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Skin and soft tissue > Infections, sweat glands, lymphedema! > Flashcards

Infections, sweat glands, lymphedema! Flashcards

1
Q

Compare eccrine and apocrine glands

A

Eccrine Gland

Apocrine Gland

Embryology

  • from epithelial cells
  • from hair follicle analogs

Function

  • thermoregulation (sweat, evaporation)
  • scent gland

Sympathetic stimulation

  • Cholinergic, respond to core temp
  • adrenergic

Time of activation

  • 1st year of life
  • puberty

Histology

  • simple tubular
  • compound tubular

Orifice

  • skin
  • pilosebaceous

Location

- highest density

  • superficial, ubiquitous
  • palms, soles, axillae
  • Axillae, anogenital, areolar

Orifice

  • skin
  • pilosebaceous

Size

  • 20 microns
  • 200 microns

Secretion

  • simple
  • decapitation secretion

Chemical composition of sweat

  • Hypotonic saline, glycogen, ‘lytes
  • sialomucin

Associated conditions

  • hyperhydrosis
  • hydradenitis suppurativa
  • bromohydrosis
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2
Q

Define hyperhydrosis

A

Define

  • objective: excessive sweating ~ > 2mL / min
  • clinical: > than required for thermoregulation
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3
Q

Classify and describe pathogenesis of hyperhydrosis

A
  • Primary - overall due to extreme non-thermoregulatory sympathetic stimulation of eccrine gland
    • Generalized - autonomic dysregulation
    • Localized - disruption / regeneration of sympathetic fibres OR abnormal # and distribution of eccrine sweat glands
  • Secondary - due to an underlying abnormality, usually generalized
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4
Q

list the differential diagnosis for secondary hyperhidrosis

A
  • Neoplastic - lymphoma, other malignancy
  • Metabolic - hypoglycemia, hyperglycemia
  • Endocrine - hyperthyroid, pregnancy, menopause, pheochromocytoma
  • Infection - TB, brucellosis, malaria
  • Drugs - cholinergics, withdrawal, alcohol
  • CNS - hypothalamic lesions
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5
Q

List the diagnostic criteria for hyperhidrosis

A
  • excessive sweating in > 1 of: axillae, palms, soles, craniofacial
  • secondary cause ruled out
  • > 6 mos duration
  • plus > 2 of:
    • +ve FHx
    • onset < 25 yrs
    • bilateral, symmetric
    • > 1 episode per week
    • affecting psychosocial function
    • cessation during sleep
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6
Q

Discuss non-operative and operative management of hyperhidrosis

A

Medical

  • Antipersperant: 20% aluminum chloride hexahyrdate based
  • Ointment: aluminum chloride based
  • Systemic medications: glycopyrolate or clonidine or CCB
  • Iontophoresis
  • Botox injection

Surgical

  • Liposuction
  • Open, direct adenectomy (excision) - “Skoog”
  • Endoscopic thoracic sympathectomy
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7
Q

what are the complications of endoscopic thoracic sympathectomy?

A

best indication is PALMAR hyperhidrosis

complications are horner’s syndrome, pneumothorax, compensatory hyperhidrosis (axillary, common 60-90%, offer these patients an open axillary procedure)

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8
Q

What is a treatment algorithm for hyperhidrosis

A
  • Palmar: topical aluminum –> oral glycopyrolate –> ionotophoresis –> botox –> ETS
  • Facial: oral glycopyrolate or clonidine –> topical aluminum –> botox –> ETS
  • Axillary: topical aluminum –> botox –> oral glycopyrolate –> open procedure vs. ETS
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9
Q

Define hydradenitis suppuritiva

A
  • A chronic recurrent inflammatory disorder of apocrine sweat glands characterized by formation of nodules, abscesses, sinus tracts
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10
Q

Describe suspected pathogenesis of hidradenitis suppuritiva

A
  • Atrophy of sebaceous gland
  • Inflammation, hyperkeratosis of pilosebaceous unit
  • Leads to hair follicle destruction, granuloma formation
  • Occlusion of opening of apocrine gland
  • Healing leads to sinus tract formation
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11
Q

What are the predisposing or risk factors associated w/ Hidradenitis suppuritiva

A
  • female : male 3:1
  • family history (possible AD; ie genetics)
  • smoking
  • obesity
  • trauma
  • poor hygeine
  • acniform disease
  • metabolic disease
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12
Q

