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The Aetiology of Pressure Sores
Journal of Tissue Viability 1994 Vol4 No 3
77
The Aetiology Of Pressure Sores James Kelly Consultant Geriatrician, Erne Hospital, Enniskillen, Co Fermanagh
The formation of pressure sores occurs within a complex mulitfactorial situation where both patient's condition, and the organisation of the clinical environment are important contributors to the overall process. This paper was presented at the Society's spring conference in Harrogate. Introduction Pressure sores, or decubitus ulcers, remain a major problem in modem medicine, affecting one in ten hospital patients' . Prevalence rates of 30-40% are not uncommon for elderly care units and rates as high as 66% have been recorded for elderly fractured neck of femur patients 2 • Only 15% of pressure sores are present on admission, therefore 85% occur while the patien~ is under hospital care3 • This represents a gross failure of care particularly on the part of the medical profession. Central to improved care is an understanding of the aetiology of pressure sores, identification of the patients most at risk and initiation of good preventive measures. Definition A pressure sore is an area of ulceration and necrosis of the skin, and/or subcutaneous fat and muscle, occurring over bony prominences as a result of prolonged, unrelieved pressure4 • Key Factors The development of a pressure sore requires one or more of a combination of key factors to be present. 1. Compressive Pressure Forces The direct pressure required to overcome normal capillary pressure of 12- 33 mm Hg, if sustained, will give rise to tissue damage. In frail elderly patients with vascular disease lower occlusion pressures may apply. Multiple short exposures to pressure with incomplete tissue recovery time can also lead to pressure sores. The skin is relatively resistant to pressure but the subcutaneous and deep tissues, particularly those in direct contact with a bony prominence, are very susceptible to damage5 • 2. Shearing Forces These forces permit relatively low contact pressures to cause large sores. This results from the tangential forces, produced by tissue layers moving in opposite directions, interrupting the deeper vascular supply via kinking, nipping and direct damage. The resultant vascular damage leads to deep full thickness pressure sores6 • 3. Friction Forces These forces are usually associated with the rapid movement of the patient's skin against the bed sheet. This most often occurs due to incorrect lifting and handling of patients. The sores produced are usually painful but superficial.
4. Moisture Even slight amounts of moisture can lead to a five fold increase in the risk of development of pressure sores. Moisture, in particular urine or faecal fluid, macerates the skin, decreasing its tensile strength. Pathophysiology The exact pathophysiology of pressure sores is unclear but certain important aspects can be outlined. 1. Ischremia This results from compressive or shearing forces. The impaired blood supply results in decreased delivery of oxygen and nutrients to the tissues and the accumulation of excess toxic metabolites. The duration of the ischaemia is critical in determining whether tissues recover, or are damaged and die7 • The reactive hyperaemia after blood flow debt represents recovery despite significant ischaemia. However, within the tissues there is considerable inflammatory cell infiltrate and oedema suggesting some damage has occurred. 2. Lymphatic Damage Pressure forces impair and damage the lymphatic system either by direct pressure damage or by secondary hypoxia. The overall effect is poor lymph flow with accumulation of toxic metabolites. 3. Tissue Necrosis Prolonged impairment of blood flow ultimately leads to cell death and tissue necrosis. Platelet aggregation occurs with the formation of multiple microthrombi in the microvasculature. At this stage a hard inelastic tumour may be felt in the subcutaneous tissues with the skin showing bluish red discoloration. This converts quickly to a black eschar with an underlying ulcerated area. 4. Infection Damage to the microvasculature and increased anaerobic metabolites encourages bacterial invasion with further bacterial multiplication. This produces mostly local effects but on occasions will give rise to bacteraemia or septicremia. 5. Reperfusion Injury The restoration of blood flow to ischremic tissues does not always result in cessation of tissue damage. The reoxygenation may produce superoxide radicals which are potentially toxic to
78
Journal of Tissue Viability 1994 Vol4 No 3
compromised tissues 8 . The role of anti-oxidants such as vit C in pressure sore prevention and healing has yet to be determined. There are a number of retiological factors, intrinsic and extrinsic to the patient, which are directly associated with increased risk of pressure sores.
