Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_781_Библиотеки_им_академика_М_И_Перельмана
.pdf
32 Aetiology
https://t.me/medicina_free
Stress– biological and immune responses associated with stress
may predispose patients to atherosclerosis.
Age– increased age increases the risk of atherosclerosis.
Acute Arterial Thrombus or Embolism
A thrombus is an unstable atheromatous plaque that can originate
from an area of diseased artery and can result in thrombus formation, for example atrial brillation. When the thrombus becomes
mobilised it gets lodged in a smaller artery, causing occlusion (Mutirangura et al. 2009). Fat and air can also embolise. Assessments of
patients suspected of a thrombus should include the six Ps (Smith
and Lilie2023):
Pain
Pallor
Paraesthesia (burning or prickling sensation)
Paralysis
Pulseless
Poikilothermia (inability to maintain a constant core tempera-
ture independent of the ambient temperature)
Inflammatory Vascular Disease
This is a rare, progressive, degenerative disease that aects small and
medium- sized arteries and veins. The artery wall becomes inamed
due to an occlusion that is surrounded by non- specic immune cells,
which deprive healthy cells local to the occlusion of oxygen and
nutrients (Blanchower and Peate2021). This results in tissue ischaemia and symptoms such as intermittent claudication – fatigue,
cramping, numbness, pain, tingling and weakness in a muscle group.
It is aggravated by exercise and relieved by rest. Chronic ischaemia
results in persistent ischaemic rest pain.
The majority of patients with leg ulcers have some degree of
venous disease. The presence of venous disease suggests that the
ulcer is likely to be of venous origin. Peripheral arterial disease is the
second most common cause of ulceration, and all patients should be
screened for signs and symptoms of arterial disease. There are many
factors that contribute to the risk of venous or arterial disease
Aetiology 33
https://t.me/medicina_free
TABLE1.7
Smoker X
High cholesterol X
Hypertension X
Previous DVT X
Pregnancy X
Varicose veins X
Oedema localised X
Oedema to lower limb X
Capillary rell <3
Hyperaemia on limb elevation (pole test) X
Intermittent claudication X
Rest pain on limb elevation X
Cool toes (consider Reynaud’s phenomenon) X
IV drug abuse X
Obesity X
Men X
Women X
Ulcer below ankle X
Punched out ulcer (cli edges) X
Shiny hairless limb (not from hair removal) X
Hairy lower limb/toes X
Family history of arterial disease X
Family history of venous disease X
Cardiac/stroke or TIA X
Staining of limb –haemosiderin. Will not disappear
but may fade, so could then be arterial
DVT, deep vein thrombosis; IV, intravenous;
TIA, transient ischaemic attack.
Risk factors forvenous andarterial disease.
Venous Arterial
seconds X
X
(Table1.7). It is essential that healthcare practitioners are aware of
these to inform assessment diagnosis and treatment.
THE SKIN
The skin is the largest organ in the body, accounting for 15% of all
body weight. It is integral to both physical and psychosocial health
and can have an impact on quality of life (Wounds UK2018). In a
34 Aetiology
Apocrine sweat gland
Lamellat
is
https://t.me/medicina_free
Hair shaft
Sweat pore
Dermal papillae
Epidermal ridges
Capillary loop
Corpuscle of touch
Eccrine sweat gland
Free nerve ending
Sensory nerve
ed corpuscles
Artery
Papillary region
Arrector pili muscle
Sebaceous gland
Reticular region
Hair follicle
Hair root
Adipose tissue
Vein
Epidermis
Dermis
Hypoderm
FIGURE1.10 The layers of the skin.
healthy individual, the skin is strong, resilient and repairs easily. It
consists of three layers (Figure1.10). The epidermis (outer layer)
provides a waterproof barrier. The dermis lies beneath the epidermis, has a rich blood supply and contains tough connective tissue,
hair follicles, sweat glands and sensory nerve endings. The hypodermis (deep subcutaneous tissue) is made of fat and connective tissue.