Discuss treatment of hidradenitis suppuritiva

A

Lifestyle

  • quit smoking
  • weight loss

Medical

  • Reasonable in most patients to start with medical treatment
  • topical Clindamycin (less severe) or PO clinda + rifampin for more severe x 3/12
  • consider Nd/YAG laser q 1 month
  • severe, refractory - consider anti-TNF-a (Remicade/Infliximab)

Surgical

  • consider intralesional kenalog
  • I&D when indicated (will recur)
  • Excision
    • and VAC
    • and allograft
    • then STSG (colonized field, consider VAC or allograft to prep bed first)
    • or locoregional flap
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13
Q

what is lymphedema?

A

lymphatic disfunction, resulting in accumulation of protein-rich interstitial fluid in the skin and subcutaneous tissue

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14
Q

describe the anatomy of a lymphatic vessel

A
  • overlapping endothelial cells (overlap acts as a valve)
  • no well defined basement membrane
  • intercellular gap allows for diffusion of proteins and fluid
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15
Q

describe the anatomy of the lymphatic system

A
  • organized into superficial and deep systems
  • superficial system:
    • unvalved vessels in the superficial and intermediate dermis, drain into valved deep dermal and subdermal plexuses
    • Dermal and subdermal plexuses follow course of superficial veins
  • deep system
    • valved vessels in subfascial channels along deep venous system
    • run in groups of 2-4 channels
    • drain fascia, muscle, tendinoligamentous supports, joints, periosteum, bone
  • superficial and deep systems only connect at supratrochlear, popliteal and groin nodes
    *
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16
Q

what anatomic regions do the thoracic duct and right lymphatic duct drain?

A
  • thoracic duct drains into left subclavian vein at junction w/ IJV
    • drains all lower extremity, left upper extremtiy/chest/neck/face
  • right lymphatic duct drains into right subclavian @ IJV
    • drains right upper extremity, chest, neck, face
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17
Q

what are the functions of the lymphatic system?

A
  1. fluid return from interstitial space to blood
  2. transport of protein
  3. aborption of GI fat
  4. immune function
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18
Q

What factors govern lymphatic flow?

A
  1. intrinsic muscle pump (smooth muscle wihtin channel wall are stimulated to contract w/ distension)
  2. skeletal muscle contraction
  3. intra-thoracic and intra-abdominal pressure changes (ie respiration)
  4. arterial pulsations
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19
Q

Describe the pathophysiology of lymphedema

A
  • disruption/excision of lymph node
  • disruption of lymphatic drainage
  • accumulation of protein-rich fluid in interstitium
  • increase pressure in interstitial causes collapse of lymphatic channels
  • progressive interstitial and channel fibrosis
  • obstruction of drainage
  • compression of normal lymphatics
  • progression of cycle
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20
Q

List long-term sequellae of lymphedema

A
  • impaired function and mobility
  • psychosocial distress
  • chronic fibrosis, dermatitis
  • chronic infection: bacterial, fungal, lymphangitis
  • lymphorrhea
  • malignancy
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21
Q

how do you stage lymphedema?

A

international society of lymphology staging system:

  • stage 0: subclinical lymphatic dysfunction
  • stage 1: early (pitting) lymphedema, resolves w/ elevation
  • stage 2: pitting edema that does not resolve w/ elevation
  • stage 3: chronic fibrosis, non-pitting edema, skin thickening, hyperpigmentation, folds, fissures, warty changes, fat deposits
    *
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22
Q

how do you classify lymphema?

A

Primary vs Secondary; status of lymph channels

  • Primary
    • Congenital lymphedema
      • since birth
      • usually spontaneous, unilateral, F>M
      • Also genetic /AD form called Millroy’s disease
        • F>M (2:1), LE>UE (3:1; bilat LE in 2/3); 2’ skin changes & ski jump toe
      • aplastic lymph channels
    • Lympheme praecox
      • adolescent (childhood - < 35)
      • F>M, usually unilateral LE to knee
      • hypoplastic
      • Familial lymphedema praecox (AD) – Associated with anomalies (vertebral defects, cerebrovascular malformations, hearing loss, distichiasis)
    • Lymphedema tarda
      • > 35 yrs
      • usually hyperplastic but obstructed, incompetent valves
  • Secondary:
    • Iatrogenic: surgery, radiation
    • Infectious: most common developed; Wucherii Bancrofti (plus others, TB)
    • Inflammation: chronic venous disease w/ ulceration
    • Trauma
    • Malignancy
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23
Q

what is risk of lymphedema after ALND? After SLNB of axilla? Of other iatrogenic regions?

