Skin and hernia Flashcards

1
Q
A

Extramammary Paget’s disease

  • Rare
  • Intraepithelial adenocarcinoma
  • Underlying invasive adenocarcinoma of apocrine glands in 30-45%.
  • Most common in apocrine dense skin- groins, axillae, natal cleft
  • Pruritus is most common symptom
  • Appearance is of well demarcated eczema
  • Treatment is with WLE
    • if surgery prohibited 5-FU, imiquimod, cryotherapy are options
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2
Q

Lymphodema stages

A

Stage 1

  • protein rich fluid acculumlation
  • Soft pitting oedema

Stage 2

  • infiltration on macrophages, fibroblasts and adipocytes
    • Local inflamatory response
  • non pitting oedema

Stage 3

  • Elephantiasis
  • local inflamatory response and recurrent infection
  • subcutaneous fibrosis and skin change
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3
Q

Primary and secondary classification of lymphoedema and causes

A

Primary

  • No identified cause
    • <1y- Congenital
      • Milroy disease
    • 1-35- Lymphoedema praecox
      • Meige Disease
    • >35- Lymphoedaema tarda

Secondary

  • Filariasis (Wucheria bancrofti)
  • Trauma
  • Surgery
    • Lymph node dissection
    • Venous
  • Radiation
  • Tumour impingement or invasion
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4
Q

Lymphoedema treatment

A

Education

  • Skin care and avoidance or trauma
  • Weight loss
  • Eczema management

Elevation and compression

  • 30-60mmHg is ideal

Physiotherapy

  • decongestive massage

Pneumatic compression

Operative management

  • Lymphaticolymphatic or lymphaticovenous bypass (if dilated lymphatics present)
  • Liposuction
  • Kontolein subcutaneous excision
  • Charles excisional operation
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5
Q

What malignancy is associated with long term >10 year lymphoedema

A

Lymphangiosarcoma

Very poor prognosis

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6
Q

Pressure injury risk factors

A

Intrinsic

  • Age
  • Diabetes
  • Malnutrition
  • Edema
  • Obesity

Extrinsic

  • Pressure sites
  • Tissue shearing during rolls and movement
  • Moisture
  • Incontinence
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7
Q

Name a scoring tool used to assist in preventing pressure sores

A

Braden score

  • Routine nursing practice
    • Subscales in:
      • Sensation
      • Moisture
      • Activity
      • Mobility
      • Nutrition
      • Friction/Shearing
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8
Q

Staging of pressure injury

A

Stage I

  • Skin reddened for longer than 1 hour after pressure relief

Stage II

  • Blister or superficial break in dermis

Stage III

  • Full thickness dermal injury with visible fat but not muscle, tendon or bone

Stage IV

  • Exposed bone, muscle or tendon
  • Often extensive undermining and tunnelling
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9
Q

Melanoma subtypes

A

Common

  • Superficial spreading (70%)
  • Nodular (15-30%)
  • Lentigo Maligna melanoma (10-15%)
  • Acral lentiginous

Rare

  • Amelanotic (most commonly nodular or desmoplastic)
  • Spitzoid melanoma
  • Desmoplastic
  • Animal type
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10
Q

major prognostic variables in primary melanoma

A

Depth of invasion

  • Continuous variable, subdivided by T staging for convenience

Ulceration

Mitotic rate

  • <1 mitosis/mm squared vs > or equal to 1

Age at diagnosis

  • Counterintuitively, young people do well

SLNB positive/ nodal staging

Presence of intransit metastasis (included in N staging)

Regression

LVI

Gender

  • Men do badly (again)
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11
Q

T Staging in melanoma

A

Always to the nearest 0.1mm (rounded)

Tis

  • Insitu (above the superficial aspect of the granular cell layer of the epidermis)

T1

  • <1mm (below the superficial aspect of the granular cell layer)

T2

  • 1-2mm

T3

  • 2-4mm

T4

  • >4mm
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12
Q

Discuss indications for SLNB in melanoma and the rate of LN positive disease in T1 melanomas

