Download Hand and wrist infection

Hand and wrist infection
Dr. YF Leung
Department of Orthopaedics and Traumatology
Tseung Kwan O Hospital
Classification
 Acute and Chronic
 Opportunistic and non-opportunistic
 Anatomical sites --- bone, joint, muscle, ligament, tendon, nerve, skin, vessel
or combination
 Germs --- virus, bacteria, fungus, protozoa, protothecal(algae), parasites
Acute vs Chronic infections:
Acute
Acute on chronic
Chronic
Days
mixed
Weeks
Fulminant/rapid progress
Indolent/slow progress
Constitutional symptoms
Usually absent
Inflammation+++
Inflammation+/-
Purulent discharge
Sinus, watery discharge, fistula, rice
bodies
Painful
Painless usually
No deformity usually
scar, joint or bone deformity
Septicaemia
Not common
Pathogenesis of infection:
 Balance between host immunity and virulence + dosage of inoculated germs
 Germs may cause tissue destruction by its own enzymes
 produce toxins result in thrombosis of vessels and ischemic tissue necrosis
 Induce immune response resulting in inflammation and secondary immune
related tissue necrosis
 SIRS(systemic inflammatory response syndrome), septicaemic shock and
death
 Chronic infection results in tissue destruction and repair with fibrosis, severe
functional deficit and limb deformity
General principles of management of UL infection:
 History: contact, contamination, compromised immune system, direct
penetration injury
 PE: constitutional symptoms, neurovascular state of UL, speed of spreading,
lymphadenitis, pain, tenderness, gas under skin, skin color, anatomical
structures involved,
 Ix: WBC, PLT, ESR, CRP, ALP, XR, Ultrasound scan, CT+/- contrast, MRI, bone
scan, diagnostic aspiration………..
 Rx: conservative & operative +/- reconstruction + antibiotics (according to
final tissue C/ST)
 Recurrent or persistent infection should alert FB, complications of bone and
joint involvement, immunocompromised patients (e.g DM, AIDs,…)
 Ask for PCR, ELIZA, immunoflurescent stain if indicated
 For chronic infection: six tissue packs for laboratory advised
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[histology, Gram stain+ C/ST, AFB stain+CST(typical &
atypical, Fungus stain+C/ST, anaerobic C/ST]
Usually caused by streptococcus, Staphylococcus aureus (SA)
About 40-50% SA infection is by MRSA-CA (community acquired)
Eikenella corrodens in human bite & Pasterella multocida in animal bite
Clostridium and mixed infection (Gram –ve rod) with gas under skin
Chronic infection with AFB, fungus, actinomycosis..….
Erysipelas & cellulitis:
 Cellulitis and erysipelas are infections of the skin and subcutaneous tissues
 variants of the same condition, elements of both often coexist within an
affected area
 If not response in 48 hours antibiotic treatment, abscess formation or resisted
strains of bacteria may be considered
MRSA-CA infection:
 Release Panton-Valentine Leukocidin (PVL), a potent toxin leads to tissue
necrosis
 Resists to cloxacillin, augmentin
 Use clindamycin, vancomycin, septrin, fusidin, Zyvox
 Wide surgical debridement sometimes needed to remove necrotic tissue
 Tissue loss is more than the superficial appearance
Paronychia:
Treatment of acute paronychia:
 7-10 days antibiotics +/- drainage under digital block
 Beware of pus under nail plate causing compressive ischemia of germinal
matrix render nail growth retardation
 Removal of 1/3 proximal nail plate may need to decompression the abscess
under nail
 Persistent infections may be due to complications include osteomyelitis of
distal phalanx and septic arthritis of DIPJ, or FB
Treatment of chronic paronychia:
 Associated with frequent water immersion and detergents
 HW, nurses, dishwashers ….
