Skin Flashcards
How does antibiotic resistance of MRSI occur
acquisition of mecA gene which encodes a penicillin binding protien (PBP2a) that has a lower binding affinitiy for beta lactams
What are risk factors for MRSI
use of fluoroquinolones; IV catheterization; more than 10 vet staff employed; post-surgery site infection
What are abx commonly used to treat MRSI
doxycyclyline and chloramphenicol
How are burns classified
on body surface area and depth of tissue
Describe the total body surface area measurements in adapted to animals
Rule of nines
Head/Neck, each front limb = 9%
Each pelvic limb, dorsal trunk, ventral trunk = 18%
What is the severity associated with TBSA in burns
Local burn < 20% less likely for SIRS
Severe burn > 20-30% Very likely SIRS
> 50% TBSA very poor prognosis
Describe a first degree burn
Epidermis only
Painful, hyperemic
Describe second degree burns
Epidermis and upper portions of dermis: pain, blistering, hair intact
If deeper portions of dermis but not complete can see yellow white skin, lost of hair (pulls out), pain only with deep pressure
Describe third degree burns
Epidermis and entire dermis
black letheary skin; eschar is sensitive to touch
Hair pulls out easily
Describe fourth degree burns
epidermis and entire dermis, deeper tissues (connective, bone, vessels etc)
Black letheary skin; eschar is sensitive touch
Hair pulls out easily
Which burn categorization method has been validated in small animals
None
What is the local response to burn
Cells closest to heat source undergo coagulation and vascular thrombosis
Surrounding tissue affected by blood stasis and edema from capillary leak syndrome
Above plus hypoperfusion lead to ischemia
How does hypoxia worsen with burns
Edema from hypoalbuminema and vasoactive substances thromboxane and inducible NO worsen hypoxia
How long before closure of burn may be considered
Up to 3 days to declare itself, may be up to 7 days.
How does frostbite result in injury
Formation of ice crystals resulting in varying degrees of severity similar to burns
Describe type 1 hypersensitivity reactions- skin
angiodema, uticaria, erythema
IgE- antigen complex binds to mast cells and basophils
Describe type 2 hypersensitivity reactions - skin
Vesicles, bullae, erosions, mucocutaneous junctions
IgM and IgG cytotoxic
antigen-antibody binding
Describe type 3 hypersensitivity reactions - skin
Uticaria, ulceration, pitting edema, wheals, papules, pinnae foot pads; MC junctions
IgG immune complexes deposited in endotheilium of vessels
Describe type 4 hypersensitivity reactions - skin
Vesicles bullae, papules, plaques, along trunk axilla, inguinal and pinnae
Antigen bound to T-cells result in tissue necrosis and activation of macrophages
What are the three types of soft tissue infections
Type 1 Polymicrobial— often MRSA
Type 2 Monomicrobial– often streptococci
Type 3 Anerobic
Why are fluoroquinolones not recommended as first line for severe soft tissue infections
In vitro induce bacteriophage-mediated lysis with increase expression of superantigens
1 study 50% were resistant
What are the phases of wound healing
Inflammation/debridement
Repair (proliferation
Maturation
What occurs in the inflammation/debridement phase of wound healing
First 48-72 hrs
Fills with blood; transient vasoconstriction then vasodilation response to histamine and IL8
Neutrophils initially then macrophages which are essential for wound healing
What occurs in the repair (proliferation) phase of wound healing
1-3 weeks
angiogensis, fibroplasia, wound contraction and epithealization
Phase change marked by increase number of fibroblasts
Type III to Type 1 collagen
How does contraction occur in the repair phase
Migration of myofibroblasts
Ceases when tension on surround skin equals the contracting forces or when epithealization is complete
What are the benifits of granulation tissue
blood supply
increase wounds resistance to infection
What occurs in the maturation phase of wound healing
Progressive gain of tissue strength revolves around collagen deposition.
Intial portion of phase at 20% after 3 weeks.
Generally will only be 70-80% of normal
Which tissue may achieve 100% strength
Bladder, Bones
What are the types of wound closure
Primary- within a few hours of wounding
Delayed primary- within 3 days— before granulation tissue formed
Secondary closure- closure after onset of granulation tissue
What are advantages to wound lavage
debride and hydrate
What is the recommended method of lavage and what pressure is ideal
8 psi
35 ml syringe with 19 ga needle
What are advantage properities of SSD
anti: Gram - , gram + and candida
In Burn resuscitation what can be deleterious
Delay beyond 2 hours ( increase mortality)
Over resuscitation just as bad as under
How does burn shock develop
Distrubitive and hypovolemic
IV volume depletion, low pulmonary artery occulusion pressure, elevated systemic vascular resistance and depressued CO
How does depressed cardiac output occur with burn injuries
Decreased plasma volume increased afterload, and decreased contractility
TNF alpha and impared calcium at the cellular level
How does fluid shift after a burn
Protein loss to interstitium as microcirculation is lost
Colloid osmotic pressure drops
Transient decrease in interstitial pressure by release of osmotic particles moving fluid to interstitium
What results due to fluid shifts after a burn
loss of circulationg plasma volume, hemoconcentration, massive edema formation
Decreased UOP, depressed cardiovascular function
When is the maximal fluid shift after a burn injury occur
at 24 hours
What is the formula most widely used to calculate volume resuscitation after a burn
Parkland formulat
4 ml/kg x % TBSA = amount LRS to give in first 24 hrs
Give 1/2 over 8 hours then give second have over 1 hours
adjust as needed based on UOP
What are colloid recommendations for burns in people based on CCM 2009 review article
alubmin increased risk of death
Hypertonic saline 4 x increase AKI, 2 x death
FFP only if coagulatpathy
What is a good way and not good way to estimate fluid volume in burn patients
No truly great way
UOP > 0.5 ml/kg/hr, if less generally under resuscitated
BAD: HCT- as will often be increased due to protein loss
In burn patients what are the benifits of vitamin C
reduced fluid requiremtns, burn tissue water content, decreased ventilator days
How does inhalation injury affect fluid requirements
Increase
In people how does inhalation injury alter developement of ventilatory associated pneumonia
70% of pateitns develop…. DONT give prophy abx
What are preventable complications of burn injuries
hypothermia, compartement syndrome, DVT, heparin induced thrombocytopenia
neutropenia, stress ulcers (give prophy), adrenal insufficency
How are signs of infection altered with burns
Burn patients have a reset of temp (often higher), increased HR and tachypenia therefore it is not always easy to tell