A

Australian cancer council guidelines state SLNB indicated in:

  • T2 disease (>1mm) or greater
  • T1b (0.8-1mm) with high risk features:
    • Mitotic rate >1/mm2
    • Ulceration
    • Maybe LVI

Likelyhood of positive SLNB

  • <5% for T1a disease
  • T1b 5-12%
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13
Q

N staging of melanoma

A

Principles

  • Number of positive nodes
  • Clinically detectible nodes
  • Presence of in-transit or satellite metastasis

N1

  • 1 node either detection
  • N1c- no nodes, but intransit/satellite met

N2

  • 2-3 nodes
  • N2c- 1 nodes with in- transit/ satellite met

N3

  • 4 or more
  • 2 nodes and intransit/satellite met
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14
Q

Clinical features useful in assessment of suspected melanoma

A

Ugly duckling sign

  • used in people with multiple naevi

ABCDE

  • Assymetry
  • Border
  • Colour variegation
  • Diameter >6mm
  • Evolution

Intransit and nodal examination

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15
Q

Hutchinsons sign

A

Hyperpigmentation of the proximal nail fold in subungual acral melanoma

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16
Q

MSLT-I

A

Multicentre Selective Lymphadenectomy Trial-I which confirmed the accuracy of SLNB in prognostication

  • Randomised trial, clinically node negative at diagnosis
    • Excision of primary and SLNB with selective lymphadenectomy if positive.
      • vs
    • Excision of primary and observation lymphadenectomy if clinical nodal recurrence
  • Intermediate thickness (1.2mm in this study) no difference in overall survival between groups but:
    • In those with nodal involvement and index lymphadenectomy vs only when clinically apparent there was a signficant survival advantage
  • Thick melanomas (>3.5mm in this study)
    • No difference in survival
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17
Q

MSLT-II

A

Patients with positive SLNB and

  • Breslow >1.2mm and/or
  • Clark level III, IV, V and/or
  • Ulceration

Randomised to immediate LND vs observation (including USS of nodes)

  • Slight improvement in disease free survival in immediate LND group but:
    • No improvement in melanoma specific survival
    • Higher rate of lymphoedema (8 vs 23%)
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18
Q

Breslow thickness

A

Depth in mm of melanoma

Measured from superficial aspect of the granular cell layer of the epidermis

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19
Q

Clark’s level

A

Level I: epidermis

Level II: Papillary dermis

Level III: to the junction of papillary and reticular dermis

Level IV: into reticular dermis

Level V: into subcutaneous fat

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20
Q

Who should be offered SLNB in melanoma

A

Clinically node negative disease and:

  • Breslow 1 mm or greater, or;
  • Breslow 0.8-1mm with high risk features
    • Ulceration
    • High mitotic rate

The risk of SLNB positive disease with breslow <1mm is <5%

  • in the 0.8-1mm group this is 7-12%
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21
Q

Genetic markers in melanoma

A

BRAF

  • BRAF inhibitors
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22
Q

Radiotherapy in Melanoma

A

TROG trial, radiotherapy after clearance

  • Presence of extranodal spread
  • >3 nodes involved
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23
Q