 DM, other skin disorders
 Separation of nail plate and eponychium
 Mixed infection with Candida albicans, SA, E.coli, AFB…
 Fibrosis and thickening of eponychium, nail deformity and decrease
vascularization
 Avoid irritants and detergents
 Local steroid with anti-fungal and anti-bacteria cream
 Separation of nail plate and eponychium
 Treat acute exaggerations
 Eponychial marsupialization in resisted cases and send cultures
 Oral antifungal + antibiotics x 4 weeks
Pulp infection (Felon):
 History of penetration injury
 Severe throbbing pain, tenderness & swelling up to DIPJ
 Infection involves multiple septal compartments (filled wit fat globules) of
pulp resulted in compartment syndrome resulted in AVN of DP and pulp
necrosis
 May complicated with osteomyelitis of DP or DIPJ septic arthritis
 Early surgical decompression via unilateral longitudinal incision to break all
septa + oral antibiotics 2/52
 Avoid incision of the flexor tendon sheath that may cause tenosynovitis
Flexor tenosynovitis:
 History of penetration injury
 Severe throbbing pain, tenderness & swelling up to distal palm
 Kanavel’s four signs (semi-flexed finger=hook sign , fusiform swelling,
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tenderness along tendon sheath, pain on passive extension)
Infection may extend proximally and complicated with infection of bursae of
the palm and Space of Parona of wrist level
Infection causes thrombosis of vincular vessels quickly results in tendon
necrosis, rupture and adhesion with fibrosis if delay in treatment
Immediate iv antibiotics +/- surgical drainage if no response in 24 hours + oral
antibiotics up to 4 wks in total
Aspiration is not advised for the risk of introduction of infection from purely
cellulitis to real tenosynovitis
Limited incision with NS irrigation, 300-500 cc, (for early case)
 Formal exploration via mid-lateral, or volar zigzag incisions, (for late case)
Radial and ulnar bursal infections:
 History of direct penetration injury of bursae
 often extend from flexor tenosynovitis
 tenderness & mild swelling of proximal palm over the thenar or hypothenar
eminences
 Infection may extend proximally Space of Parona of wrist level
 Involvement of both bursae = horseshoe abscess
 prompt surgical drainage + copious saline irrigation + drains+ oral antibiotics
up to 2-4 wks in total
 Two-incision technique with one incision just proximal to A1 pulley oblique
and the other at distal forearm just proximal to carpal tunnel (similar to
limited approach to flexor tenosynovitis)
 Formal zigzag incision is required in late case
Deep space infections:
Potential spaces between bursae/flexor tendons and intrinsic muscles (exclude
lumbricals), Mid-palmar space infection with loss of palmar concavity, Thenar space
infection
Surgical incisions for deep space infections-Prompt surgical drainage + copious saline irrigation + drains+ oral antibiotics up to 24 wks in total
Web space infection(dumbbell, collar-button abscess):
Parona’s space abscess:
Potential space between flexor tendons and pronator quadratus, may present as
acute CTS, Use US for diagnosis, Incision like open carpal tunnel release for isolated
Parona’s space abscess
Septic arthritis:
 Primary haematogenous or extends from nearby infection sources
 Joint distension with pus resulted in flexion deformity, pseudoparalysis of
limbs, pain on passive motion of joint
 Bacterial enzymes and inflammatory chemicals causes rapid destruction of
articular cartilage then complicate with osteomyelitis and resulted in joint
instability + deformity
 DDx: gout, pseudogout, RA, SLE, psoriatric arthritis, acute rheumatic fever,
sarcoidosis, Reiter syndrome…….
 Joint aspiration is helpful for Gram stain, crystals and C/ST
 Emergent surgical intervention needed to confirm the diagnosis if clinically
suspected or unresponse to antibiotics after 24 hours
 Arthroscopic lavage (for wrist joint, sometimes CMCJ, MCPJ) or open
arthrotomy
Osteomyelitis:
 Primary haematogenous (in children) or extends from nearby infection
sources
 Associated with compound fracture and iatrogenic after ORIF for UL fractures,
immunocompromise, vascular insufficiency…..
