Parker Definitions Flashcards
Abscess
Cavity lined by granulation tissue containing pus (alive & dead bacteria, alive & dead neutrophils, tissue debris, serum) Pre-disposing factors: foreign body within the wound, haematoma formation, ischaemia Commonest superficial abscess organisms; staph aureus, streptococcus pyogenes e.g. infected sebaceous cyst, breast abscess, pilonidal abscesses Clinical features; calor, rubor, dolor, tumour Commonest deep abscess organisms; gram neg - Escherichia coli, anaerobes - bacteroides e.g. diverticular, subphrenic, anastomotic leaks Clinical feautres; swinging pyrexia, tachycardia, tachpnoea
Treatment of abscesses
Rx- drainage, often under GA.
ABx have poor penetraction and can -> chronic inflammatory mass (antibioma)
Superficial abscess: incision and drainage, cruciate incision (alowing for dependent drainage), loculi within avscess should be broken down and necrotic tissue excised & pus sent for microbiology, dressing inserted into the wound.
Deep abscess: US or CT guided aspiration. Multiloculated abscess may require open drainage
Pus
alive & dead bacteria, alive & dead neutrophils, tissue debris, serum
Cyst
collection of fluid in a sac lined by endothelium or epithelium which usually secretes the fluid. • 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.
Classification of cysts
True: lined by endo/epithelium False: from exudation/degeneration- eg pancreatic pseudocyst, cystic degeneration of tumour Congenital: dermoid cyst, branchial cyst, hyatidid of Morgagni Acquired: sebacous, thyroid/ovarian, parasitic, pseudocysts
Sinus
blind epithelial track, lined by granulation tissue which extends from a free surface into the tissues, e.g. pilonidal sinus.
Fistula
abnormal communication between two epithelial surfaces. It is lined by granulation tissue and colonized by bacteria, e.g. fistula-in-ano, pancreaticocutaneous, colovesical, vesicovaginal.
Ulcer
breach in an epithelial surface.
Diverticulum
Outpouching of a hollow viscous (true = includes all tissue layers), false= only mucosa & muscularis mucosae eg bowel, bladder, oesophagus
Atherosclerosis
Degenerative disease of large and medium-sized arteries characterized by lipid deposition and fibrosis.
Thrombus
solid mass of blood constituents formed within the vascular system.
Embolism
mobile mass of material in the vascular system capable of blocking its lumen.
Clot
Solid collection of blood cells in a fibrin network
Ischaemia
Tissue effect from insufficient oxygen
Infarction
Tissue death from insufficient oxygen
Gangrene
Ischaemic tissue necrosis with desiccation (dry) or putrefaction (wet) Can be secondary to thrombosis (eg appendicular artery)/ embolism eg in PVD/extrinsic compression eg in facture or tourniquet use
Metaplasia
Reversible transformation of one type of terminally differentiated cell into another fully differentiated cell type. Eg Baratt’s oesophagus (squamous to columnar) Adaptive response of a tissue to environmental stress. It is mediated by changes in expression of genes involved in cellular differ- entiation. It does not progress to malignancy: if the environmental changes persist, dysplasia may result and progress to malignancy
Dysplasia
Potentially premalignant condition characterized by increased cell growth, atypical morphology, and altered differentiation. May be a response to chronic inflam- mation or exposure to carcinogens. Early forms may be reversible: severe dysplasia has a high risk of progression to malignancy,
Neoplasia
Autonomous abnormal growth of cells which persists after the initiating stimulus has been removed.
Inflammation
local physiological response to tissue injury. It can be acute or chronic.
Granuloma
Aggregate of epitheloid histiocytes to isolate infection or foreign body
Necrosis
Abnormal tissue death with inflammatory changes- not energy depedant
Apoptosis
Physiological process or ‘programmed cell death’ affecting a single cell in a population of healthy cells process of removing effete and abdnormal cells normal cells divide to replace the lose cells Cell degradation via intracellular enzyme activation Energy dependant with no inflammatory response assoc with maintenance of organ size in adults, organ development and physiological atrophy or involution
Coagulative necrosis
Preserved tissue architecture nucleus fades (karyolysis), becomes more dense (pyknosis), fragments (karyorrhexis) Coagulation of proteins to preserve architecture eg kidney/heart/spleen Eg when tissue placed in boiling water
Colliquative necrosis
Liquefactive necrosis occurring in lipid-rich tissue Lysosomal enzymes active to break down fat to denature it resulting in liquefaction eg in brain
Caseous necrosis
Unstructured necrosis where tissue architecture cannot be identified secondary to necrosis eg in TB Contains amorphous proteins and degenerate lipids
Wet gangrene
From venous & arterial occlusion Necrosis and putrefaction by gram negative bacteria- bacterioides & clostridia
Dry gangrene
Tissue desiccation with no infection and often autoamputates eg in diabetic foot
Gas gangrene
- infection with gas-forming anaerobic bacteria resulting in surgical emphysema & crepitus