A
  • ALND: 10 - 40% (~ 30%)
  • SLNB: 5-10%
  • others: sarcoma (30%, all sites); melanoma (%16%, all); gynecologic (%20), GU (10%)
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24
Q

describe your history for patient presenting with unilateral leg swelling & suspected lymphedema

A
  • Evolution, infections, ADLs, pain, asymmetry or increased circumference of an extremity, family history
  • previous surgery (ie. node dissection), radiation, trauma; compliance & response to compression
  • travel (ie. to region with endemic filariasis)
  • malignancy must always be considered
  • Sudden onset, rapid progression, or associated pain (may indicate direct tumor growth or metastatic disease in the regional lymph node basin)
  • consideration of ddx of unilateral leg swelling: acute DVT, malignancy/recurrence, post-thrombitis, arthritis
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25
Q

what is your ddx for unilateral and bilateral leg swelling (ie for pt presenting for evaluation of lymphedema?)

A
  • Bilateral:
    • obesity, lipedema, malignancy, low protein state, cardiac failure, venous insufficiency
  • Unilateral:
    • acute DVT, post-thrombitis, arthritis, malignancy/recurrence
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26
Q

what are goals of therapy for lymphedema

A
  1. prevent infections and long-term sequellae
  2. reduce swelling
  3. improve function
  4. improve appearance
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27
Q

Outline non-surgical therapy for lymphedema

A
  • initate therapy early
  • strict compliance required
  • lifestyle
    • elevation
    • weight reduction
  • compression
    • compression garments - 20-30mmHg graded compression
    • manual lymphatic drainage
    • complex lymphatic therapy: manual lymph drainage + compression garments + PT
  • medications
    • antibiotics - therapeutic, consider prophylactic w/ multiple recurrent infections
    • diurectics (controversial)
    • Benzopyrones/ coumariins - no good evidence
  • others: sequential pneumatic compression, ultrasound, limiation of triglycerides, intra-arterial injection w/ autologous lymphocytes (experimental)
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28
Q

outline surgical therapy for lymphedema

A
  • Ablative
    • Excisional: charles (total circumferential subcutaneous excision & STSG); sistrunk (wedge excision, staged subcutaneous excision)
    • Liposuction
  • Physiologic
    • Lymphaticolymphatic anastomosis
    • Lymphaticovenous shunt
    • Lymph node transfer
29
Q

outline indications for surgical intervention for lymphedema

A
  • Failed conservative therapy with;
    • Impaired extremity function
    • Gross extremity size & weight
    • Recurrent lymphangitis (>3 episodes / year)
    • Severe skin changes
    • Localized 2° lymphatic obstruction or 1° with obstructive pattern, stage I/II/+-early III (for physiologic techniques)
30
Q

what are complications of surgical intervensions for lymphedema?

A

· Dehiscence

· Infection

· Seroma/hematoma

· Skin necrosis

· Recurrence or exacerbation of edema

· Injury to cutaneous nerves

lymphorrhea

31
Q

discuss management principles for post-mastectomy (ALND) lymphedema

A
  • Wait at least 6 months after resection for resolution of swelling
  • Continue conservative measures
  • Rule out recurrence and metastasis
  • Test quality of donor channels by lymphoscintigraphy
  • Evaluate suitability as surgical candidate
32
Q

discuss lymphangiosarcoma

A

· risk - chronic lymphedema (10% at 10 years); but overall rare with incidence overall and among mastectomy patients < 1%

o post-mastectomy lymphedema, lymphangiosarcoma = stewart-treves syndrome

· nodular, red-purple nodular lesion with satellites

· poor prognosis (< 10% at 5 yrs); not radio- or chemo-responsive; therefore amp

33
Q

What is your differential for hidradenitis suppurativa

A
  • infected bartholin cyst
  • pilonidal cyst
  • perirectal abscess
  • TB, actinomyces
  • cat scratch disease
34
Q

How do you classify the severity of hidradenitis suppurativa?