 Persistent infection despite treatment of nearby infection
 XR, MRI, CT scan with contrast may required to confirmed the diagnosis
 Needle aspiration of subperiosteal abscess
 MRI is extremely useful for assessment of the extent of osteomyelitis and
sequestrum thus help to plan the surgery and later reconstruction
 May extend to joint and result in septic arthritis especially less than one year
old because of vascular continuity between metaphysis and epiphysis via the
epiphyseal plate arteries
Treatment of osteomyelitis -- Antibiotics for 6-8 weeks +/- repeated surgical debridement
 Removal implants or sequestrum
 External fixator across the infected bone +/- antibiotic impregnated cement
or gentamycin beads
 Reconstruction with bone graft, bone lengthening, bone transport, joint
fusion, amputation etc.
Special type of UL infections
(Necrotizing fasciitis)
 Exposed to contaminated water
 Streptcoccus, non-cholerae Vibrio species, or other Gram –ve bacteria, rarely
fungus (mucormycosis) that secreting hyaluronidase, collagenase,
streptokinase, lipase etc.
 Admitted with septicaemia shock, tachycardia, confusion, DIC
 Rapid progression within hours, initial skin lesions such as bullae, purpura and
edema with punctate ecchymosis, dusky blue skin, diminished skin sensation,
tenderness beyond erythema, later skin necrosis because of thrombosis of
nutrient vessels
 Increase or normal WBC, decrease platelets count, low HB, increase CPK,
impaired renal function, undiagnosed DM
 High mortality ~ 50% in hospital, increase with age
 Important differential diagnosis is gas gangrene
 Clostridium infection
 more rapid progression and fetal within hours
 Alpha & theta toxin cause myonecrosis, hemolysis, cardiac depression
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Treatment principle same but usually needs amputation
Urgent debridement under GA, ICU care
Intra-operatively, fatty watery fluid from subcutaneous plane, infected
fasciitis with necrosis, muscles are usually intact
Try to incise and drain extensively but preserve as much as skin if possible, get
tissue for microscopy+ C/ST, fungal CST for immunocompromise patients
Wounds laid open with adding some stitches loosely to prevent skin
contracted down
Repeated debridement if needed 24-48 hours if necessary
 Secondary skin coverage
 Amputation when infection cannot be controlled
 Use clindamycin (immunomodulant benefit), penicillin + board spectrum
antibiotics
(Prothetic infections)
 Joint replacement of UL becomes more common
 Early or late septic loosening
 Immunocompromise such as RA, DM
 Aspiration yielding low
 MRI, bone scan, surgical exploration + frozen section (< 5 polymorphs per
high-power field)
 Removal of implants, temporary filling of the dead space with antibioticimpregnated cement
 Send tissue C/ST, send implant for microscopy or PCR(polymerase chain
reaction) or ELISA(enzyme-linked immunosorbent assay) tests of the biofilms
(bacteria secrete an exopolysaccharide matrix whick protect them from host
defense mechanism and antibiotics)
 Antibiotic for 6/52
 Fusion or reimplantation (two stages preferred) depends on the risk factor,
bone stock, organism and surgeons’ experience
(Herpetic Whitlow)
 Herpes simplex virus (HSV) type 1, 2
 Finger sucking, dental professionals, hints on lesions of lip’s mucosa
 Important differential diagnosis of other bacterial hand infections Severe
pain, vesicles, index or thumb are more common
 May have lymphadenitis or lymphangitis
 Diagnosis by clinical, fluid for viral culture, elevation of immunofluorescent
serum antibody against HSV
 Treatment with acyclovir (or other anti-HSV agents), no operations
(Cutaneous anthrax)
 Rarely seen in HK because not many farmers here
 Gram + aerobic rod Bacillus anthracis
 Cutaneous(95%), gastroointerstinal and inhalational types
 Non-cutaneous types point to biological weapons in USA (CDC= Centers for
