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CHAPTER 3 Surgical pathology
152
Atherosclerosis
Atherosclerosis is a degenerative disease of large and medium-sized
arteries characterized by lipid deposition and fi brosis.
Aetiology
Reversible risk factors include smoking, hypercholesterolaemia, obesity,
and hypertension. Irreversible risk factors include diabetes, male sex, age,
and family history.
Pathological features
• There are three stages of atheromatous lesion; fatty streaks are linear
lesions on the artery lumen, composed of lipid-fi lled macrophages, and
which progress to fi brolipid plaques and fi nally, complex lesions.
• In sites predisposed to atherosclerosis (sites of vessel bifurcation,
turbulent fl ow, post-stenotic areas, areas denuded of endothelial
cells), lipid-laden macrophages enter the vessel wall via gaps between
endothelial cells.
• A fi brolipid plaque contains a mixture of macrophages and smooth
muscle cells which migrate into the plaque, capped by a layer of
fi brous tissue.
• Growth factors, particularly platelet-derived growth factor (PDGF),
stimulate the proliferation of intimal smooth muscle cells and the
synthesis of collagen, elastin, and mucopolysaccharide.
• Lipid accumulates within the plaque extracellularly and in the
myocytes, ultimately producing foam cells.
• Cell death eventually ensues with the release of intracellular lipids,
calcifi cation, and a chronic infl ammatory reaction.
• High levels of circulating LDL-cholesterol are thought to lead to
atherosclerosis by damaging endothelium, both directly by increasing
membrane viscosity and indirectly through free radical formation, and
by inducing secretion of PDGF.
• In larger vessels such as the aorta, atherosclerotic plaques may release
atheroemboli and mural thrombus or impinge on the vessel media,
causing tissue atrophy resulting in aneurysm formation or dissection.
• Acute MI is caused by three processes in coronary vessels: progressive
atherosclerosis, disruption of unstable plaque with acute thrombosis,
and acute haemorrhage into the intima around the plaque.
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CHAPTER 3 Surgical pathology
154
Thromboembolic disease
Thrombus
A thrombus is a solid mass of blood constituents formed within the
vascular system.
The formation, structure, and appearance of thrombus and clot are completely different. Clinical features of thrombus—see b p. 120.
Aetiology
Described by Virchow, the three types of risk factors for thrombus are
called Virchow’s triad (see Box 3.1). Not all three are needed: any one
of them may result in thrombus formation in arteries or veins. Arterial
thrombus is most commonly associated with atheroma, venous thrombus
with stasis.
Box 3.1 Virchow’s triad
• Disruption in the blood vessel endothelium.
Atheromatous plaque, e.g. acute MI.•
Thrombophlebitis, e.g. DVT.•
Trauma, e.g. from pressure, surgery, fractures, previous thrombus.•
• Disruption in the pattern of blood fl ow.
Stasis, e.g. immobilization, surgery, low CO states.•
Turbulence, e.g. post-stenotic, atherosclerotic plaques.•
• Changes in blood constituents.
Age.•
Smoking.•
Malignancy.•
DIC, HITT.•
Pregnancy, oral contraceptive pill.•
Thrombus formation
Wherever thrombus forms, the principal mechanisms are similar.
• Initial trigger is one or more of Virchow’s triad.
• Fibrin deposition on vessel wall and formation of platelet layer.
• Red cells trapped in fi brin meshwork on top of platelet layer.
• Mass projects into lumen, causing turbulent blood fl ow.
• Thrombus grows in direction of blood fl ow: propagation.
• In veins, alternating patterns of white platelets and red blood cells may
be seen: lines of Zahn.
• Thrombophlebitis is infl ammation of veins secondary to thrombus.
• Phlebothrombosis is thrombus formation secondary to phlebitis.
• Phlegmasia alba dolens (white painful leg) occurs after slow thrombosis
formation in the ileofemoral veins and is a chronic condition.
• Phlegmasia cerulean dolens (blue painful leg) is due to acute massive
ileofemoral venous thrombosis and can result in shock and gangrene.
• Thrombophlebitis migrans are transient thromboses in previously
healthy veins anywhere in the body, suggesting visceral cancer.
THROMBOEMBOLIC DISEASE
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Embolism
An embolism is a mobile mass of material in the vascular system capable
of blocking its lumen.
Types of embolism
The aetiology is very different, depending on the cause of embolism.
The clinical effects depend on the territory supplied by the vessel that is
blocked. Emboli can be divided into:
• Systemic emboli (see b p. 642) (cause stroke, end-organ ischaemia, MI);
• PE (see b p. 120).
Both types of embolism can be further classifi ed by the substance
involved:
Thrombus.• Most emboli are derived from thrombi.
