33 and 34 - Soft Tissue Infections Flashcards

1
Q

3 clinical patterns of infection

A
  • Cellulitis
  • Abscess
  • Necrotizing fasciitis
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2
Q

Cellulitis

A

o Skin and connective tissue infection and inflammation WITHOUT necrotic or purulent collections
o Cellulitis can start out as just inflammation then become as an abscess, but by definition, cellulitis is NOT purulent in nature

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3
Q

Abscess

A

o Deep tissue infection WITH necrotic tissue and or purulent collections
o Involving tissue compartments, joints, tendon sheaths or deep spaces

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4
Q

Necrotizing fasciitis

A

o Extremely rapid progression
o Life and limb threatening

NOTE: not really going to talk about this today

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5
Q

Clinical signs and symptoms of cellulitis

A

o Erythema, edema
o Pain, fever, chills, malaise
o In diabetics with neuropathy, they will not have pain

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6
Q

Clinical signs and symptoms of abscess

A

o Erythema, edema
o Fluctuance, purulence, necrosis (coming from the inside out)
o Treat with antibiotics
o Pain, fever, chills, malaise

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7
Q

Clinical signs and symptoms of necrotizing fasciits

A

o Rapid wide spread necrosis
o Severe systemic symptoms (sepsis)
o CANNOT just treat with antibiotics, NEED to debride the necrosis

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8
Q

Common organisms

A
  • NOTE: you need to know what the most common organism is to start antibiotic therapy
    o For cellulitis, there is no opening in the skin to culture, so we need to assume
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9
Q

Common organisms in cellulitis

A

Strep. Group A, Staph. aureus

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10
Q

Most common organism in abscess and post-operative infections

A

Staph. aureus

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11
Q

Common organisms in a puncture wound

A

o Staph. aureus

o P. aeruginosa (osteomyelitis)

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12
Q

MOST common organism in diabetic infections

A

o **Staph aureus ** (staph is almost ALWAYS present)

o Can be POLYMICROBIAL (challenging to treat)

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13
Q

Community vs hospital acquired infections in terms of antibiotic resistance

A
  • Community acquired infection has less antibiotic resistance
  • Hospital acquired infection has more antibiotic resistance
  • Healthy person is less likely to have an abx resistant infection (community acquired)
  • If a NH patient comes in with an infection, we assume methicillin resistance
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14
Q

Effect of long standing antibiotic therapy on antibiotic resistance

A
  • Patients on long standing antibiotic therapy select out resistant organisms
  • *****Prophylactic antibiotics should be limited in timing and spectrum (1 dose 30 min prior to surgery for staph) – Should NOT be doing 2 weeks of prophylactic antibiotics after surgery
  • You can’t put everyone on abx just to be safe – that will cause more problems in abx resistance
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15
Q

Polymicrobial infections

A
  • Diabetic infections are in many cases poly-microbial
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16
Q

MRSA

A
  • MRSA is a major player in community and institutional acquired infections
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17
Q

Clinical findings associated with soft tissue infection

A
  • Fever
  • Leukocytosis
  • Lymphadenopathy
  • Lymphangitis
  • Bullae, purpura and other skin changes
  • Increased ESR or C-reactive protein (Erythrocyte sedimentation rate and C-reactive protein measure overall inflammation in the body)
  • Bacteremia (+ blood cultures)
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18
Q

Fever

A
  • > 100.5 degrees F
  • Exogenous and endogenous pyrogens
  • Individual variation and diurnal variation
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19
Q

Fever patterns

A
o	Continuous
o	Intermittent (spiking fever – common in abscess)
o	Remittent (parasitic – goes away, comes back few days later)
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20
Q

Immunocompormised patient’s fever

A
  • **NOTE ** If the patient is immunocompromised they may not mount a febrile reaction – A diabetic with renal failure will NOT have a high fever, even with a limb-threatening infection
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21
Q

White blood count

A

WBC
o Leukocytosis > 12K

“With diff” - differential
o PMN percentage
o Left shift (immature WBCs, band cells, in blood stream)

o In immuno-compromised, you will not see a huge peak in WBC, but you will see slight elevation that will start to come down once abx therapy has been initiated