Excision margins in melanoma

A
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24
Q

FAMMM

A

Familial Atypical Mole and Melanoma syndrome

  • AKA dysplastic naevis syndrome
  • CDKN2A gene
    • Chromosome 9p21
      • encodes p16, loss of function leads to inappropriate progression through S phase
  • Autosomal dominant inheritance
  • Life time risk of melanoma approaches 100%
  • Associated risk of pancreatic, lung and breast cancers
    • also brain and leukemia
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25
Gorlin syndrome
Rare Autosomal dominant PTCH1 gene syndrome of: * multiple BCCs * odontogenic keratocysts of the jaw * developmental delay
26
BCC epidemiology
Common, lifetime risk ~30% in fair skinned people Risk increases with age closer to the equator increases risk men 1.3:1 women
27
BCC risk factors
UV exposure * probably more UVA than UVB Tanning beds Arsenic exposure Radiation exposure Fair skin, red hair Family history of skin cancer Pigment disorders * xeroderma pigmentosum, albinism Immunosuppression * HIV, transplant, CRF
28
BCC origin cell
Basal layer of epidermis
29
BCC subtypes
More indolent * Nodular (most common, ~80%) * Superficial * Pigmented BCC (6%) * Fibroepithelial (most indolent) More aggressive * Infiltrative/mopheaform * Micronodular * Basosqumaous (part BCC part SCC)
30
Macroscopic features of BCC
Pearly rolled edge, depressed centre Ulceration common Teleangiectasia centrally is common Locally invasive, extremely rarely metastatic 80% are found on the face and neck
31
BCC excision margins
4-5mm Although those with 2mm margins only recur 4%
32
Imiquimod
5% cream Immune response modifier * Promotes innate immune response * Activation of Toll-like receptor 7 incites cells to produce cytokines * IFN-a, IL-6, TNF-a Dosing regimens vary per indication * Warts 3x weekly until clearance max 8/52 * BCC 5x weekly for 6/52
33
Topical fluorouracil
5% cream Antimetabolite * Thymidylate synthase * inhibits DNA synthesis Apply 1-2x per day for 2-4 weeks, avoid contact with, or decontaminate, non diseased skin (esp the applying fingertip)
34
Clinical features of pyoderma gangrenosum
* Rapid course of lesion development * Initial lesion consistent with papule, pustule, or vesicle * Pain out of proportion to lesion * History of preceding trauma (pathergy) * History of disorders associated with PG * Ulcerated lesion with violaceous margin and undermining
35
Pathophysiology of pyoderma gangrenosum
Neutrophilic dermatosis Neutrophil infiltration, dysfunction and inapproprate action Often associated with systemic inflamation * IBD, Arthritis Progressive dermatitis and erosion of skin and soft tissue, neutrophil mediated * TNFa implicated * Responds to antiTNFa treatment (infliximab)
36
Treatment of pyoderma gangrenosum
Key is diagnosis with biopsy If associated with IBD surgery for that disease may lead to resolution Treatment is immunosuppression * Systemic glucocorticoids * Topical tacrolimus * Single small RCT using infliximab shows good resolution Analgesia Wound cares Avoidance of trauma Surgery is reserved for infection/necrosum
37
Hidradenitis supparativa pathophysiology
Follicular epithelial hyperplasia * hyperkeratosis * follicular plugging and distension * Mechnical stress forces esp. in intertrigonous areas * duct rupture, leakage of keratin fragments, sebum and bacteria into tissue * foreign body granulomatous response NB: Likely not from sweat glands as the name suggests
38
Hidradenitis treatment
Education and wound care * Avoid Trauma * Avoid tape * Smoking cessation (and nicotine) * Weight loss Hurley I * Topical clindamycin * Punch debridement Hurley II-III * Doxycycline 100mg OD-BD * OCP, spironolactone may help * Surgery * Simple excisions * Excision and grafting
39
Staging of Hidradenitis supparativa
Hurley Classification * Stage I – Simple abscess * Abscess formation (single or multiple) without sinus tracts and cicatrization/scarring * Stage II – Sinus/fibrosis without confluence * Recurrent abscesses with sinus tracts and scarring, single or multiple widely separated lesions * Stage III – Confluence * Diffuse or almost diffuse involvement, or multiple interconnected sinus tracts and abscesses across the entire area
40
Cutaneous SCC clinical features
