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FRACS study > Skin and hernia > Flashcards

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
Q

Gorlin syndrome

A

Rare

Autosomal dominant

PTCH1 gene

syndrome of:

  • multiple BCCs
  • odontogenic keratocysts of the jaw
  • developmental delay
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26
Q

BCC epidemiology

A

Common, lifetime risk ~30% in fair skinned people

Risk increases with age

closer to the equator increases risk

men 1.3:1 women

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27
Q

BCC risk factors

A

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
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28
Q

BCC origin cell

A

Basal layer of epidermis

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29
Q

BCC subtypes

A

More indolent

  • Nodular (most common, ~80%)
  • Superficial
  • Pigmented BCC (6%)
  • Fibroepithelial (most indolent)

More aggressive

  • Infiltrative/mopheaform
  • Micronodular
  • Basosqumaous (part BCC part SCC)
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30
Q

Macroscopic features of BCC

A

Pearly rolled edge, depressed centre

Ulceration common

Teleangiectasia centrally is common

Locally invasive, extremely rarely metastatic

80% are found on the face and neck

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31
Q

BCC excision margins

A

4-5mm

Although those with 2mm margins only recur 4%

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32
Q

Imiquimod

A

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
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33
Q

Topical fluorouracil

A

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
Q

Clinical features of pyoderma gangrenosum

A
  • 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
Q

Pathophysiology of pyoderma gangrenosum

A

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
Q

Treatment of pyoderma gangrenosum

A

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
Q

Hidradenitis supparativa pathophysiology

A

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
Q

Hidradenitis treatment

A

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
Q

Staging of Hidradenitis supparativa

A

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
Q

Cutaneous SCC clinical features

A

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
Q

Staging for cutaneous SCC

A

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
Q

Merkel cell cancer cell theories of cell origin

A

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
Q

Virus implicated in Merkel cell cancers

A

Merkel Cell Polyomavirus

(present on PCR in 80% of tumours)

44
Q

AEIOU of Merkel cell cancers

A
  • 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
Q

Lumbar herniae and their boundaries

A

Inferior (Petit)

  • between
    • external oblique
    • iliac crest
    • latissimus dorsi

Superior (Grynfeltd)

  • between
    • quadratus lumborum
    • internal oblique
    • 12th rib
46
Q

What are the recommended biopsy types for melanoma

A

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
Q

Should prophylactic parastomal mesh be used

A

STOMAMESH trial shows no reduction in the incidence of parastomal hernia at 1 year

48
Q

How can necrotizing fasciitis be subtyped

A

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
Q

Bacteriology of type 1 necrotizing soft tissue infection

A

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
Q

Bacteriology of type II necrotizing soft tissue infection

A

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
Q

Risk factors for necrotizing soft tissue infection

A
  • 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
Q

Clinical findings in necrotizing soft tissue infection

How frequently are they found

A
  • 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
Q

Fournier Gangrene

A

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
Q

Vibrio vulnificus

A

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
Q

Antibiotic management of necrotizing fasciitis

A

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
Q

How does thermal injury cause tissue loss

A

By coagulative necrosis

57
Q

how can burns be classified by cause

A

Flame

Scald

Hot (or cold) surface contact

Chemical

Electricity

58
Q

How do chemical and electrical injuries cause tissue loss

A

Direct cellular membrane injury and thermal injury.

  • induces both colliquation and coagulative necrosis
59
Q

What are the three zones of burn injury

What is their significance

A

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
Q

How should burns be classified by depth

A

Superficial

Partial

  • Superficial partial
  • Deep partial

Full thickness

4th degree

61
Q

Superficial burns

A
  • 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
Q

Superficial-partial burns

A
  • 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
Q

Deep-partial thickness burns

A
  • 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
Q

Full thickness burns

A
  • 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
Q

Fourth degree burns

A

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
Q

Name 3 methods of burn area estimation

A

Lund browder chart (most accurate, especially in children)

Rule of 9’s

Palm method

67
Q

what depths of burn are included in burn area estimations

A

All except superficial burns are included

68
Q
A

Modified Lund Browder chart

The most accurate method of burn area prediction

69
Q

Rule of Nines

A

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
Q

Palm method of burns area estimation

A

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
Q

Signs of airway injury in burns

A
  • 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
Q

Who should receive formal fluid resuscitation in burns

A

>15% TBSA

  • Calculated as any burn greater than superficial
73
Q

Choice of crystalloid in burns resus

A

Hartmanns or Lactated Ringers

74
Q

How are burns resuscitaion fluids managed

A

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
Q

FAMMM diagnostic criteria

Recommendations on surveillance

A

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
Q

Discuss the anatomical issues associated with IVC obstruction in groin hernia surgery

A

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
Q

What are the borders of a femoral hernia neck

A

Medial

  • lacunar ligament

Posterior

  • pectineal ligament

Anterior

  • inguinal ligament

Lateral

  • femoral vein
78
Q

High risk SCC size

A

2cm or greater

79
Q

What are the medical treatment options in metastatic melanoma

A

BRAF inhibitors

  • vemurafenib

PD1 inhibitors

  • pembrulizumab

Systemic chemotherapy

  • doxirubicin
    • not very effective and quite toxic
80
Q

What are the 5 key characteristics to consider in mesh for hernia repair

how does each effect the repair

A

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
Q

What is your prefered mesh choice in a routine Lichtenstein hernia repair

why

A

Atrium prolite mesh

  • good tensile strength (too high at 138 N/m2)
  • lightweight (80g/m2)
  • polypropylene monofilament construction
  • nonabsorbable
  • large pore size (0.8mm)

FRACS study (13 decks)

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