Intrinsic Factors These are factors inherent to the individual patient that place him or her at increased risk of a pressure sore. 1. Age More than seventy per cent of all pressure sores occur in the elderly 9 • Many of the intrinsic factors below occur most frequently in this age group. Age related tissue changes also play a role. This group therefore, requires special targeting of preventive measures and resources. 2. Body State/Clinical State The frail or poorly nourished patient is at particular risk. Obese patients may have more protective padding but they have increased risk through weight induced immobility. 3. Circulatory Problems Arterial insufficiency due to peripheral vascular disease, primary cardiac dysfunction or anaemia frequently results in pressure sore problems. 4. Mental Awareness Confused patients and patients with lowered level of consciousness are at particularly high risk of sore development. Similarly, patients with sensory problems are also vulnerable. 5. Mobility Poorly mobile patients, and in particular, chairbound patients are at very high risk of pressure sores 10 • 6. Chronic Debilitating Diseases Any chronic debilitating condition such as rheumatoid arthritis, uraemia or diabetes mellitus exposes the patient to pressure sore problems. 7. Additional Acute Illness Frequently patients perceived to be at only mild to moderate risk develop pressure sores due to an additional acute illness such as a respiratory or urinary tract infection. Any change in the patient's clinical state should warrant immediate reassessment of the Waterlow or Norton score.
Extrinsic Factors These are factors relating to the environment in which a patient is managed or treated. 1. Waiting Times Long periods lying on AlE trolleys, operating tables and in Xray departments are associated with increased risk. Trolley 'toppers' can reduce this risk but patients should be 'fast tracked' out of these departments to a pressure relieving bed/mattress at the earliest opportunity. 2. Equipment The standard hospital mattress and bed have no pressure relieving properties and actually place patients at increased risk, particularly if they are poorly maintained. Similarly the
inappropriate use oflow pressure relieving mattresses or overlays for high risk patients without associated patient turning leads to pressure sores. 3. Enforced Immobilisation Traction and splints if incorrectly applied or poorly monitored frequently cause pressure sores. 4. Chairs The widespread practice of using chairs without adequate pressure relieving cushions remains a majorproblem in hospitals and nursing homes. 5. Medication Inappropriate use of sedatives or hypnotics and inadequate analgesia promotes the development of pressure sores. 6. Staffing Insufficient staffing, incorrect skill mix or poorly trained staff can result in poor pressure sore prevention. 7. Patient Handling Incorrect lifting or handling of an at risk patient by poorly trained staff or relatives may result in pressure sores. Constant awareness of the many intrinsic and extrinsic risk factors combined, with a good scoring system and appropriate pressure relieving equipment, leads to pressure sore prevention reducing patient suffering, staff workload and unit costs.
Address for Correspondence Dr James Kelly Consultant Geriatrician, Erne Hospital, Enniskillen, Co Fermanagh, N Ireland, BT74 6AY.
References 1. BarbenelJ C, Jordan M M, NicolS M, OarkM 0. Incidence of pressure sores in the Greater Glasgow Health Board Area Lancet. 1977; ii: 548-50. 2. Versluysen M. How elderly patients with femoral fracture develop pressure sores in hospital. Br Med11986; 292:1311-13. 3. Norton D, McLaren R, Exton-Smith AN, eds. An Investigation of geriatric nursing problems in hospital. Edinburgh: Churchill Livingstone. 1975. 4. Sheenaq S M, Dinh T A Decubitus Ulcers. How to prevent them andinterveneshouldpreventionfail. PostgradMed. 1990; 87: 91-5. 5. Groth KE. Oinical observations and experimental studies on the origin of decubiti. Acta Chir Scand. 1942; 87 Suppl76: I, 1-209. 6. Bader D L, Bowker P. Mechanical characteristics of skin and underlying tissues in vivo. Biomaterials. 1983; 4: 305-8. 7. Bader D L, Gant C A Changes in transcutaneous oxygen tension as a result of prolonged pressures at the sacrum. Clin Phys Physiol Meas. 1988; 9: 33-40. 8. Michel C C, Gillon H. Microvascular Mechanisms in Stasis and Ischremia. In: Bader DL ed, Pressure Sores Clinical Practice and Scientific Approach. London: Macmillan. 1990: 153-62. 9. Bliss M. Geriatric Medicine. In: Bader D Led, Pressure Sores Clinical Practice and Scientific Approach. London: Macmillan. 1990:65-80. 10. Bliss M. Is bed really badforold people? Geriatric Medicine. 1992; 22: 41-4.