- Clostridial spores from:
- clostridium welchii
- Clostridium oedematiens
- Clostridium septicum
- Microscopy = gram positive bacilli, rectangular without spore formation, anaerobic culture on blood agar show haemolytic colonies (C. welchii) and ‘stormy’ clot reaction with litmus milk + C.welchii -> positive Nagler reaction due to lecithinase reaction of alpha exotoxin
- Clinical = toxic and unwell. Features = shock, jaundice, haemolysis, ARF, myositis, myonecrosis, gas formation, palpable crepitus, mottled discolouration of overlying skin
- Plan XR -> gas and subcutaneous tissue and fascial plains
- Treatment = vigorous resuscitation and early surgery, debridement/amputation, sensitive to penicillin, hyperbaric O2, (ABx benzylpenicillin prophylaxis - contaminated wounds, diabetic undergoing elective peripheral vasc surgery)
Atrophy
decrease in organ size due to a reduction in cell size or number Cause: - Gradual diminution in blood supply - reduction in functional activity - interrupted nerve supply - endocrine deficiency - pressure
Calcification
abnormal deposits of calcium salts either: - Dystrophic - deposition of calcium that occurs when necrotic tissue is not absorbed or tissues undergo slow degeneration - Metastatic - calcification occurs when serum calcium is elevated for a long period of time. Assoc with increased calcium absorption due to high vit D levels, resorption of bone, mobilisation of calcium due to PTH excess and chronic renal failure Ca is deposited in arterial walls, kidneys, lungs, stomach wall
Amyloid
abnormal protein that is deposited in extracellular tissue - around basement membrane and capillaries and is resistant to degradation - Primary; due to unknown cause - Secondary; due to tuberculosis, pyogenic infection, fheymatoid arthritis, myeloma, hodgkin’s disease Affects - heart, intestinal tract, kidneys Results in atrophy due to pressure Transufation of proteins due to increased permeability, assoc with vessel narrowing Pathologically detected by congo red due -> apple green fluorescence in polarised light
Hypersensitivity reactions
exagerated immunological response to antigen by normal immune system requiring previous exposure to antigen. 1. Type I - anaphylactic - IgE 2. Type II - Cytotoxic - IgM/G & phagocyte/K cells 3. Type III - immune complex - IgG 4. Type IV - cell mediated or delayed - T lymphocytes & macrophages
Type I hypersensitivity
Immediate/anaphylactic hypersensitivity occurs within 10-15mins of antigen exposure mild- to- life threatening Clinical features: urticaria, conjuncitivitis, rhinitis, bronchospasm IgE mediated & mast cells/basophil, amplified by platelets and eosinophils Exposure to Ag -> IgE production, bind cell surface receptors on mast cells, cross linking -> mast cell degranulation via Ca influx, mediators released incl: histamine, tryptase, kinogenase, leukotriene B4, prostaglandin D2, platelet activating factor Degranulation can be triggered by - exercise, stress, chemicals and anaphylatoxins Rx - agents that block histamine receptors, inhibit mast cell degranulation and leukotriene receptor blockers e.g. hay fever, drug allergy
Type II hypersensitivity
Cytotoxic Various organs and tissues Ag = endogenous Reaction occurs in hrs Mediated via IgM and IgG antibodies and complement Phagocytes & K cells play a role e.g. good pasteur’s
Type III hypersensitivity
immune complex hypersensitivity Affects general/individual tissues Several hrs after exposure to Ag Mediated via soluble immune complexes and complement, IgG class Ag can be exogenous (bacteria, virus, parasite) or endogenous (systemic lupus erythematosis, rheumatoid arthritis)
Type IV Hypersensitivity
Cell mediated/delayed type peak after c.48hrs mediated via T lymphocytes, monocytes, macrophages with cytotoxic T cells -> direct damage T helper cells -> cytokines that recruit and activate macrophages Major lymphokines: monocyte chemotactic factor, interleukin 2, TNF alpha Autoimmune and infectious disease e.g. TB, tocoplasmosis
Psoas abscess
- Iliopsoas comparment (extraperitoneal space) contains psoas and iliacus muscle
- Psoas lies close to abdo structures/organs e.g. sigmoid colon, ureter, appendix + infection can spread to muscles
- Muscles have good blood supply pre-disposing to haematogenous spread of infection
- Aetiology primary: haematogenous spread of inf and seen in immunocompromised e.g. DM, IV drug use, renal failure
- Aetiology Secondary:
- crohn’s
- diverticulitis
- appendicitis
- UTI
- Septic arthritis
- Femoral vessel cannulation
- Commonly staph aureus/gut related organisms, occasionally TB
- Clinical features: flank, back, abdo pain, fever, limp, malaise, WL, lump in groin
- Investigation: WCC/Inflammatory markers raised, AXR - nomal, CT - fold standard, MRI - useful
- Management: ABx, drainage (percutaneous)
Cellulitis
- spreading infection in the subcutaneous tissue
- post skin abrasion/similar trauma
- B haemolytic streptococcus/staph aureus
- Produce enz that degrade tissue and allow spread of infection
- Clinical features: well demarcated area of inflammation, malaise, fever, waised LCC, if not Rx -> lymphangitis, lymphadenitis, skin necrosis