The functions of the skin include the following (Mitchell2022):
Protection: intact skin acts as a protective barrier and prevents
internal tissues from trauma, ultraviolet light, toxins, pathogens
and allergens, and changes in environmental temperature.
Barrier to infection: part of this is the physical barrier, but also
the presence of sebum, a natural antibiotic chemical in the epidermis, and a surface acidic environment.
Sensory perception: nerve endings in the skin respond to painful
stimuli, temperature, vibrations, touch and itch.
Aetiology 35
https://t.me/medicina_free
Temperature regulation: the rich blood supply in the skin can act
as a ‘heat dump’ to enable body cooling. The subcutaneous fat
acts as a heat source and heat insulation.
Production of vitamin D and melanin: vitamin D is important for
bone development; melanin is responsible for colouring the skin
and protecting from sunlight and radiation damage.
Communication: the skin is a sensory organ that enables com-
munication through touch and physical appearance.
The skin is constantly exposed to injury and any wounding to the
skin compromises function and integrity.
WOUND HEALING
Wounds can be divided into two sub- categories, ‘acute’ and ‘chronic’.
All leg ulceration will begin as a new or acute wound when the break
in the integrity of the skin rst occurs, yet often people with new ulceration do not present to clinical services until much later when the
wound has been there for some time. There has been a drive nationally
to challenge the use of the word ‘chronic’ in leg ulceration; this is mirrored in the long- term condition management world where terms
such as ‘chronic disease management’ have been rejected in favour of
‘long- term conditions management’. This adaption of the description
is rationalised by the argument that the use of the term ‘chronic’ is
negative and relates to the normalisation of delayed wound healing
(Hopkins and Ritchie2021). As discussed later in this book, the underlying cause of leg ulceration is indeed a long- term condition, requiring
lifelong management, but with the correct treatment the episode of leg
ulceration need not be a long- standing condition in itself.
Leg ulcers are often complex due to factors such as wound location. Simply put, this is due to the eects of gravity: a wound on the
arm has less gravity to overcome than a wound on the leg. On rst
presentation to a healthcare professional many person- centred complexities (for example co- morbidities, medications, health beliefs)
and system- level complexities (workforce, nances and stang
issues) will have led to an already established wound that will require
proactive clinical treatment with the correct dose of compression
therapy to promote healing (EWMA2008).
36 Aetiology
https://t.me/medicina_free
PHASES OFWOUND HEALING
Wound healing is commonly described in four stages (Table1.8).
In every wound type, the healing process runs through a cascade
of phases that partly overlap in time, and so while described here
as a linear process, it is important to acknowledge the overlap of
phases and also the possibility that in wounds that have become
hard to heal, there is potential for a wound to have become ‘stuck’
in one of the phases of wound healing. Most commonly in hard- toheal wounds the wound has become trapped in the inammatory phase.
Haemostasis
The rst phase is known as the vascular phase. Following initial
wounding the degree of blood loss is controlled by a series of events.
The blood and lymphatic vessels undergo vasoconstriction of the
capillaries to slow and reduce the ow of blood to the wounded area
and the production of a brinous blood clot. Haemostasis can continue from the development of a wound for up to ve days
(Ozgok Kangal and Regan 2023). Damaged blood vessels release
blood and platelets that gather, forming a blood clot in the wound.
This process minimises injury and initiates the inammatory phase
(Mitchell2020).
TABLE1.8
Phase Normal timing
Vascular (clotting) 0–5 days
Inammatory phase
(clearing- up phase)
Proliferative phase (rebuilding) 3–24
Maturation Can take up to 2 years depending on
Source: Adapted from Ozgok Kangal and Regan (2023).
Phases ofwound healing.