Gas.• Injection or entraining of air, decompression sickness.
Fat.• Long bone fractures, severe burns, extensive soft tissue
trauma.
Amniotic fl uid.• i Intrauterine pressure forces fl uid into uterine veins
and into systemic circulation.
Septic emboli.• Vegetations from heart valves.
Atheromatous plaque.• Peripheral vascular disease, iatrogenic.
Tumour.• Common route of metastasis.
Foreign bodies.• IV drug users, medically inserted catheters.
Clot
A clot is a solid collection of blood cells within a fi brin network.
Clot forms in vessels after death or outside the body as part of the
response to trauma. Activation of the clotting cascade (see b p. 119)
results in formation of fi brin from fi brinogen, resulting in the formation of
fi brin meshwork that enmeshes cells in a solid, elastic clot.
Ischaemia and infarction
Ischaemia is tissue effect due to insuffi cient oxygen delivery.
Infarction is tissue death due to insuffi cient oxygen delivery.
155
Oxygen supply-demand mismatch is caused by:
• Vascular narrowing (atherosclerosis, thrombus, embolus, spasm).
• Global hypoperfusion (shock, cardiopulmonary bypass).
• Hypoxaemia (anaemia, hypoxia).
• Vascular compression (ventricular distension, venous occlusion).
• Increased oxygen demand (exercise, pregnancy, hyperthyroidism).
Pathological features
The shape of the infarct depends on the territory and perfusion of the
occluded vessel.
• Seconds. Change from aerobic to anaerobic metabolism.
• Minutes. d Contractility of muscle, cell and mitochondria swell.
CHAPTER 3 Surgical pathology
156
• Hours. Myocyte death, coagulation necrosis, muscle pale, oedematous.
• Days. Infl ammatory exudates with polymorphonuclear leucocytes, then
fi broblast infi ltration beginning scar formation; macroscopically, the
infarcted area appears yellow and rubbery with haemorrhagic border.
• Weeks. Neovascularization and margins.
• Months. Scar maturation—tough, white, contracted area.
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CHAPTER 3 Surgical pathology
158
Gangrene and capillary ischaemia
Gangrene is ischaemic tissue necrosis with dessication (dry gangrene)
or putrefaction (wet gangrene).
Gangrene
Aetiology
• Thrombosis, e.g. appendiceal artery secondary to infl ammation.
• Embolus, e.g. atherosclerotic emboli in peripheral vascular disease.
• Extrinsic compression, e.g. fracture, organ torsion, tourniquet.
Clinical appearances
Dry gangrene
The affected limb, digit, or organ is black because of breakdown of haemoglobin, dry, and shrivelled. Dry gangrene shows little or no tendency
to spread. A zone of demarcation appears between the dead and viable
tissue and separation begins to take place by aseptic ulceration in a few
days.
Wet gangrene
Veins as well as arteries are blocked. Pain is initially severe, but lessens as
the patient becomes more septic. There is always infection (putrefaction).
The skin and superfi cial tissues become blistered. There is a broad zone
of ulceration which separates it from normal tissue. Proximal spread is a
feature, leading to septicaemia and death.
Gas gangrene
Gangrene complicated by infection with gas-producing anaerobic bacteria,
e.g. Clostridium perfringens. Gases elaborated from putrefaction lead to
surgical emphysema and crepitus (see b p. 175).
Principles of treatment
• Systemic treatment.
Aggressive fl uid resuscitation is often necessary.•
Pain relief (IV morphine 5–10mg).•
IV antibiotics—broad-spectrum (e.g. benzylpenicillin, metronidazole, •
piperacillin/tazobactam, or according to microbiological advice).
• Conservative treatment. Only possible for non-vital organs affected
by dry gangrene (e.g. toes/forefoot). Aim is to let the affected areas
mummify and spontaneously separate.
• Surgical salvage procedures. Conservative excision possibly combined
with reconstruction or restoration of blood supply (e.g. foot
amputation and bypass surgery for distal lower limb gangrene).
• Radical surgical excision. Only possible where affected organ is
completely resectable (e.g. limbs, perineal tissues)—excision must
be radical in spreading or gas gangrene. Ensure all pus is released, all
affected tissue (not just the necrosed area) is excised back to bleeding
healthy tissue. Often requires ‘relook’ surgery to ensure adequate
excision of infected tissue.
GANGRENE AND CAPILLARY ISCHAEMIA
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• Palliative care. Consider for unresectable gangrene (e.g. retroperitoneal
gangrene, very extensive intestinal gangrene) or for elderly sick
patients where surgery is inappropriate.
Capillary ischaemia
This is ischaemia mediated by injury to capillaries.