- Risk factors: lymphoedema, venous stasis, DM, Surgical wounds
- Management: rest and elevate, ABx oral/IV if no improvement
- Benzylpenicillin, flucloxacillin
Necrotising soft tissue infection
- result from skin infection with virulent bacteria
- bacterial toxins -> widespread skin and fascial necrosis
- e.g. necrotising fascitis
Necrotising fascitis
- immunocompromised pr - DM, alcoholic, IV drug abusers
- Chr- after cuts, abrasions, bites, post op abdo surgical wounds, perineum secondary to anorectal sepsis, male genitalia (fornier’s)
- Polymicrobial infection inv faculative aerobes, streptococcal species or escherichia coli and anaerobes
- Exotoxin produced by organisms -> severe systemic toxicity
- Clinical: like cellulitis + warning signs = severe pain out of proportion to clinical signs, systemic toxicity, cutaneous gngrene, H’gge fluid leaking from wound, -> organ failure, mortality of 30%, plain XR -> gas in subcutaneous tissue
- Management: early and rapid treatment, HDU, fluid resusc and organ support, early surgical debridement with extension beyong apparently normal tissue, +/- amputation/fasciotomy, ?defunctioning colostomy if perineal, ABx (benzylpenicillin, metronidazole, gentamicin), hyperbaric O2
Wound infection
- 75% nosocomical infections occur in surgical patients
- Most post op infections are from pt own bacterial flora
- commonest sites - UTI (40%), wound (35%), Resp tract (15%), bacteraemia (5%)
- Wound contamination - pt residual flora/skin, surgeon’s hand, contaminated instruments, dressings, drains, catheters, IV line, airborne, heamatogenous spread
- Types of wound infections:
- surgical site infection
- superficial incisional infections
- Deep incisional infections
- Organ space infections
Surgical site infection
- within 30 days of surgery
- involves skin and subcutaneous tissue
- purulent discharge from superficial infection/organisms isolated from aseptically obtained wound culture
- signs of infection
Microbiology for wound infection
- Staphylococcus aureus
- enterococci
- coagulase-negative staphylococci
- Escherichia coli
- pseudomonas aeruginosa
- enterobacter species
- proteus mirabilis
- klebsiella pneumoniae
- candida species
Predisposing factors to wound infection
- general factors:
- age, obesity, malnutrition
- endocrine and metabolic disorders
- hypoxia, anaemia
- malignant disease
- immunouppression
- Local factors:
- necrotic tissue
- Foreign bodies
- Tissue ischaemia
- haematoma formation
- poor surgical technique
- Microbiological contamination:
- type and virulence of organism
- size of bacteriological dose
- antibiotic resistance
Wound infection prevention
- Exogenous methods:
- sterilisation of instruments and sutures
- positive pressure ventilation of operative theatres
- Laminar air flow in high risk areas
- exclusion of staff with infections
- Endogenous
- skin prep
- mechanical bowel prep
- antibiotic prophylaxis
- good surgical technique
4 categories of surgeries
- Clean
- incision through non-inflamed tissue and wound primarily closed
- no brach in aseptic technique
- no viscus opened
- e.g. mastectomy, hernia repair
- wound infection rates = 1-2%
- Contaminated
- left open or created by penetrating trauma, <4hrs old
- viscus may be opened with inflammation/spillage of contects/break in sterile technique
- e.g. appendicectomy & stab wounds
- infection rates = 15-20%
- Clean-contaminated
- emergency surgery or reoperation via clean incision within 7 days of original surgery
- viscus may be opened but no spillage of gut contents
- minor break of aseptic technique
- e.g. right hemicolectomy and cholecystectomy
- Infection rates <10%
- Dirty
- presence of pus, intraperitoneal abscess formation or visceral perforation
- penetrating trauma >4hrs old
- e.g. perforated abdo viscera
- Infection rates >40%
Antibiotic prophylaxis - reduces infection rates, used in ops with high incidence of post op infection (e.g. colonic surgery) or where infection would be disasterous (e.g. prosthetic valves)
Tetanus
- Develops following deep/penetrating wound in relatively avascular area
- microbiology - infection with clostridium tetani, gram positive spore forming rods, microscopy = drum-stick appearance with terminal spore, found in env/soil, strict anaerobe, exotoxin (resistant to autoclaving), NOT antigenic therefore repeat infections occur
- Pathogenesis: germination of spores -> exotoxins, effect the NS and reach CNS via peripheral nerves, acts on pre-synaptic terminals of inhibitor nerves and reduces the release of inhibitory neurotransmitters (e.g. glycine), excess activity of motor neurones -> muscle spasm
- Fascual muscle spasm -> trismus, face = ‘risus sardonicus’, back muscle spasm = opisthotonos, exhaustion & resp failure -> death, Dx = clinical
- Treatment - active immunisation with tetanus toxoid with booster every 5-10 yrs, adequate toilet of contaminated wounds, passive immunisation with hyperimmune immunoglobulin in pt @ risk. In suspected cases ->passive immunisation with anti-tetanus immunoglobulin, adqeuate wound debridgement, IV benzylpen and IC support
- Mortality is c.50%