1–7 days
days
the severity of the wound and the
person’s general health and
well- being
Aetiology 37
https://t.me/medicina_free
Inflammatory Phase
The second phase is the Inammatory response, which begins once
haemostasis has been achieved. Vasodilation follows vasoconstriction, which causes hyperaemia; this presents as a red, warm, swollen
area with increased pain. This usually starts within the rst 24 hours
of injury and can last for up to two weeks in normal wounds. For
hard- to- heal wounds, this can be considerably longer. The blood vessels dilate to allow essential cells into the wound bed. Growth cells
are released, which attracts the migration of phagocytic cells– neutrophils, monocytes and macrophages. The primary function of these
cells is to host an immune response autolysing any bacteria, necrotic
or sloughy tissue within the tissue spaces (Nguyen etal.2009). This
is known as phagocytosis. The neutrophils, monocytes and macrophages release soluble mediators such as pro- inammatory
cytokines and growth factors, which are involved in the recruitment
and activation of broblasts and epithelial cells. These prepare the
wound bed for the next phase of healing. Capillary hydrostatic pressure is increased as a result of greater blood ow and presents externally as redness and heat (Mitchell2020), which are normal in the
sequence of wound healing and should not be mistaken for wound
infection at this stage (Ozgok Kangal and Regan2023; Reinke and
Sorg 2012). The eectiveness of normal blood osmotic pressure
increases capillary permeability, which leads to protein- rich uid
leaking into the interstitial tissue. The viscosity of the blood increases
as the uid moves out of the capillaries, slowing down the ow. This
results in the blood cells clumping together, forcing white cells to
move towards the endothelium of the vessels and causing swelling
and pain. During this process, there is an increased demand for nutrients and oxygen to the wounded area, which increases the individual’s core body temperature and metabolic rate.
Proliferation Phase
The third phase is the proliferative phase (also known as rebuilding),
which occurs at between 3 and 24 days and can be sub- divided into
the granulation stage and the re- epithelisation stage. It is a complex
process where broblasts and growth factors are released from the
surrounding tissues and rapidly multiply.
38 Aetiology
https://t.me/medicina_free
Granulation: angiogenesis is the formation of new blood cells.
This process ensures that the nutrients, gas and metabolic
exchange are provided for granulation tissue formation, which is
essential for wound healing. The broblasts from surrounding
tissues activate growth factors released in the inammatory
phase. These produce a collagen- rich matrix through replication,
which builds strength and elasticity in the wound (Mitchell2020). The red, velvety appearance of granulation tissue on
the wound bed gives an indication of healthy tissue. Dark, discoloured granulation that bleeds easily may be an indication of
infection and poor vascular supply to the tissue (Peate and
Stephens2019).
Contraction: a push/pull eect to contract the wound edges is
created by the myobroblasts.
Epithelisation: once healthy granulation tissue is laid down, the
re- epithelisation stage can begin (Gantwerker and Hom2012).
The epithelial cells change shape to migrate across the wound
bed, forming islands of epithelisation that in time multiply to
cover the wound. Once migration has completed and the wound
has closed, the epithelial cells reattach themselves to the basement membrane.
Maturation Phase
Also known as remodelling, this is the nal stage of wound healing.
The granulation tissue matures into a scar and tissue tensile strength
is increased. This phase can take up to two years to complete. It
involves the reorganisation and maturation of the collagen bres to
maximise tensile strength. This strength will most likely only remain
at 80% of the strength of unwounded skin (Ozgok Kangal and
Regan2023). The collagen bres reorganise themselves and crosslink to strengthen and remodel the scar tissue to complete the woundhealing process. Once the wound has progressed through all four
phases it is healed. However, it is important to remember that scar
tissue is always vulnerable, and for a leg ulcer the underlying pathophysiology that has caused the ulceration remains and requires lifelong management to prevent reoccurrence (see Chapter9).
An understanding of wound healing is essential for the overall
assessment of a wound to identify the stage of healing, or indeed if the
Aetiology 39
https://t.me/medicina_free
ulcer has become ‘trapped’, perhaps in the inammatory stage. It is
also important to be able to recognise abnormal wound healing, which
may be indicative of more unusual ulceration, discussed in Chapter3.
CONCLUSION
A good understanding of the vascular system and associated disorders is important for healthcare professionals so they can gather all
the information needed to aid diagnosis, complete lower limb assessments, plan treatment and care, and educate patients.
REFERENCES
Aysert Yıldız, P., Özdil, T., Dizbay, M. etal. (2018). Peripheral arterial disease
increases the risk of multidrug diabetic foot infections. Turkish Journal of Medical Sciences 48 (4):
845–850.
