Cysts
Classifi cation Congenital
• Sequestration dermoid. Due to displacement of epithelium along embryonic fi ssures during closure, e.g. skin. Sites include outer and inner borders of orbit, midline of the body, anterior triangle of neck (brachial cyst), (cf. implantation dermoid due to skin implantation from injury).
• Tubulo-dermoid/tubulo-embryonic. Abnormal budding of tubular structures, e.g. enteric cysts, post-anal dermoid, thyroglossal cyst.
• Dilatation of vestigial remnants. For example, urachal, vitellointestinal, paradental and branchial cleft cysts, hydatid of Morgagni, Rathke’s pouch.
Acquired
• Retention cysts. Due to the blocking of a glandular or excretory duct, e.g. sebaceous cyst (sweat gland); ranula (salivary gland); and cysts of the pancreas, gall bladder, parotid, breast, epididymis, Bartholin’s glands, hydronephrosis, hydrosalpinx.
• Distension cysts. Due to the distension of closed cavities as a result of exudation or secretion, e.g. thyroid or ovarian cysts; hygroma (lymphatic cysts), hydrocoele, ganglia, bursas (false cysts).
• Cystic tumours. For example, cystadenoma, cystadenocarcinoma of ovary.
• Parasitic cysts. For example, hydatid cysts (Taenia echinococcus).
• Pseudocysts. Due to necrosis of haemorrhage with liquefaction and encapsulation, e.g. necrotic tumours, cerebral softening, or coalescence of infl ammatory fl uid collections, e.g. pseudocyst of pancreas.
Clinical features Subcutaneous/superfi cial
Smooth, spherical, soft, and fl uctuant when palpated in two planes with the fi ngers at right angles to each other. If tense contents, may produce pain in the cyst or surrounding tissue. If the fl uid is clear, the swelling will transilluminate. Ultrasound and aspiration of contents are methods of determining whether a given swelling is cystic and may differentiate a cyst from a lipoma. May compress surrounding tissues. May produce pain if complications supervene. They are also subject to infection, torsion if on a pedicle, haemorrhage, and calcifi cation.
A cyst is a collection of fl uid in a sac lined by endothelium or epithelium which usually secretes the fl uid.
• True cysts are lined by endo- or epithelium.
• False cysts are the result of exudation or degeneration, e.g.
pseudocyst of pancreas, cystic degeneration in a tumour.
CYSTS, SINUSES, AND FISTULAS
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Treatment
• Excision. Only if symptomatic, cosmetic, or concern over diagnosis.
• Marsupialization (deroofi ng and suture of the lining to skin). If chronic or infected.
• Drainage (deep site). If symptomatic or complicated. Not if concern over malignancy.
Sinuses/fi stulas
Causes
• Specifi c disease, e.g. Crohn’s.
• Abscess formation and spontaneous drainage, e.g. diverticular abscess discharging into vagina with fi stula formation.
• Penetrating wounds.
• Iatrogenic (e.g. anastomotic leak discharging via wound).
• Neoplastic.
Persistence of a fi stula is due to the following
• Presence of foreign material, e.g. suture/bone in a sinus.
• Distal obstruction of the viscus of origin.
• Continuing active sepsis, e.g. TB, actinomycosis.
• Epithelialization of the track.
• Chronic infl ammation, e.g. Crohn’s.
• Malignancy in the track.
Investigation
Establish the extent by sinography/fi stulogram. MRI scan is often helpful.
Treatment
Principles of sinus treatment:
• Ensure adequate drainage, laying it open and remove granulations.
• Remove septic material, foreign bodies.
• Biopsy sinus wall if concern over underlying diagnosis.
• Loose packs may be used to help drainage.
Principles of fi stula treatment:
• Treat any sepsis, fl uid imbalances, and poor nutrition if associated.
• Ensure good drainage to prevent fi stula extension.
• Identify the anatomy, use examination under anaesthetic (EUA) or imaging if required.
• Biopsy the fi stula if concern over underlying diagnosis.
• Defi nitive treatment requires:
Excision of the organ of origin or closure of the site of origin.
•
Removal of chronic fi stula track and surrounding infl amed tissue.
•
Closure of ‘recipient’ organ if internal or drainage of external site
• if to skin.
• A sinus is a blind epithelial track, lined by granulation tissue which extends from a free surface into the tissues, e.g. pilonidal sinus.
• A fi stula is an abnormal communication between two epithelial surfaces. It is lined by granulation tissue and colonized by bacteria, e.g. fi stula-in-ano, pancreaticocutaneous, colovesical, vesicovaginal.
Atherosclerosis
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.
Atherosclerosis is a degenerative disease of large and medium-sized arteries characterized by lipid deposition and fi brosis.