77
The Aetiology Of Pressure Sores James Kelly Consultant Geriatrician, Erne Hospital, Enniskillen, Co Fermanagh
The formation of pressure sores occurs within a complex mulitfactorial situation where both patient's condition, and the organisation of the clinical environment are important contributors to the overall process. This paper was presented at the Society's spring conference in Harrogate. Introduction Pressure sores, or decubitus ulcers, remain a major problem in modem medicine, affecting one in ten hospital patients' . Prevalence rates of 30-40% are not uncommon for elderly care units and rates as high as 66% have been recorded for elderly fractured neck of femur patients 2 • Only 15% of pressure sores are present on admission, therefore 85% occur while the patien~ is under hospital care3 • This represents a gross failure of care particularly on the part of the medical profession. Central to improved care is an understanding of the aetiology of pressure sores, identification of the patients most at risk and initiation of good preventive measures. Definition A pressure sore is an area of ulceration and necrosis of the skin, and/or subcutaneous fat and muscle, occurring over bony prominences as a result of prolonged, unrelieved pressure4 • Key Factors The development of a pressure sore requires one or more of a combination of key factors to be present. 1. Compressive Pressure Forces The direct pressure required to overcome normal capillary pressure of 12- 33 mm Hg, if sustained, will give rise to tissue damage. In frail elderly patients with vascular disease lower occlusion pressures may apply. Multiple short exposures to pressure with incomplete tissue recovery time can also lead to pressure sores. The skin is relatively resistant to pressure but the subcutaneous and deep tissues, particularly those in direct contact with a bony prominence, are very susceptible to damage5 • 2. Shearing Forces These forces permit relatively low contact pressures to cause large sores. This results from the tangential forces, produced by tissue layers moving in opposite directions, interrupting the deeper vascular supply via kinking, nipping and direct damage. The resultant vascular damage leads to deep full thickness pressure sores6 • 3. Friction Forces These forces are usually associated with the rapid movement of the patient's skin against the bed sheet. This most often occurs due to incorrect lifting and handling of patients. The sores produced are usually painful but superficial.
4. Moisture Even slight amounts of moisture can lead to a five fold increase in the risk of development of pressure sores. Moisture, in particular urine or faecal fluid, macerates the skin, decreasing its tensile strength. Pathophysiology The exact pathophysiology of pressure sores is unclear but certain important aspects can be outlined. 1. Ischremia This results from compressive or shearing forces. The impaired blood supply results in decreased delivery of oxygen and nutrients to the tissues and the accumulation of excess toxic metabolites. The duration of the ischaemia is critical in determining whether tissues recover, or are damaged and die7 • The reactive hyperaemia after blood flow debt represents recovery despite significant ischaemia. However, within the tissues there is considerable inflammatory cell infiltrate and oedema suggesting some damage has occurred. 2. Lymphatic Damage Pressure forces impair and damage the lymphatic system either by direct pressure damage or by secondary hypoxia. The overall effect is poor lymph flow with accumulation of toxic metabolites. 3. Tissue Necrosis Prolonged impairment of blood flow ultimately leads to cell death and tissue necrosis. Platelet aggregation occurs with the formation of multiple microthrombi in the microvasculature. At this stage a hard inelastic tumour may be felt in the subcutaneous tissues with the skin showing bluish red discoloration. This converts quickly to a black eschar with an underlying ulcerated area. 4. Infection Damage to the microvasculature and increased anaerobic metabolites encourages bacterial invasion with further bacterial multiplication. This produces mostly local effects but on occasions will give rise to bacteraemia or septicremia. 5. Reperfusion Injury The restoration of blood flow to ischremic tissues does not always result in cessation of tissue damage. The reoxygenation may produce superoxide radicals which are potentially toxic to
78
Journal of Tissue Viability 1994 Vol4 No 3
compromised tissues 8 . The role of anti-oxidants such as vit C in pressure sore prevention and healing has yet to be determined. There are a number of retiological factors, intrinsic and extrinsic to the patient, which are directly associated with increased risk of pressure sores.