Bevan, G. and White Solaru, K. (2020). Evidence based medical management
of peripheral arterial disease. Arteriosclerosis, Thrombosis, and
Biology 40 (3): 541–553.
Blanchower, J. and Peate, I. (2021). Fundamentals of Applied Pathophysiol-
ogy: An Essential Guide. Chichester: Wiley-
Browse, N.L. and Burnard, K.G. (1982). The cause of venous ulceration.
Lancet ii: 243–245.
Chant, A.D.P. (1988). Tissue pressure, posture and venous ulceration. Lancet
336: 1050–1051.
Coleridge- Smith, P.D., Thomas, P., Scurr, J.M., and Dormandy, J.A. (1988).
Causes of venous leg ulceration: a new hypothesis. British Medical Jour-
nal 296: 1726–1727.
European Wound Management Association (2008). Hard- to- Heal Wounds: A
Holistic Approach. EWMA Position Document. London: MEP.
Gantwerker, E. and Hom, D. (2012). Skin: histology and physiology of wound
healing. Clinical Plastic Surgery 39 (1): 85–97. https://doi.org/10.1016/
j.cps.2011.09.005.
Green, J., Jester, R., McKinley, R. etal. (2014). The impact of chronic venous
leg ulcers: a systematic review. Journal of Wound Care 23: 601–612.
https://doi.org/10.12968/jowc.2014.23.12.601.
Grey, E. and Patel, K. (2022). Venous and arterial leg ulcers. In: ABC of
Wound Healing, 2e (ed. A. Price), 34–40. Chichester: Wiley.
resistant bacteria and amputation in
Vascular
Blackwell.
40 Aetiology
https://t.me/medicina_free
Guest, J.F. and Fuller, G.W. (2023). Cohort study assessing the impact of
COVIDcomes in clinical practice in the UK. BMJ Open 13 (2): e068845.
Guest, J.F., Fuller, G.W., and Vowden, P. (2018). Venous leg ulcer manage-
ment in clinical practice in the UK: costs and outcomes. International
Wound Journal 15: 29–37. https://doi.org/10.1111/iwj.12814.
Guest, J., Fuller, G., and Vowden, P. (2020). Cohort study evaluating the bur-
den of wounds to the UK’s National Health Service in 2017/2018: update
from 2012/2013. BMJ Open 10: e045253. https://doi.org/10.1136/
bmjopen-
Henning, R. (2021). Obesity and obesity-
contribute to atherosclerosis: a review of the pathophysiology and
treatment of obesity. American Journal of Cardiovascular Disease 11
(4): 504–529.
Herrick, S.E., Sloan, P., McGurk, M. etal. (1992). Sequential changes in histo-
logical pattern and extracelluar matrix deposition during the healing of
chronic venous ulcers. American Journal of Pathology 14 (5): 1085–1095.
Higley, H.R., Ksander, G.A., Gerhardt, C.O., and Falanga, V. (1995). Extrava-
sion of macromolecules and possible trapping of transferring growth
factor in ulceration. British Journal of Dermatology 132: 79–85.
Hopkins, A. and Ritchie, G. (2021). The legs matter campaign: the need to
change culture not dressings. Wounds UK 17 (2): 23–24.
Lee, J. and Cooke, P. (2011). The role of nicotine in the pathogenesis of ath-
erosclerosis. Atherosclerosis 215 (2): 281–283. https://doi.org/10.1016/
j.atherosclerosis.2011.01.003.
Linton, M., Yancey, P., Davies, S. etal. (2014). The Role of Lipids and Lipopro-
teins in Atherosclerosis. Bethesda, MD: National Library of Medicine.
London, G. and Pannier, B. (2010). Arterial functions: how to interpret the
complex physiology. Nephrology Dialysis Transplantation 25 (12):
3815–3823.
Lusis, A. (2010). Atherosclerosis. Nature 407 (6801): 233–241.
