in pressure areas which do not change color rapidly to the red of reactive hyperemia, as they would in a healthy person. Rather, the white patches remain for many minutes before slowly returning directly to a more normal skin color with little or no reactive hyperemia being observable. Similar effects can be seen in critical care patients who are on high doses of inotropes, such as adrenaline.


20.2.2 Indirect Causes (Associated Factors)




1.

Age-related physiological alterations can lower the threshold for pressure-induced injury in elderly patients. For example, an increase in the fragility of blood vessels and connective tissue and a loss of fat and muscle leading to a reduced capacity to dissipate pressure.

 

2.

Any condition that is associated with prolonged, impaired wound healing such as diabetes mellitus, which affects 11 % of adults over the age of 70 years.

 

3.

Oxygen is required for all stages of wound healing; thus, any condition that is associated with a low tissue oxygen tension is a major cause of pressure ulcers. These include heart failure, atrial fibrillation, myocardial infarction, and chronic obstructive pulmonary disease.

 

4.

Peripheral vascular disease, which affects 20 % of older adults, has a negative impact on wound healing.

 

5.

Contractures and spasticity can contribute by repeatedly exposing tissues to pressure through flexion of a joint.

 

6.

Loss of sensations – the pain signal that would normally cause an immobile individual to change position – is lost.

 

7.

Paralysis and insensibility may produce atrophy of the skin leading to a thinning. This renders the skin more susceptible to the friction and shear forces a patient experiences when being moved.

 

8.

Nutritional insufficiency conditions such as malnutrition [14], hypoproteinemia [15], and anemia [16] can cause significant delays in wound healing and hasten the formation of pressure ulcers [17].

 

9.

Moisture causes maceration which predisposes the skin to injury. De-epithelialization caused by trauma leads to transdermal water loss that creates maceration and adherence of the skin to clothing and any other supports in contact, resulting into further injury [8].

 

These associated factors that (independently or combined) can cause pressure ulceration such as being elderly and unable to move the body or specific parts without help or any condition that is associated with weakened wound healing (such as chronic diseases as diabetes mellitus or vascular disease), incontinence, and/or mental disability (often after brain or spinal injury) [18, 19] are explained below in some details:


20.2.2.1 Mobility Problems


Person with mobility problem is unable take preventive actions to pain signal; possible reasons for having a mobility problem are the following:

1.

Spinal cord injury that causes some or all limbs to be paralyzed

 

2.

Brain damage caused by an event such as a stroke or severe head injury, which results in paralysis

 

3.

Progressive damage to the nerves used to move parts of the body, such as Alzheimer’s disease, multiple sclerosis, or Parkinson’s disease

 

4.

Severe pain that makes it difficult to move some or all body parts as seen in skeletal secondaries of malignant diseases

 

5.

Fractures in limbs causing immobility and abnormal limb posture

 

6.

In postoperative phase – particularly if left on a ventilator or with an epidural catheter

 

7.

Coma

 

8.

Extremely painful joint movements such as rheumatoid arthritis

 


20.2.2.2 Poor Nutrition


Reasons that the patient’s diet may lack nutrition include the following:

1.

Anorexia nervosa – a mental health condition where a person has an unhealthy obsession with maintaining a low body weight

 

2.

Dehydration

 

3.

Dysphagia – esophageal cancer, oropharyngeal cancer, and severe stomatitis

 

4.

Loss of appetite – stomach cancer

 


20.2.2.3 Health Conditions




1.

Type 1 diabetes and type 2 diabetes – the high levels of blood sugar associated with diabetes can cause accelerated atherosclerosis and progressive ischemia.

 

2.

Peripheral arterial disease – the blood supply in the legs becomes restricted due to the gradual narrowing of the lumen of the arteries of the legs – by spasm, angiitis, thrombus deposition, and luminal obliteration.

 

3.

Heart failure – previous damage to the heart means it is no longer able to pump enough blood around the body.

 

4.

Kidney failure – which can lead to a buildup of dangerous toxins and products of metabolism in the blood that can cause tissue damage.

 

5.

Chronic obstructive pulmonary disease (COPD) – the low levels of oxygen in the blood associated with COPD can make the skin more vulnerable to anoxia and ischemic damage.

 


20.2.2.4 Aging Skin


With age, the skin loses some of its elasticity (stretchiness), which makes it more vulnerable to damage by minimal shearing force. Aging also results in reduced blood flow to the skin and a reduction in the height of the subcutaneous fat.


20.2.2.5 Incontinence


Both urinary incontinence (inability to control your bladder) and bowel incontinence (inability to control your bowels) can cause certain areas of the skin to become moist and prone to infection. This can trigger pressure ulcers to develop.


20.2.2.6 Mental Health Conditions


People with severe mental health conditions such as schizophrenia or severe depression have an increased risk of pressure ulcers for a number of reasons:

May 13, 2017 | Posted by in GENERAL SURGERY | Comments Off on Pressure Ulcers of the Lower Limb
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