The clinical appearance of invasive cSCC often correlates with the level of tumor differentiation. * Well-differentiated lesions usually appear as indurated or firm, hyperkeratotic papules, plaques, or nodules. * Lesions are usually 0.5 to 1.5 cm in diameter but may be much larger. * Ulceration may or may not be present. * In contrast, poorly differentiated lesions are usually fleshy, granulomatous papules or nodules that lack the hyperkeratosis that is often seen in well-differentiated lesions. * Poorly differentiated tumors may have ulceration, hemorrhage, or areas of necrosis.
41
Staging for cutaneous SCC
Clinical nodal assessment * FNA CT CAP if high risk features * Bone, muscle, fascia involvement * Large size (\>2cm) * Breslow \>2mm * Nodal involvement * Near or invading major nerves * In transit mets PET- no evidence No evidence for (or against) SLNB
42
Merkel cell cancer cell theories of cell origin
Two theories * Traditional (and still valid) view is origin in Merkel cells * Neural mechanoreceptor cell of the basal layer of the dermis * Alternative view is origin in dermal totipotential cell * Acquires neuroendocrine features during malignant transformation
43
Virus implicated in Merkel cell cancers
Merkel Cell Polyomavirus | (present on PCR in 80% of tumours)
44
AEIOU of Merkel cell cancers
* Asymptomatic * 88 percent * Expanding rapidly * (significant growth in ≤3 months) * Immune suppression * HIV infection, solid organ transplant recipient, chronic lymphocytic leukemia * Older than 50 years age * Most common \>80 * Ultraviolet (UV)-exposed area in a fair-skinned individual
45
Lumbar herniae and their boundaries
Inferior (Petit) * between * external oblique * iliac crest * latissimus dorsi Superior (Grynfeltd) * between * quadratus lumborum * internal oblique * 12th rib
46
What are the recommended biopsy types for melanoma
Excision biopsy to 2mm margin is the recommended by the australian cancer council. Of the incomplete biopsy methods incisional biopsy has the lowest false negative rate (1.4%)
47
Should prophylactic parastomal mesh be used
STOMAMESH trial shows no reduction in the incidence of parastomal hernia at 1 year
48
How can necrotizing fasciitis be subtyped
Type I * polymicrobial * both anaerobic and aerobic Type II * Lancefield group A streptococci * pyogenes * or other beta haemolytic strep Type III * gas gangrene, or clostridial myonecrosis
49
Bacteriology of type 1 necrotizing soft tissue infection
Polymicrobial with anaerobic and aerobic bacteria * Typically at least one each of: * Anaerobe * Bacteroides * Clostridium * Peptostreptococcus * Enterobacteriaceae (gram neg family) * E.coli * Enterobacter * Klebsiella * Proteus * Facultative anaerobic Streptococci (other than GAS) * Enterococci * Strep. agalactiae * Fungi occasionally implicated
50
Bacteriology of type II necrotizing soft tissue infection
Monomicrobial * Beta haemolytic streptococcal infection * Group A Strep, almost always pyogenes * M protein is the important virulence factor * bacterial strains can produce pyrogenic exotoxins * important mediator of toxic shock syndrome * Staph aureaus * Uncommon * Vibrio vulnificus * Salt water injuries * Aeromonas hydrophila * Fresh water injuries
51
Risk factors for necrotizing soft tissue infection
* Major penetrating trauma * Minor laceration or blunt trauma * Skin breach (esp IVDU) * Recent surgery * Mucosal breach * hemorrhoids, rectal fissures, episiotomy * Immunosuppression * (diabetes, cirrhosis, neutropenia, HIV infection) * Malignancy * Obesity * Alcoholism * In women: pregnancy, childbirth, pregnancy loss, gynecologic procedures
52
Clinical findings in necrotizing soft tissue infection How frequently are they found
* Erythema * (without sharp margins; 72 percent) * Oedema that extends beyond the visible erythema * (75 percent) * Severe pain * (out of proportion to exam findings in some cases; 72 percent) * Fever * (60 percent) * Crepitus * (50 percent) * Skin bullae, necrosis, or ecchymosis * (38 percent)
53
Fournier Gangrene
Type I (polymicrobial) necrotizing soft tissue infection of the perineum * More common in men * often involves penis and scrotum * Diabets and obesity are major risk factors
54
Vibrio vulnificus
Gram negative aquatic organism often implicated in salt water soft tissue infections treatment with fluoroquinolones or tetracyclines * In severe infection a 3rd generation cephalosporin may be helpful (ceftriaxone, cefotaxime)
55
Antibiotic management of necrotizing fasciitis