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22
Q

Timing of sed rate and WBC increase in infection

A

o For sed rate, there is a lag time… You may see the sed rate continue to peak following WBC decline post-abx therapy, but the sed rate will start to come down after that
o Not as easy as just looking at the numbers – need to relate it to the patient

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23
Q

Lymphatic involvement in soft tissue infection

A
  • Inflammatory reaction in lymph channels
  • Erythematous lymphatic streaking
  • Palpable or painful lymph nodes
  • Example: you can see red line coming down the leg, inguinal lymph nodes would likely be swollen, painful
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24
Q

Blood cultures in soft tissue infection

A
  • Identification of bacteremia
  • Important to consider with profound systemic symptoms
  • May be helpful to identify pathogen when local culture material is not available
  • May be difficult to obtain positive culture with intermittent bacteremia of cellulitis and abscess
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25
Q

Sepsis

A

Sepsis is a systemic response to a local infection

Example
o Foot ulcer (red hot swollen) and meet the criteria for SIRS = SEPSIS

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26
Q

Why is sepsis important to evaluate for?

A

VERY IMPORTANT TO UNDERSTAND***

o Need to know this because it determines admittance to the hospital

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27
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

o Temp 100.5
o HR > 90
o Respirations > 20
o PaCO2 12K

Need 2-3 criteria

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28
Q

Types of sepsis (4)

KNOW THIS ***

A

Sepsis
o SIRS + Documented Infection

Severe Sepsis
o Sepsis + Organ dysfunction
o 25-30% Mortality

Septic Shock
o Sepsis + Acute persistent circulatory Failure
o 40-70% Mortality

Multi Organ Failure Syndrome

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29
Q

Organ dysfunction

A
  • Altered mental status
  • Edema
  • Cardiac index > 3.5
  • Acute oliguria
  • Arterial hypoxemia
  • High CR
  • INR > 1.5
  • Platelet count 1
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30
Q

What are the disease states that will contribute to a soft tissue infection?

A
  • THESE WILL ALTER THE PATIENT’S SYMPTOMS AND IMMUNE RESPONSE*
  • Elderly
  • Diabetes
  • Transplant and HIV
  • Steroid use
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31
Q

How does diabetes contribute?

A

o Immune-suppression
o Altered immune response (Fever, WBC, SIRS)
o PVD (Poor healing)
o Neuropathy (Reduced patient perception)

32
Q

How does HIV and transplant contribute?

A

o Immune-suppression

33
Q

How does steroid use contribute?

A

o Altered immune response

o Blunted clinical symptoms

34
Q

General treatment guidelines for infection

A
  • Cellulitis can be treated with empiric antibiotics
  • *Incision and Drainage must be priority if abscess or necrosis are present - do not leave isolated pockets of necrosis or purulence
  • Delayed closure in most cases (open it and leave it open to drain)
  • Culture deep tissues

Post I&D Antibiotics based on clinical scenario and patient health factors…
o Institutionalized patients may have MRSA
o Diabetic infections may be poly-microbial

35
Q

Culture technique

A
  • Superficial swipe is inaccurate for identification of deep pathogens
  • Avoid skin contact to limit confusion of skin flora and pathogens
  • Tissue is better than pus for culture material – DEEP TISSUE*
  • Aerobic, anaerobic, fungal, acid fast
  • Quantitative cultures
36
Q

Antibiotic selection

A

Empiric choice first followed by culture directed drug of choice

***Best guess of the likely pathogens based on the patient medical history and clinical circumstances of the infection

37
Q

Characteristics to look for in the drug of choice

A

o Highest specificity
o Lowest risk
o Lowest cost

38
Q

Oral vs. IV antibiotics

A

o Oral drugs can have very good tissue penetration

o Do not always need IV in otherwise healthy

39
Q

Duration

A

This will vary based on the patient’s health status

40
Q

IDSA guidelines for CELLULITIS

A

Very good guidelines to reference

Community Acquired:
o Strep. / Staph.
o Nafcillin – Cefazolin - Clindamycin

MRSA Suspected:
o TMP/SMZ - Clindamycin

Nosocomial (hospital-acquired)
o Vancomycin

41
Q

IDSA guidelines for DIABETIC FOOT INFECTIONS

A

Mild (with no previous antibiotics)
o Dicloxacillin – Cephalexin – Clindamycin
o Nafcillin – Cefazolin - Clindamycin