A

Hurley stages

Stage 1

  • single or multiple abscesses, localized
  • no sinus/scarring

Tx: topical clinda, kenalog inj, +/- NdYAG qmonthly, infliximab as last non-op option

Stage 2

  • multiple abscesses, + sinuses+scarring

TX: oral clindamycin + rifampin x10wks, +/- Nd:YAG monthly, infliximab as last non op option

Stage 3

  • multiple abess interconnected, + sinus + scarring, diffuse disease

Tx: Surgical excision + trial of preop non-op options

35
Q

DEFINE SKIN AND SOFT TISSUE INFECTION

A
  • presumed bacterial infection
  • bacterial invasion and multiplication in skin, subcutaneous tissue, fascia or muscle with local or systemic toxic effects
36
Q

List RFs for development of SSTI:

A
  • breach in epidermis/dermis
  • dry, cracked, irritated skin
  • immunocompromise (2’ >>>>> 1’; ie DM, PVD)
  • chronic venous insufficiency
  • chronic lymphatic insufficiency
  • chronic neuropathy
37
Q

what is the difference between a simple and complication SSTI?

A
  • complicated is SSTI
    • involves deep soft tissue
    • requires surgical intervention
    • factors associated w/ decreased delivery or effectiveness of medical therapy
      • DM, obesity, vascular insufficiency/compromise, immunocompromise
38
Q

define and classify surgical site infections

A
  • SSI is defined as infection at the site of surgery within 30 days of surgery (or 1 year if implantable device) and one of the following:
    • surgeon diagnosis of SSI
    • culture+ sample from aseptically obtained fluid, tissue
    • purulence or abscess with clinical, laboratory, re-operative or histopathological confirmation
    • surgical site is reopened PLUS at least 1 sign of infection: pain/tenderness, erythema, warmth, fever
  • subclassified as:
    • superficial - skin and subcutaneous
    • deep - deeper soft tissues like fascia, muscle
    • organ / space - specific organ involved or space not mentioned above
39
Q

what are risk factors for primary immunodeficiency?

A
  • 4+ infections / year
  • recurring infection not responsive to abx
  • abnormal location or type of infection
  • chronic or recurring intermittent fevers
  • recurrent deep abscesses of soft tissue, LN, organs
  • FHx of 1’ immunodeficiency
40
Q

differentiate between SIRS, sepsis and septic shock

A
  • SIRS - systemic inflammatory response to infectious or non-infectious stimulus
    • HR > 90
    • Temp > 38 or < 36
    • RR > 20 or PaCO2 < 32mmHg
    • WBC > 12 or < 4 or > 10% immature bands
  • Sepsis: SIRS due to documented infection
  • Septic shock is: SIRS, infection, hypotension
41
Q

define necrotising soft tissue infection

A
  • rare life-threatening necrotising infection of skin, subcutaneous fat, fascia or muscle
  • caused by toxin-producing bacteria
  • characterized by rapid progression and 3 D’s: disproportionate pain, dermatologic findings, deranged physiology
42
Q

how do you classify NSTI

A
  • type 1: polymicrobial gram + and gram - infection
    • RF: older, comorbid, immunocompromised
    • occult skin break / bacterial translocation from abscess, perineal, anorectum
  • type 2: monomicrobial (typically gram + infection): GAS >>>>> S. aureus > both > other
    • RF: can be healthy and younger (or not), skin break may be known - recent surgery or other skin trauma, IVDU
  • type 3: poly or monomicribial infection of vibrio species
    • warm water area
43
Q

What factors wiht group A strep infection promote a necrotising soft tissue infection

A
  1. Rapid spread & necrotising to skin & soft tissues:
    1. by exotoxins - hyaluronidase, streptokinase, stretolysin - obliteration of fascial planes
  2. Profound systemic inflammatory response and physiologic derangement
    1. M proteins activate T cells / cellular immunity at 200x normal
    2. promotes massive SIR & catstrophic sepsis
44
Q

what factors w/ clostridial source promote an NSTI?