My choice * Meropenem, and * Vancomycin, and * Clindamycin General principles are: * Broad spectrum coverage against gram negatives, gram positives and anaerobes * Tazosin is a reasonable alternative to a carbapenem * Cover MRSA * Vancomycin * Clindamycin * Suppresses bacterial toxin production * Decreases penicillin binding protein production (synergistic beta lactam effect)
56
How does thermal injury cause tissue loss
By coagulative necrosis
57
how can burns be classified by cause
Flame Scald Hot (or cold) surface contact Chemical Electricity
58
How do chemical and electrical injuries cause tissue loss
Direct cellular membrane injury and thermal injury. * induces both colliquation and coagulative necrosis
59
What are the three zones of burn injury What is their significance
Zone of coagulative necrosis * Irreversible cellular injury at time of insult Zone of stasis * Vascular damage and leaky endothelium * poor tissue perfusion * Thromboxane A2 is an important mediator of burn induced vasoconstriction in the zone of stasis * May be reversible or progress to coagulative necrosis Zone of hyperaemia * Vasodilation and inflammation * Usually not at risk for further necrosis
60
How should burns be classified by depth
Superficial Partial * Superficial partial * Deep partial Full thickness 4th degree
61
Superficial burns
* Involve only the epidermal layer of skin. * Do not blister but are painful, dry, red, and blanch with pressure. * Over two to three days the pain and erythema subside, and by approximately day 4, the injured epithelium peels away from the newly healed epidermis. * Such injuries are generally healed in six days without scarring. * This process is commonly seen with sunburns.
62
Superficial-partial burns
* Characteristically form blisters within 24 hours between the epidermis and dermis. * Painful, red, and weeping and blanch with pressure. * Burns that initially appear to be only epidermal in depth may be determined to be partial thickness 12 to 24 hours later. * Generally heal in 7 to 21 days * A layer of fibrinous exudates and necrotic debris may accumulate on the surface, which may predispose the burn wound to heavy bacterial colonization and delayed healing. * These burns typically heal without functional impairment or hypertrophic scarring * pigment changes may occur.
63
Deep-partial thickness burns
* Extend into the deeper dermis * Deep burns damage hair follicles and glandular tissue. * Painful to pressure only * Almost always blister (easily unroofed), are wet or waxy dry, and have variable mottled colorization from patchy cheesy white to red * Do not blanch with pressure. * If infection is prevented and wounds are allowed to heal spontaneously without grafting, they will heal in two to nine weeks. * These burns invariably cause hypertrophic scarring. If they involve a joint, joint dysfunction is expected even with aggressive physical therapy. * A deep partial-thickness burn that fails to heal in two weeks is functionally and cosmetically equivalent to a full-thickness burn. * Differentiation from full-thickness burns is often difficult.
64
Full thickness burns
* Extend through and destroy all layers of the dermis and often injure the underlying subcutaneous tissue. * Burn eschar, the dead and denatured dermis, is usually intact. * can compromise the viability of a limb or torso if circumferential. * Usually anesthetic or hypo-aesthetic. * Skin appearance can vary from waxy white to leathery gray to charred and black. * Skin is dry and inelastic and does not blanch with pressure * Hairs can easily be pulled from hair follicles. * Vesicles and blisters do not develop. * Pale full-thickness burns may simulate normal skin except that the skin does not blanch with pressure. * Eschar eventually separates from the underlying tissue and reveals an unhealed bed of granulation tissue. * Without surgery, these wounds heal by wound contracture with epithelialization around the wound edges. * Scarring is severe with contractures; complete spontaneous healing is not possible.
65
Fourth degree burns
Fourth-degree burns are deep and potentially life-threatening injuries that extend through the skin into underlying soft tissue and can involve muscle and/or bone.
66
Name 3 methods of burn area estimation
Lund browder chart (most accurate, especially in children) Rule of 9's Palm method
67
what depths of burn are included in burn area estimations
All except superficial burns are included
68