Moderate (or with previous antibiotics)
o Ampicillin / Sulbactam – Clindamycin + Levaquin

42
Q

Diabetic foot infections

A
  • Poly-microbial (Aerobes, Anaerobes, G+, G-)
  • Multi-system disease (Cardiac, Renal, PAOD, Neuropathy, Immunosuppression)
  • Less amenable to out-patient care
  • Patient may not exhibit symptoms* (No pain – Neuropathy, low white count and fever – Immunosuppression)
43
Q

IDSA guidelines for animal and human bites

A
  • Non allergic (Ampicillin / Sulbactam)
  • PCN allergy (Clindamycin + Levaquin)
  • Most common organism in a dog bite = Pasturella
44
Q

Paronychia - general

A

o Superficial nail fold infection
o Has characteristics of both cellulitis and abscess
o Well localized, usually not very deep or proximal infections
o In immunocompromised, it will be much more severe

45
Q

Paronychia - clinical characteristics

A

Pain, erythema, purulence, granuloma, usually well localized, nail changes

46
Q

Paronychia - treatment

A

o Incision & drainage is the mainstay
o Antibiotics rarely needed except for compromised host
o Culture only in special situations
o Staph., **Strep., Candida (= most common)
o We don’t usually even need abx
o NEED SURGICAL TREATMENT – ABX WILL NOT BE ENOUGH
**

47
Q

Cellulitis - clinical characteristics

A

o NO PURULENCE

o Erythema, warmth, pain, fever, chills, malaise, leucocytosis with left shift, contiguous source, no necrosis or pus

48
Q

Cellulitis - treatment

A

o Empiric antibiotics, most commonly strep and staph
o Culture is usually not possible
o Admit to the hospital if the patient has profound symptoms, compromised host or failure of out-patient therapy

49
Q

Criteria for hospital admission

A
  • Profound clinical symptoms (Sepsis)
  • One or more contributing disease states
  • Antibiotics requiring inpatient monitoring
  • Failure of out-patient therapy
  • Suspicion of abscess requiring I&D
50
Q

ISDA guidelines for admission

A

They revolve around SEPSIS

  • Hypotension
  • Increased creatinine
  • Low bicarb
  • Increased CPK
  • Significant left shift
  • C-reactive protein > 13
51
Q

Monitoring recovery of soft tissue infections

A
We look at all of this to determine the next steps in treatment (debride again, send home, keep them in hospital, etc.)
o	Clinical appearance
o	Temperature
o	Symptoms (pain, chills) 
o	WBC and differential
o	ESR or C reactive protein
o	Serial cultures???
52
Q

Describe the controversy regarding serial cultures

A
  • Some say 3 clean cultures before you can close the wound

- MOST wounds will not have clean cultures ever, so need to look at more than this – whole patient approach

53
Q

Deep infections

A
  • Includes: abscess and puncture wound
54
Q

Abscess - clinical characteristics

A

o Pain, cellulitis, lymphangitis, spiking fever, fluctuance, focal collection of necrotic material

55
Q

Abscess - treatment

A

o I&D/Culture – every hour we are not opening it up, more tissue is dying
- THERE ARE TEST QUESTIONS ON THIS – Incision and drainage is the MOST IMPORTANT THING
o Empiric antibiotics
o Medical Evaluation
o Vascular and other Testing
o Directed antibiotics after cultures are available
o Open wound management
o Delayed closure or reconstruction – do NOT close this right away

56
Q

What do you NEED to remember about an abscess?