Mansilha, A. and Sousa, J. (2018). Pathophysiological mechanisms of chronic
venous disease and implications for venoactive drug therapy. Interna-
tional Journal of Molecular Sciences 19 (6): 1669.
McCance, K.L., Huether, S.E., Brashers, V.L., and Rote, N.S. (2018). Patho-
physiology: The Biologic Basis for Disease in Adults and Children, 8e.
St Louis, MO: Mosby.
Mitchell, A. (2020). Assessment of wounds in adults. British Journal of Nurs-
ing 29 (20): S18–S24.
Mitchell, A. (2022). Skin assessment in adults. British Journal of Nursing
31 (5): 274–278.
Mutirangura, P., Ruangsetakit, C., Wongwanit, C. etal. (2009). Clinical dif-
ferentiation between acute arterial embolism and acute arterial
19 on venous leg ulcer management and associated clinical out-
2020- 045253.
induced inammatory disease
Aetiology 41
https://t.me/medicina_free
thrombosis of the lower extremities. Journal of the Medical Association
of Thailand 92 (7): 891–897.
National Institute for Health and Care Excellence (2016). Physical activity:
brief advice for adults in primary care. Public health guideline [PH44].
https://www.nice.org.uk/guidance/ph44
National Institute for Health and Care Excellence (2023). Leg ulcer– venous.
https://cks.nice.org.uk/topics/leg-
Nelson, E. and Adderley, U. (2016). Venous leg ulcers. British Medical Jour-
nal Clinical Evidence 2016: 1902.
Nguyen, D.T., Orgill, D.P., and Murphy, G.F. (2009). The pathophysiologic
basis for wound healing and cutaneous regeneration. In: Biomaterials
for Treating Skin Loss (ed. D.P. Orgill and G.F. Murphy), 25–57. Cambridge: Woodhead Publishing.
Ozgok Kangal, M. and Regan, J. (2023). Wound healing. In: StatPearls. Treasure
Island, FL: StatPearls Publishing https://www.ncbi.nlm.nih.gov/books/
NBK535406.
Peate, I. and Stephens, M. (2019). Wound Care at a Glance, 2e. Chichester:
Wiley- Blackwell.
Reinke, J.M. and Sorg, H. (2012). Wound repair and regeneration. European
Surgical Research 49: 35–43. https://doi.org/10.1159/000339613.
Shammeri, O., AlHamdan, N., Al-
insuciency: prevalence and eect of compression stockings. Interna-
tional Journal of Health Sciences 8 (3): 231–236.
Smith, D. and Lilie, C. (2023). Acute arterial occlusion. In: StatPearls. Treas-
ure Island, FL: StatPearls Publishing https://www.ncbi.nlm.nih.
gov/books/NBK441851.
Tan, M.N.A., Lo, Z.J., Lee, S.H. etal. (2018). Review of transmetatarsal ampu-
tations in the management of peripheral arterial disease in an Asian
population. Annals of Vascular Diseases 11 (2): 210–216.
Tucker, W., Arora, Y., and Mahajan, K. (2022). Anatomy, Blood Vessels.
Bethesda, MD: National Library of Medicine.
Urwin, S., Dumville, J.C., Sutton, M. et al. (2022). Health service costs of
treating venous leg ulcers in the UK: evidence from a crosssurvey based in the northwest of England. BMJ Open 12: e056790.
https://doi.org/10.1136/bmjopen- 2021- 056790.
White, J. and Ryjewski, C. (2005). Chronic venous insuciency. Perspectives
in Vascular Surgery and Endovascular Therapy 17 (4): 319–327.
https://doi.org/10.1177/153100350501700406.
Wounds UK (2018). Best practice statement: Maintaining skin integrity. https://
wounds- uk.com/best- practice- statements/maintaining- skin- integrity
Wounds UK (2022). Best practice statement: Holistic management of venous
leg ulceration (second edition). https://wounds- uk.com/best- practicestatements/holistic- management- venous- leg- ulceration- second- edition
ulcer- venous
hothaly, B. etal. (2014). Chronic venous
sectional
Соседние файлы в папке Библиотека им академика М.И. Перельмана