Fascia Pathology

8/13/2019 Fascia Pathology

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FASCIA PATHOLOGY


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Definition and anatomyThe dense connective tissue that

envelopes muscles grossly, and alsosurrounds every bundle of musclefibers and each individual muscle cell.

This connective tissue is inextricablylinked with the muscle, and is

continuous with the tendons andperiosteum


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Fascia is composed of cells includingfibroblasts,macrophages ,mast cellsand extracellular matrix.

The extracellular matrix (ECM) iscomposed of ground substance,collagen and elastin fibers.

Its richly innervated


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Fibrosis and adhesions

One of the hallmarks of fascia is its mutability andremodeling in response to mechanical stress.

However, under certain conditions excess

mechanical stress, inflammation or immobilitythis process can result in excessive anddisorganized collagen and matrix depositionresulting in fibrosis and adhesions eg in plantarfascitis


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What is Necrotizing Fasciitis?

life-threatening, progressive, rapidly spreading,inflammatory infection located in the deep fascia.

infection rapidly destroy the skin and soft tissuebeneath it

Also known as: flesh-eatingbacteria.

Other names: -hemolytic streptococcal gangrene,Meleney ulcer, acute dermal gangrene, hospitalgangrene, and necrotizing cellulitis.

3 types of NF. Type I : a polymicrobial flora.

Type IIGroup A -Streptococcus bacteria(most common case)

Type III : marine vibrio gram-negative rods.


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How does one contract NF?

exposed to an individual with anopeningin their skin. direct contactwith someone carrying the

bacteria the bacterium being carried by the person

itself.

enter through weakened skin, as acontusion, a bruise, a blister, or even an

abrasion.


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Cofactors that Increase risks

Diabetes

Alcoholism

Immuno-suppression Severe illnesses: heart, lung, or liver

disease

Obesity


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Whats going on inside yourbody?

Bacteria eat away at tissue between skin and muscle

Increase in sensitivity or anaesthetic feel to the skin itself

Inflammatory response by immune system

Bacterial toxins released

Cytokines impede function of phagocytic cells

Anaerobes thrive speeding up necrotic process Endothelial cells become damaged;

Increased permeability of the lining of vessels in the body

Poor blood supply inhibit:

Inflammatory response process

Ability for the immune system to properly work

Ability to transfer antibiotics to the affected fascial layer Vasoconstriction and thrombosis edema hypoxia necrosis of

the fascia, skin, soft tissue, and muscles.

Additional necrosis involving the subcutaneous nerves.


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Exams and Laboratory Testing

1. Blood samples2. Testing for elevated or lowered creatinine,glucose, CPK, bicarbonate, albumin, andcalcium levels.

3. X-ray4. CT, and MRI scanning5. And most importantly antibiotic culture andsensitivity tests


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Symptoms

Bone pain or tenderness

Carpal tunnel syndrome

Muscle weaknessTenderness and swelling of upper and

lower limbs

Thickened skin with puckeredappearance


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Pathology

In early disease there is oedema of thefascia and subcutaneous tissue with alymphocytic infiltrate containingplasma cells and eosinophils.

With time the collagen becomesthickened and sclerotic with

extension into the subcutaneousfibrous tissue


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The tissue eosinophils may be focalaround adnexal structures or diffusewithin the tissue infiltrate

In more extensively involved cases thechanges can extend to the dermis

The epidermis is typically not involved,

though mild atrophy can be seen in aminority of cases


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Tests done

Gamma globulins

ESR

MRISkin biopsy:Full thickness


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FASCIA TUMOURS


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NODULAR FASCITIS

Common lesion that typically presents as arapidly growing mass on the flexorforearm, chest, back or elsewhere

Arises from superficial fascia, occasionallyintramuscular or intravascular

Similar lesions may also develop within the

breasts, bladder,cervix, intra-articular,prostate, vagina and vulva


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Epidemiology:Peaks at age 40 years; priortrauma in 10% of cases

Benign behavior, but sometimesmisdiagnosed as sarcoma based oncellularity, mitotic figures and rapidgrowth


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Gross

Tan-white-gray, myxoid appearance,usually 3 cm or less (reconsiderdiagnosis if greater than 3 cm)

Nodular with poorly defined margins

May be centered in subcutis, maygrow into skeletal muscle


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Microscopy

Zonation effect with hypocellular central regionand hypercellular periphery

Composed of uniform, plump, immature,

spindled to stellate fibroblasts ormyofibroblasts without atypia, with a feathery,"tissue-culture" like growth pattern due toabundant ground substance

Often with mucoid/myxoid pools (microcysts),a very useful diagnostic finding

Uniform elongated nuclei with punctate nucleoliand without significant nuclear atypia