A

ALWAYS INCISION AND DRAINAGE FIRST – EMERGENT* (I&D) TEST QUESTION*
o “There will be test questions on this”
o Take culture at the same time
o If you start antibiotics before you take a culture, you have just altered the culture

57
Q

Open wound management goals

A

Used for most infections after I&D to:
o Promote granulation
o Sequentially remove necrotic and infected tissue.
o Manage dead space
o Prevent subsequent sequestration

58
Q

Basics of open wound management

A
  • Continuously wet bandaging
  • Serial debridement (have to be able to continue debriding the wound in the office or OR)
  • Complete when granulation occurs and cellulitis and other signs resolved
59
Q

CASE STUDY I

A
  • 27 y/o healthy male just back from a camping trip, foot has been red for 3 days
  • Severe pain, sweats and chills, tender in groin, oral temp 101.8, WBC 15.6K, ESR 32
  • Draining for 1.5 days*** (tells you it is an abscess and not cellulitis), X-ray negative
  • Diagnosis and plan: Abscess – I&D RIGHT NOW**
  • Diagnosis is abscess in the foot with systemic sepsis because he has systemic symptoms as well
60
Q

Criteria for hospital admission (recall from above)

A
  • Abscess requiring I&D
  • Profound clinical symptoms (sepsis)
  • One or more contributing disease states
  • Antibiotics requiring inpatient monitoring
  • Failure of out-patient therapy
61
Q

Plan for CASE STUDY I

A
  • Plan: Hospital Admission, Emergent I&D, empiric antibiotics until cultures complete, medical optimization, saline bandages until the wound is clean and systemic symptoms have resolved, delayed closure when wound clean and granular
62
Q

Delayed wound closure

A
  • Primary closure vs. skin graft?
  • Antibiotics after closure?

PLAN:
o Continue antibiotics for 5 days in otherwise healthy patient responding to treatment
o May need to consider longer course of abx if diabetic or if osteomyelitis
- 3 days later skin has recovered, wound is granular and very healthy looking

63
Q

CASE STUDY II

A
  • 70 y/o female with RA and DM, callus broke open 1 week ago and has been draining
  • Painful in arch and ankle, feels weak
  • N&V this AM, “thinks she has the flu”
  • Oral temp 100.6 (can’t make a decision based on this due to immunocompromised)
  • WBC 9.5K (can’t make a decision based on this due to immunocompromised)
  • They think it is the flu and they are not associating it with the foot because it is not painful
  • Arch compression yields drainage
  • Plan: hospital admission, emergent I&D, empiric antibiotics until cultures complete, medical evaluation and optimization, vascular evaluation, directed antibiotics, saline bandages until wound is clean and systemic symptoms are resolved
64
Q

CASE STUDY III

A
  • 64 y/o male with NIDDM x 15 years
  • Redness x 10 days, starting to drain, feels like he is getting the flu
  • Oral temp 99.6, WBC 8.4K, blood sugar 270, non-palpable pulses
  • Diagnosis is abscess with necrosis – NO vascular supply, so AFTER we halt the infection, we will get a vascular consult ASAP (I&D tonight, vascular consult tomorrow)
  • Plan: hospital admission, emergent I&D, medical evaluation, empiric abx until cultures complete, vascular testing, advanced imaging, saline bandages until wound is clean and systemic symptoms have resolved
65
Q

CASE STUDY IV

A
  • 47 y/o IDDM with ulcer for 6 months, recent swelling in 2nd toe & forefoot
  • No pain, feels fine, has had multiple past ulcers
  • Temp 99.2, WBC 6.7K, ESR 55, x-ray shows extensive bone destruction, pulses palpable
  • Most important factors in this patient is the multiple past ulcers, bone destruction, swelling in toe – Now we have an abscess in the toe
  • Probably traveled up the tendon sheath – now you have a closed space infection, an abscess
  • Plan: hospital admission, I&D, medical evaluation, empiric antibiotics, advanced imaging, directed abx, serial debridement and wound care
  • Once infection has cleared, need to figure out how to close the wound – toe flap
  • Eventually needed a transmetatarsal amputation, which removed the deforming forces to treat the ulcer as well as the infection – it was a functional amputation stub
66
Q