Intrinsic Factors These are factors inherent to the individual patient that place him or her at increased risk of a pressure sore. 1. Age More than seventy per cent of all pressure sores occur in the elderly 9 • Many of the intrinsic factors below occur most frequently in this age group. Age related tissue changes also play a role. This group therefore, requires special targeting of preventive measures and resources. 2. Body State/Clinical State The frail or poorly nourished patient is at particular risk. Obese patients may have more protective padding but they have increased risk through weight induced immobility. 3. Circulatory Problems Arterial insufficiency due to peripheral vascular disease, primary cardiac dysfunction or anaemia frequently results in pressure sore problems. 4. Mental Awareness Confused patients and patients with lowered level of consciousness are at particularly high risk of sore development. Similarly, patients with sensory problems are also vulnerable. 5. Mobility Poorly mobile patients, and in particular, chairbound patients are at very high risk of pressure sores 10 • 6. Chronic Debilitating Diseases Any chronic debilitating condition such as rheumatoid arthritis, uraemia or diabetes mellitus exposes the patient to pressure sore problems. 7. Additional Acute Illness Frequently patients perceived to be at only mild to moderate risk develop pressure sores due to an additional acute illness such as a respiratory or urinary tract infection. Any change in the patient's clinical state should warrant immediate reassessment of the Waterlow or Norton score.
Extrinsic Factors These are factors relating to the environment in which a patient is managed or treated. 1. Waiting Times Long periods lying on AlE trolleys, operating tables and in Xray departments are associated with increased risk. Trolley 'toppers' can reduce this risk but patients should be 'fast tracked' out of these departments to a pressure relieving bed/mattress at the earliest opportunity. 2. Equipment The standard hospital mattress and bed have no pressure relieving properties and actually place patients at increased risk, particularly if they are poorly maintained. Similarly the
inappropriate use oflow pressure relieving mattresses or overlays for high risk patients without associated patient turning leads to pressure sores. 3. Enforced Immobilisation Traction and splints if incorrectly applied or poorly monitored frequently cause pressure sores. 4. Chairs The widespread practice of using chairs without adequate pressure relieving cushions remains a majorproblem in hospitals and nursing homes. 5. Medication Inappropriate use of sedatives or hypnotics and inadequate analgesia promotes the development of pressure sores. 6. Staffing Insufficient staffing, incorrect skill mix or poorly trained staff can result in poor pressure sore prevention. 7. Patient Handling Incorrect lifting or handling of an at risk patient by poorly trained staff or relatives may result in pressure sores. Constant awareness of the many intrinsic and extrinsic risk factors combined, with a good scoring system and appropriate pressure relieving equipment, leads to pressure sore prevention reducing patient suffering, staff workload and unit costs.
Address for Correspondence Dr James Kelly Consultant Geriatrician, Erne Hospital, Enniskillen, Co Fermanagh, N Ireland, BT74 6AY.
References 1. BarbenelJ C, Jordan M M, NicolS M, OarkM 0. Incidence of pressure sores in the Greater Glasgow Health Board Area Lancet. 1977; ii: 548-50. 2. Versluysen M. How elderly patients with femoral fracture develop pressure sores in hospital. Br Med11986; 292:1311-13. 3. Norton D, McLaren R, Exton-Smith AN, eds. An Investigation of geriatric nursing problems in hospital. Edinburgh: Churchill Livingstone. 1975. 4. Sheenaq S M, Dinh T A Decubitus Ulcers. How to prevent them andinterveneshouldpreventionfail. PostgradMed. 1990; 87: 91-5. 5. Groth KE. Oinical observations and experimental studies on the origin of decubiti. Acta Chir Scand. 1942; 87 Suppl76: I, 1-209. 6. Bader D L, Bowker P. Mechanical characteristics of skin and underlying tissues in vivo. Biomaterials. 1983; 4: 305-8. 7. Bader D L, Gant C A Changes in transcutaneous oxygen tension as a result of prolonged pressures at the sacrum. Clin Phys Physiol Meas. 1988; 9: 33-40. 8. Michel C C, Gillon H. Microvascular Mechanisms in Stasis and Ischremia. In: Bader DL ed, Pressure Sores Clinical Practice and Scientific Approach. London: Macmillan. 1990: 153-62. 9. Bliss M. Geriatric Medicine. In: Bader D Led, Pressure Sores Clinical Practice and Scientific Approach. London: Macmillan. 1990:65-80. 10. Bliss M. Is bed really badforold people? Geriatric Medicine. 1992; 22: 41-4.