A

alpha toxin and omega toxin

  1. necrosis to soft tissues through vascular thrombus formation, decreased endothelial cell integrity
  2. phyiologic derangement through various SIR mechanisms
45
Q

what factor of gram negative infections associated w NSTI

A

lipopolysaccharide chains –> profound SIR

46
Q

what is the pathophysiology of dermatologic findings in NTSI

A
  • rapid spread along fascial planes
  • infarction of perforating blood vessels and cutaneous nerves
  • ascending necrosis and progressive anaesthesia
47
Q

Discuss treatment of established or highly suspected NSTI

A
  1. Consults & critical care
    1. ICU consult & bed arranged for fluid resuscitation, chemical hemodynamic support, ventilatory support, pain control, ability to return to OR quickly, closely monitored
    2. Dietician - will have supra-physiologic nutritional requirements
    3. Infectious disease - should be consulted every time
  2. Medical therapy - Antibiotics
    1. Standard 1st line regime in pen-appropriate patient: Pip-tazo, clindamycin, vancomycin
      1. alternate 1st lines - use a carbapenem instead of pip-tazo w/ above
      2. use aminoglycoside or fluorquinolone PLUS metronidozole instead of pip-tazo or carbapenem
    2. If GAS speciated: Pen G + Clinda
  3. Medical therapy - other adjuncts
    1. IVIG - consider for GAS speciated infections
    2. HBO - not currently recommended based on weak evidence and organizational difficulties
  4. surgery is definitive care
    1. debride all necrotic and infected tissue
    2. plan for take-back and repeat debridement in 24-48hrs
    3. Interim dsg w/ betadine packs, eventually something moist (acticoat/jelonet base layer) +/- VAC ONCE ALL NECROTIC/INFECTED TISSUE DEBRIDED
    4. Ultimate coverage as indicated by defect
48
Q

Why is clindamycin utilized in treatment of NSTI

A
  • utilized in first line if potentially a GAS or clostridial infection; otherwise contineud after speciation only if GAS or clostridum
  • neutralizes exotoxins produced (not to target the bacterium itself)
    • clostridial - alpha toxins
    • strep - M proteins
49
Q

what is the potnetial benefit of IVIG in certain NSTI

A

for staph or strep

thought to bind exotoxins and decrase compliment cascade and systemic inflammatory response

50
Q

Describe the pathophysiology of diabetic foot ulcer

A
  1. Triad of polyneuropathy, neuro-ostearthropathy (Charcot arthropathy), motor neuropathy - lead to altered biomechanics, lack of protective sensation, altered pressure distribution - leads to skin break down
  2. Skin break down becomes colonized by polymicrobial agents, can form biofilm
  3. Altered phagocytic immune function (hyperglycemia) and associated vascular insufficiency lead to diminished ability to fight early bacterial coloization/contamination/infection; becomes deeply invasive
51
Q

list bacteria common to human bite

A
  • gram +ve aerobe: staph aureus, strep (pyogenes(
  • gram -ve areobe/anaerobe: eikenella corrodens, bacteroids, fusobacterium, prevotella, peptostreptococcus
52
Q

list bacteria common to dog or cat bite

A
  • gram + aerobe: staph aureus, strep pyogenes & viridans
  • gram - anaerobe: pasteurella multicoda, bacteroides, fusobacterium, prevotella
53
Q

what is bacteria predominantly associated w cat scratch fever

A
  • bartonella henselae
54
Q

what are bacteria associated w/ marine infections

A
  • gram + aerobe: strep iniae
  • gram - anaerbe or aerobe: vibrio, aeromonas hydrophilia, mycobacterium marinum
55
Q

compare tetanus prone to tetanus not-prone wounds

A

Clinical Features

Tetanus-Prone Wounds

Non Tetanus-Prone Wounds

Age of wound

> 6 hours

< 6 hours

Configuration

Stellate wound, avulsion, abrasion

Linear wound

Contaminants (dirt, feces, soil, saliva, etc)

Present

Absent

Depth

>1cm

<1cm

Devitalized tissue

Present

Absent

Denervated, and/or ischemic tissue

Present

Absent

Signs of infection

Present

Absent

Mechanism of injury

Missile, crush, burn, frostbite

Sharp surface (eg, knife, glass)

56
Q

which patients require tetanus booster? which patients require tetanus immunoglobulin?