CASE STUDY V

A
  • 54 y/o female IDDM x 25 years, redness and swelling 5 days after twisting ankle
  • No pain, feels fine, oral temp 98.5, WBC 8.9, HgA1c 9%, palpable pulses, swelling to the knee both extremities
  • Ankle sprain or abscess? They made an incision and it was highly purulent, lots of drainage
67
Q

CASE STUDY VI

A
  • 62 y/o male with multiple episodes of gout, current episode x 7 days
  • Severe pain, not responding to indomethacin, no response to oral abx, getting blisters on toes
  • Fever and chills, oral temp 101.5, WBC 11K, tender in arch
  • This is an abscess due to gout with necrosis of the toe, which is spreading proximally – the gout was traveling with the infection so there were crystals
  • This is a deep space abscess in a single compartment of the plantarfoot
  • Plan: admission, emergent I&D, medical evaluation, empiric abx, advanced imaging, serial debridement and wound care, reconstruction
  • Gout – sodium urate tophi which “eats everything in its path” – there was no tendon capsule or bone left, just the sodium urate accumulation which can become acutely infected
68
Q

CASE STUDY VII

A
  • 75 y/o IDDM male with redness and L calf pain @ rest, acute onset 10 days ago, seen by two other doctors and treated with 2 courses of oral antibiotics
  • Not responding to oral antibiotics and colchicine, uric acid 4.0, no open lesions, oral temp 99.0, WBC 5.0K, pulses not palpable, extensive heart disease history
  • Diagnosis: PAD – occlusive vascular disease, determined this by testing for dependent rubor and elevation pallor
69
Q

CASE STUDY VIII

A
  • 67 y/o female admitted for cellulitis not responding to broad spectrum antibiotics
  • Leg pain, temp 98.6, WBC 8.0, ESR 12, history of DVT
  • Diagnosis: venous stasis – elevation makes it better, not the antibiotics
70
Q

Puncture wound - general concepts

A
  • Must determine the specific circumstances of trauma – environment, object, force of injury, timing of presentation, retained foreign body
  • Get a detailed PMHx
  • Initiate immediate treatment
  • A lot of the same concepts as abscesses
71
Q

Puncture wound treatment

A
  • *****The aggressiveness of treatment is based on the zone of involvement
  • *****I&D is the cornerstone of treatment
  • Antibiotics are carefully considered
  • Timing is extremely important
  • Suspect Pseudomonas in osteomyelitis
  • Always get X-ray
72
Q

Puncture zones and risk associated

A
  • Zone 1 - High risk***
  • Zone 2 - Low risk (Zone 2 is a low risk because there is a lot of distance to the bone, muscle, tendon, etc.)
  • Zone 3 - Mod risk
73
Q

Clinical characteristics of puncture wounds

A
  • History of trauma, pain
  • Physical exam does not always tell the whole story
  • Remember diabetics may have no symptoms or not be aware of trauma
  • Should be treated aggressively before signs of cellulitis or abscess begin
  • Everything is the same – don’t need to belabor this
  • Depends on the environment of the injury***
  • Depends on zone ***
74
Q

Zone 1 puncture wounds

A
  • Aggressive I&D and lavage in all cases, open management is necessary
  • Antibiotics not mandatory unless high risk environment, compromised host, definite bone contact or fracture
  • All injuries with bone penetration are treated with aggressive I&D
  • Example: Puncture wound on the bottom with infection on the top – we know there is abscess because it has travelled to the joint – only way it can get to the top of the foot
75
Q

Zone 2 and 3 puncture wounds

A

Local I&D, antibiotics carefully considered

Open management if:
o Deep penetration / Bone contact
o Contaminated environment
o Compromised host

Zone 2 in a Healthy Patient
o	Local anesthesia
o	Mini I&D
o	Extensive lavage
o	 open

Zone 2 in a Patient with Systemic Complication
o Aggressive I&D
o Antibiotics
o Leave open

76
Q

General concepts in the treatment of puncture wounds

A
  • The aggressiveness of treatment is based on the zone of involvement
  • I&D is the cornerstone of treatment
  • Antibiotics are carefully considered
  • Timing is extremely important
  • Always get X-ray
  • KEY – EVERYTHING we learned about in infection plus ZONE OF INVOLVEMENT***