• Frostbite. Exposure to cold with freezing results in fi xed capillary
contraction, ischaemia, and infarction.
• Trenchfoot. Exposure to cold without freezing results in capillary
contraction followed by fi xed dilation.
• DIC (see b p. 116).
• Cryoglobulinaemia, sickle cell, parasites.
159
CHAPTER 3 Surgical pathology
160
Tumours
Defi nitions
• Metaplasia. Reversible transformation of one type of terminally
differentiated cell into another fully differentiated cell type.
• Dysplasia. Potentially premalignant condition characterized
by increased cell growth, atypical morphology, and altered
differentiation.
• Neoplasia. Autonomous abnormal growth of cells which persists
after the initiating stimulus has been removed.
• A neoplasm is a lesion resulting from neoplasia.
Metaplasia
This represents an adaptive response of a tissue to environmental stress.
It is mediated by changes in expression of genes involved in cellular differentiation. It does not progress to malignancy: if the environmental changes
persist, dysplasia may result and progress to malignancy. For example:
• Change from ciliated to squamous cells in the respiratory epithelium of
the trachea and bronchi in smokers;
• Change from squamous to columnar cells in the oesophageal
epithelium of patients with gastro-oesophageal refl ux disease
(Barrett’s) (see b p. 280).
Dysplasia
Potentially premalignant condition. May be a response to chronic infl ammation or exposure to carcinogens. Early forms may be reversible: severe
dysplasia has a high risk of progression to malignancy, for example:
• Dysplasia arising in colonic epithelium due to chronic ulcerative colitis.
• Squamous dysplasia in the bronchi of smokers (sputum cytology).
Classifi cation of tumours
Use this classifi cation to give a differential diagnosis for any neoplasm.
• Tissue of origin. Organ and tissue type (see Table 3.1).
• Behaviour. Benign or malignant.
• Primary or secondary.
Benign tumours
• Slow growing, usually encapsulated, do not metastasize, do not recur
if completely excised, rarely endanger life. Effects are due to size and
site.
• Histology: well differentiated, low mitotic rate, resemble tissue of
origin.
Malignant tumours
• These expand and infi ltrate locally, encapsulation is rare, metastasize
to other organs via blood, lymphatics or body spaces, endanger life if
untreated.
• Histology: varying degrees of differentiation from tissue of origin,
pleomorphic (variable cell shapes), high mitotic rate.
TUMOURS
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Table 3.1 Structural classifi cation
Tissue of origin Tumour type
Epithelium Benign: papilloma, adenoma (glandular epithelium)
Malignant: carcinoma (adenocarcinoma, squamous cell
carcinoma indicate cell types)
Connective tissue Benign: fi broma (fi brous tissue), lipoma (fat),
Neural tissue These arise from nerve cells, nerve sheaths, and
Haemopoietic The leukaemias, Hodgkin’s disease, multiple myeloma,
Melanocytes Melanoma
Mixed origins E.g. fi broadenoma, nephroblastoma, teratoma (all three
Developmental
blastomas
chondroma (cartilage), osteoma (bone), leiomyoma
(smooth muscle), rhabdomyoma (striated muscle)
Malignant: sarcoma, e.g. fi brosarcoma, osteosarcoma,
etc. (if well differentiated); spindle cell sarcoma, etc.
(if poorly differentiated)
supporting tissues, e.g. astrocytoma, medulloblastoma,
neurilemmoma, neuroma, etc.
lymphosarcoma, reticulosarcoma
germ layers), choriocarcinoma
E.g. neuroblastoma (adrenal medulla), nephroblastoma
(kidney), retinoblastoma (eye)
Invasion
Invasion is the most important single criterion for malignancy and is also
responsible for clinical signs and prognosis as well as dictating surgical
management. Factors that enable tumours to invade tissues include:
• Increased cellular motility.
• Loss of contact inhibition of migration and growth.
• Secretion of proteolytic enzymes, such as collagenase, which weakens
normal connective tissue bonds.
• Decreased cellular adhesion.
Metastasis
Metastasis is a consequence of these invasive properties: it is the process by which malignant tumours spread from their site of origin (primary
tumour) to form secondary tumours at distant sites. Carcinomatosis
denotes extensive metastatic disease. The routes of metastasis are:
• Haematogenous. Via the bloodstream.
Five tumours—breast, bronchus, kidney, thyroid, prostate—•
classically metastasize via haematogenous spread to bone.
Lung, liver, and brain are common sites for secondaries.•
• Lymphatic. To local, regional, and systemic nodes.
• Transcoelomic. Across pleural, pericardial, and peritoneal cavities.
• Implantation. During surgery or along biopsy tracks.
161
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