Cellular areas may have storiform or fascicularpatterns (S or C shaped)


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Often frequent mitotic figures (but no atypicalforms), lymphocytes and macrophages, redblood cell extravasation, bands of keloid-type

collagen Vasculature is usually prominent

Walls of small to medium sized vessels areinvolved by reactive process at periphery of

lesion May infiltrate adjacent fat

May have metaplastic bone, focal cystic areas,ganglion type cells but no cells with large,

hyperchromatic, atypical nuclei


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Cranial fascitis

Nodular fascitis variant

Infants or children < 2 years old

Rare; usually boys

Soft tissue of scalp and underlying cranial bones

Develops from galea aponeurotica, erodes outertable of cranium and may infiltrate dura

Some cases show dysregulation of Wnt/-catenin

pathway, suggesting a potential relationship todesmoid fibromatosis rather than nodularfasciitis


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May be related to birth trauma, craniectomy or bespontaneous

Congenital in a minority of cases

PainlessTypically associated with focal calvarial lytic

change at the lesional site

Grows quickly like nodular fasciitis, but same

benign behavior


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Morphology

Gross:1-3 cm white to pink, mildly mucoid torubbery mass,unencapsulated but wellcircumscribed

Micro:Loosely arranged broad fascicles of delicatefusiform cells with edematous to myxoid-appearing interstitium

Nuclear atypia minimal or absent

Mitotic figures ranged from 1-5 per 10 high powerfields

No compact cellularity, no short fascicles, noregional variations compared to nodular

fasciitis


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Radiography

Lytic defect of skull with sclerotic rim onxray

Treatment: Surgical excision


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Intravascular Fascitis

Variant of nodular fasciitis that involves wall andlumen of small to medium-sized veins andarteries

Slower growth than classic nodular fasciitis butsame behavior

Uncommon

Typically seen in 1st through 3rd decades, but can

occur at any ageSlightly more common in men


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Most often found in upper extremity or head andneck region

Less common sites include the lower extremity

and trunkEtiology:Unclear

Conservative excision


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Morphology

Usually 2 cm or less

Nodular or plexiform

Resembles nodular fasciitis (proliferation of plump

spindle cells in a loose "tissue culture"arrangement), but with a less prominentmucoid matrix and numerous osteoclast-likegiant cells

May be intra- or extravascular


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Dupuytrens Contracture

Also known as palmar

Nodular proliferative process of palmaraponeurosis, surrounding adipose and

occasionally dermis, due to fibroblasts,myofibroblasts and fibrocytes

Most common type of fibromatosis (1-2% ofpopulation), prevalence increases with age

(24% at age 65+)


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Puckers overlying skin as it agesCauses flexion contracture of digits 4 and 5due to cord-like expansion of digitalaponeurotic slipsDoes not involve deep structures such astendons or skeletal muscleMay be caused by fibrogenic cytokines


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Morphology

Small nodules or nodular masses associated withaponeurosis and subcutaneous fat, with gray-yellow-white cut surface (color depends oncollagen content)

Proliferative phase:Uniform, plump, immature spindle cells(myofibroblasts and fibroblasts) with blandnuclei and indistinct nucleoliModerate collagen and elongated vessels


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Older lesions:More dense collagen, less cellularityVariable mitotic figuresOccasional attachment to dermis orcartilaginous metaplasiaUsually no infiltration of surrounding tissuebeyond subcutis


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Morphology

Gross: 2-3 cm nodules associated with

aponeurosis and subcutis, with gray-yellow-white cut surface (color depends on collagencontent)

Micro

Proliferative phase:Hypercellular collection of uniform, plump,immature spindle cells with bland nuclei andindistinct nucleoliModerate collagen and elongated vesselsVariable multinucleated giant cells


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Older lesions:Denser collagen, less cellularityOften prominent chronic inflammation,

variable mitotic figures and hemosiderin


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Penile fibromatosis

Also known as Peyronies disease

Fibrous thickening of dermis and Bucks fasciabetween corpora cavernosa and tunica

albuginea, causing curvature towards side oflesion and restricting movement of thesestructures during erection

Etiology may be related to Parc protein or Wnt2


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Typically age 40+ years, rarely age 40 or

lessVarious etiologies (microvascular trauma ,

urethritis, sclerosing inflammatory process,idiopathic), appears to differ from othersuperficial fibromatoses although associatedwith themPrevalence 3-9%, associated with plaques,

pain, induration, deviation, palmar fibromatosisUsually dorsolateral penis, 30% have

inflammatory component


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Morphology

Disorganization of collagen of tunica albugineawith formation of nodules, often hyalinizingfibrosis, perivascular lymphocytic infiltrate in1/3, linear band of calcification in 1/4

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Fascia Pathology