A

Tetanus history

Not tetanus prone

Tetanus prone

Td

TIG

Td

TIG

Unknown or < 3 doses

Yes

No

Yes

Yes

> 3 doses, < 5 yrs ago

No

No

No

No

> 3 doses, > 5 yrs, < 10 yrs ago

No

No

Yes

No

> 3 doses, > 10 yrs ago

Yes

No

Yes

No

Td: tetanus and diphtheria (0.5cc sc)

TIG: tetanus immunoglobulin (250cc IM)

Td & TIG given simultaneously: inject at different sites with different syringes

57
Q

discuss management of periorbital cellulitis

A
  • History and physical exam: OPQRST plus vision changes, diplopia, proptosis, painful EOM, chemosis, headache, fever, mental status
  • serologic wu
  • Image: CT scan - consider for all pts (I would); also for all suspected post-septal and/or pre-septal not responding to medical management after 24-48 hrs
  • medical management
    • all pre-septal, some post-septal (small periosteal abscesses, young patients, early, no gas, no proptosis, no detnal infection) - ceftriaxone vs. clinda +/- flagyl
  • surgical management
    • open fronto-ethmoidectoy
    • transcaruncular access
    • FESS - functional endoscopic sinus surgery
58
Q

what differentiates preseptal from post septal cellulitis?

A
  • based on chandler classification, defining features are proptosis, ophthalmoplegia, vision change
59
Q

define biofilm

A
  • a structured community of microorganisms
  • encapsulated by a self-made polymeric matrix
  • and strongly adherent to a living or inert surface
60
Q

what is the gold standard way to diagnose the bacteria involved in biofilm?

A

polymerase chain reaction

61
Q

what is HIV?

A
  • HIV is an chronic, progressive illness/ infection by the HIV retrovirus causing a deficient cell-mediated immunity and characterized by ultimate development of opportunistic infections, malignancies and neurologic diseases
62
Q

List dermatologic manifestations of HIV

A
  • recurrent herpes zoster or herpes simplex infections
  • oral candidiasis
  • hairy leukoplakia (oral)
  • folliculitis
  • seborrheic dermatitis
  • Kaposi sarcoma
63
Q

what is the overall risk of seroconversion after health care worker exposure to HIV?

what are higher risk factors?

A
  • Overall 0.3%
  • Higher risk factors
    • delay AZT
    • Hollow bore needle, draws blood
    • Long duration of contact or deep injury
    • Large volume of exposure
    • Patient high viral load/severe HIV/AIDS
    • visible blood on needle
    • vascular procedure
64
Q

what is the current recommendation for PEP? ·

A

· Zidovudine (AZT) and Lamivudine (3TC) +/- third agent Nelfinavir (high titre of source, deep injury)

65
Q

what is HIV associated lipodystrophy? what areas are affected and briefly how would you treat?

A
  • HIV + patients undergoing active arv treatment; typically associated w/ protease inhibitor treatments
  • variable areas of lipoatrophy and lipohypertrophy
  • lipohypertrophy: dorsal cervical fat pad, abdomen, breasts - tx w/ liposuction
  • lipoatrophy: face - cheeks, nasolabial fold; extremities
    • implants: medpore or silastic implants to face (cheek)
    • synthetic filler - scultra (poly-L-lactic acid is FDA approved for this indication), historic was bioalchimid - now associated w/ late granulomatous infection
    • autogenous filler - fat
66
Q

discuss treatment of HIV associated kaposi sarcoma

A
  • disease management - reduce viral load (undetectable), increase CD4 count - disease can enter remission or resolve [OPTIMIZATION OF HIV ARV IS CORNERSTONE]
  • surgery - indicated for symptomatic lesions (bleeding)
  • radiotherapy - if several symptomatic lesions in same field (very radiosensitive)
  • chemotherapy - for diffuse/disseminated KS, outside single xrt field
67
Q

what do you do if someone is bitten by a stray racoon that was acting weird?

A
  1. copiously irrigate the wound with soap & water, then iodine +/- alcohol scrub (to decrease viral load)
  2. XR to rule out assocatied fracture or retained FB
  3. debride any necrotic or non-viable tissue
  4. do not close - dress open and reassess within a week
  5. contact animal control/public health - try to obtain and test the animal
  6. if animal tests + or if high risk then treat with rabies prophylaxis
    1. rabies immunoglobulin 20u/kg x 1 - sc around injury as much as possible, rest IM
    2. rabies human/chick derived vaccine 1mL IM - day 0, 3, 7, 14 (+ 28 if immunosuppr)
68
Q

what is risk of seroconversion/transmission after occupational exposure of HIV, HCV, HBV?

A
  • HIV 0.3%
  • HCV 3-10%
  • HBV 2-40% (varies on vaccination status, titres of patient and occupational exposed)
69
Q
A

Skin and soft tissue (13 decks)

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