Diseases Control and prevention)
 Diagnosis by clinical, small painless read macule progresses to papule and
then vesciular, ruptures, ulcerates then form a classical brown black eschar,
CST of fluid or PCR
 Treatment with penicillin, doxycyclines x 8-10 weeks, no operation because of
risk of spreading infection
(Pyogenic granluoma)
 Red friable lesion, contact bleeding
 Inflammatory response to minor trauma
 Overgrowth preclude wound healing
 No truly infection, culture -ve
 Treatment with cauterization or excision
(Pyoderma gangrenosum)
 often misdiagnosed as infection
 Progressive necrotizing and ulcerative disease of skin
 Immunocompromised hosts
 Associated with ulcerative colitis, Crohn’s disease, myelodysplastic syndrome
 Centrifual creeping ulcer surrounding by a rough serpentine undermining
black-blue rim, which is further encircled by a 5-10mm rim of raised purplish
erthyma covered by a translucent gray epidermis
 Diagnosis is clinical only, biopsy is of little value, culture –ve
 Treatment with oral prednisone
 No surgical intervention is indicated
(Actinomycosis)
 Normal flora of oral cavity, soil
 Gram –ve anaerobic bacilli, Actinomyces israelii (the commonest)
 Occurs in clenched fist injury, farming,
 Inflammatory reaction persists, multiple sinuses discharge continuously with
“yellow sulfur granules” (microorganisms)
 Subcutaneous induration, spread slowly, locally invasion of bone
 Treatment with penicillin 6-12 months, or tetracylcines, clindamycine
 No surgery
(Mycetoma)
 Chronic infection produces granulomatous lesion histologically
 Clinically slow evolving nodular lesions, often painless, formation of abscesses
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with sinuses discharge, fistula
Microscopy showed granules(bunch of grapes) like microorganisms
Can be caused by aerobic bacteria (Actinomycetoma) or fungi (Eumycetoma)
Six tissue packs for laboratory investigations
Diagnosis based on biopsy, bacterial and fungal culture
MRI is useful to assess the extent of lesion including bone and joint invasion
Look for underlying immunocompromise factors
Common fungi include Pseudallescheria boyii, Madurella mycetomatis,
Scedosporium, Arthrographis, Torula, Aspergillus, crytococccus
 Common bacteria include Nocardia, Acetinomadura, streptomyces,
 4 Stages: (1) one or more small firm, painless subcutaneous nodules under
skin for 2-3 months called nodular stage (2) nodules become abscesses and
drain granules (organisms) through sinuses termed sinusoidal stage
(3)progress to involved bone and osteomyelitis as skeletal stage (4) extend
along lymphatics to chest wall or other sites after many years resulted in
metastatic stage
 no constitutional symptoms, remissions with exacerbations, deformity of
limbs
 Treatment according to sensitivity tests of antibiotics or antifungal agents,
wide surgical debridement is indicated
 Antibiotics include streptomycin, dapsone, septrin, amikacin
 Antifungal agents include ketoconazole, itraconazole, fluconazole,
amphotericin B(lipid formula)
(cutaneous fungal infections)
 Fungi metabolize keratin for their nutrition but rarely invade beneath skin
 Very common encountered in clinical practice
 Cause skin and nail infections only
 Commonly Candida albicans, dermatophytes (eg. trichophyton, Microsporum)
caused Tinea,
 Diagnosis: skin or nail scrapings in 10% KOH on a glass slide under microscopy
showed branching mycelia and spores + fungal C/ST
 Antifungal agents include oral ketoconazole, itraconazole, fluconazole, topical
antifungal cream, KMnO4 bath, Loceryl nail paint, etc
(subcutaneous fungal infections)
Sporotrichosis(Rose thorn disease), Candida infection
(deep fungal infections)
Aspergillosis of skin and extensor tendons, Histoplasmosis osteomyelitis of distal
radius, Coccidioidomycosis flexor tenosynovitis, Blastomycosis fungal arthritis of
MCPJ
 Other fungi such as Crytococcosis, Mucormycosis, Exophiala ….etc.