Modified Lund Browder chart The most accurate method of burn area prediction
69
Rule of Nines
For adult assessment, the most expeditious method to estimate TBSA in adults is the "Rule of Nines" * Head represents 9 percent TBSA * Each arm represents 9 percent TBSA * Each leg represents 18 percent TBSA * The anterior and posterior trunk each represent 18 percent TBSA
70
Palm method of burns area estimation
Small or patchy burns can be approximated by using the surface area of the patient's palm. * The palm of the patient's hand, excluding the fingers, is approximately 0.5 percent of total body surface area * The entire palmar surface including fingers is 1 percent in children and adults
71
Signs of airway injury in burns
* Persistent cough, stridor, or wheezing * Hoarseness * Deep facial or circumferential neck burns * Nares with inflammation or singed hair * Carbonaceous sputum or burnt matter in the mouth or nose * Blistering or edema of the oropharynx * Depressed mental status, including evidence of drug or alcohol use * Respiratory distress * Hypoxia or hypercapnia * Elevated carbon monoxide and/or cyanide levels
72
Who should receive formal fluid resuscitation in burns
\>15% TBSA * Calculated as any burn greater than superficial
73
Choice of crystalloid in burns resus
Hartmanns or Lactated Ringers
74
How are burns resuscitaion fluids managed
The Parklands formula * The traditional formula is * 4ml x (patient body weight in kg) x (TBSA in %) * Half is given over the first 8 hours * Half over the subsequent 16 hours * This is likely to overestimate fluid requirements * In our local unit a modified Parklands of 3ml/kg/TBSA% is used for initial resus An early switch to goal directed therapy and urine output monitored resuscitation is recommended with a goal of 0.5ml/kg/hour * there is evidence that this improves outcomes
75
FAMMM diagnostic criteria Recommendations on surveillance
Diagnostic criteria debated but: * Large number of naevi at an early age * Multiple atypical naevi (at least 2) * Classical description is \>100 naevi * At least one \>8mm * One or more atypical Screening should begin at 10 years of age, melanoma may develop in teens * Monthly self exam and specialist dermatologist review recommended
76
Discuss the anatomical issues associated with IVC obstruction in groin hernia surgery
The inferior epigastric vessels (both superficial and proper) form anastomotic arcades with the superior epigastrics and form the thoracoepigastric veins * These are a site of large volume shunting from IVC to SVC in IVC obstruction
77
What are the borders of a femoral hernia neck
Medial * lacunar ligament Posterior * pectineal ligament Anterior * inguinal ligament Lateral * femoral vein
78
High risk SCC size
2cm or greater
79
What are the medical treatment options in metastatic melanoma
BRAF inhibitors * vemurafenib PD1 inhibitors * pembrulizumab Systemic chemotherapy * doxirubicin * not very effective and quite toxic
80
What are the 5 key characteristics to consider in mesh for hernia repair how does each effect the repair
Elasticity and tensile strength * mesh must be able to conform to the abdominal wall in motion or it would cause distorsion, tissue disruption and pain * tensile strength of 16 N/cm2 is the maximum tensile strength required Porosity * large pores permit integration with tissues and most importantly integration of immune competent tissue * microporous meshes \<100µm are associated with chronic infection and fibrosis Density (weight) * lower density meshes have lower burden of foreign body per unit area, they therefore are associated with a decreased inflammatory response and better tissue integration. Constitution * mesh can be either monofilament or polyfolament weave * the microporous areas within polyfilament weave are associated with increased bacterial infection * monofilament is generally more stiff Absorption * mesh can be either absorbable or non absorbable * absorbable mesh relies on scar formation which is never as strong as the initial tissue and may increase the risk of recurrence * non absorbable mesh may stiffen and contract over time and if there is infection it will persist
81
What is your prefered mesh choice in a routine Lichtenstein hernia repair why
Atrium prolite mesh * good tensile strength (too high at 138 N/m2) * lightweight (80g/m2) * polypropylene monofilament construction * nonabsorbable * large pore size (0.8mm)