 Also cause deep infection in immunocompromised hosts
 High index of suspicion especially in chronic lesions in months or years
 Relied on fungal microscopy + C/ST and biopsy
(Leprosy- Hansen’s disease)
 Acid fast bacillus(AFB) Mycobacterium leprae cause infection of peripheral
nerves
 ulnar > median > radial nerves
 Neuropathy resulted from infection, immunologic response and compressive
neuropathy (both intraneural or extraneural)
 3 cardinal signs: anesthetic skin patch, nerve thickening, hypopigmented skin
patch with diminished sensation
 WHO classification: Paucibacillary (PB) with good host immune response,
multibacillary (MB) of little host immunity
 Diagnosis by lepromin skin test, slit skin smear for AFB stain and microscopy,
skin biopsy, sural (thickened) nerve biopsy, PCR
 Treatment with dapsone, rifampicin + surgical nerve decompression (external
epineurotomy & internal neurolysis), rarely drainage of nerve abscess
 Late cases complicated with nerves palsy + fingers resorption from repeated
trauma to insensate skin, Charcot joints
(Mycobacterial infection)
 Mimic all UL lesions
 ddx of RA, OA, all other types of infections, tumors….
 Caseating granuloma formation, Langhans giant cells,
 Multi-drugs resistant trend
 Clinical presentation similar to other chronic UL infections
 Can affect any anatomical structures: cutaneous, subcutaneous,
tenosynovitis, arthritis, osteomyelitis,
 mild or moderate elevated ESR
 Associated with HIV or immunocompromise hosts if ESR is high that points to
low defense of hosts
 Non-tuberculous mycobacteria (NTM or atypical TB) and tuberculous
mycobacteria (TM or classical TB)
 Diagnosis: principles are the same as other chronic infections, relied on
biopsy and C/ST
 Classifications based on growth rate
 (1) slow – M. avium complex, M.kansasii, M. tuberculosis
 (2) Intermediate – M. marium
 (3) Fast – M. fortuitum, M. Chelonae, M. abscessus
 Their growth rate dictates the clinical presentation and speed of spreading
and destruction as well as the culture time for diagnosis
 NTB generally treated with clarithromycin, ciprofloxacin, rifampicin,
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doxycyclines, septrin etc.
TB classically treated with 1st line anti-TB drugs of isoniazid, rifampicin,
ethambutol, pyrazinamide
Duration of chemotherapy(multi-drugs regime advised to prevent resistance)
depends on the response
In general, 2-3 months for rapid growth AFB, 6 months for slow growth AFB,
deep infection may double the time, resistant cases may need longer duration
Surgical debridements sometimes needed especially in poorly response to
chemotherapy and resistant cases infected by M. marium, avium, fortuitum
etc.
 E.g. Mycobacterial extensor tenosynovitis, Mycobacterial Arthritis (M.
marium)
(Protozoal infection)
 Cutaneous Leishmaniasis of hand transmitted by sandfly
 Treatment by topical paramomycin cream or intralesional injection
 of antimony compounds weekly for three months
 Prevention with DEET spray on exposed skin when travelling to
 Endemic areas
(Parasitic infection)
 Roundworm –Gnathostomiasis (common in Thailand)
 A chronic cutaneous migrating larval infection
 Ingestion of contaminated undercooked seafoods
 Increased eosinophil count
 Treatment by surgical exploration and removal of larva
[protothecal (algae)]
 Immunocompromised patient presented with erosive arthritis
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Diagnosis by microscopy and culture
Prototheca Wickerhamii common algae in human
Treatment by surgical debridement + anti-algae agents for 3 months
E.g. Itraconazole
(occupational infections)
 Interdigital pilonidal sinus
 In barbers, sheep shearers, cow milkers
 Pentration by the hair cut implanted in the interdigital skin resulted in foreign
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body reaction and formation of granuloma
Sinus or cyst with secondary bacterial Infection and intermittent discharge
Treatment by surgical excision and closure + antibiotics
imunocompromised patient presented with erosive arthritis
(HIV related viral infection)
Herpes Simplex type 2 --- Usually multiple and abundant, caused by Herpes Simplex
virus-2
Kaposi’s sarcoma --- Purple vascular tumor, Malignant, rapid progression may
metastasize, Caused by Herpesvirus type 8
(Warts)
Verruca vulgaris (common wart) 95%, Verruca Plana (flat wart) 5%
 Caused by human papilloma viruses (HPV)
 Often spontaneous resolution in few years
 Chemical destruction by keratolysis such as salicylic acid paint 2/52 or
Intralesional injection of bleomycin
 Physical destruction by cryotherapy, electrocauterization, surgical excision