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65 Cards in this Set

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What is pernio syndrome?
slow freeze

aka chilblains
What are signs of hypersensitivity to cold?
cold urticaria: due to allergy, autoantigen, vasomotor disturbances
acute pernio syndrome
-cyanotic dermatitis
-erethematous
-edema
-intense itching and burning
-clears in 7-10 days
-may remain hyperpigmented for weeks
-due to vasospasm of cold skin
-avoid scratching skin
-avoid heat when rewarming
chronic pernio syndrome
-repetitive exposure to cold and humid conditions
-lesions are erythematous and may ulcerate
-may reulcerate in cold and heal in warm weather
What is a pathological change that occurs with chronic pernio?
Angiitis:
-thickened arterial walls, -necrosis of paniculus adiposis, -chronic inflammatory reaction of the subcutaneous tissue
Diagnosis of chronic pernio
-chronic erythema
-ulcerating skin
-burn/itch
-red and elevated lesions
-bullae may develop
-hyperpigmentation
Conditions similar to chronic pernio
erythema nodosum:
-spring and fall
-NEVER ULCERATE
-resolve without hyperpigmentation

Idiopathic Nodular Vasculitis
-more painful
-rarely ulcerate
Trench foot/immersion foot
-change in peripheral circulation due to exposure to cold and dampness
-imflammatory reaction
-usually due to exposure to cold water
-mild medial fibrosis of small arteries
3 phases of trench/immersion foot
1. initial vasospastic phase
2. post immersion hyperemia
3. late vasospastic phase
initial vasospasm phase of trench/immersion foot
-ischemia
-pale, cyanotic, cold
-decreased pulses
-edema
-violaceous ulcers may appear
-lesion may be anesthetic
post immersion hyperemia
-after injury during rewarming
-red and hot
-pulses return
-bullae may appear with hemorrhagic or serous fluid
-burning paresthesia
-last 2 weeks
-may develop gangrene with possible bleeding around site
late vasospastic
-further ischemia
-can be prevented
-2 weeks to months after injury
-feet become hyperhydrotic
-extreme sensitivity to cold
-gangrene ensues
treatment of trench/immersion foot
-preserve body heat
-elevate feet and legs
-prevent exercise and trauma
-vasodilators
-amputation
frostbite
freezing of tissue due to cold
Direct frostbite
slow freezing
-extracellular ice crystals
-most common
rapid freezing
-intracellular ice crystals
-rare
-supercooled liquids or metals
indirect frostbite
-vasomotor response to cold
-occurs in later stages of frostbite
-due to AV shunting
4 stages of cold injuries
1. prefreeze
2.freeze-thaw
3. vascular stasis
4. ischemic late phase
prefreeze stage of frostbite
-arteriole vasoconstriction
-venodilation
-leaking of intracellular fluids
freeze thaw phase of frostbite
extracellular ice crystal formation due to ruptured cell membranes

tissue damage is reversible if injury is stopped
vascular stasis phase of frostbite
AV shunting

distal tissue hypoxia
ischemic late phase of frostbite
-prolonged hypoxia and neural damage
-nerve and muscle damage
-muscles swell and necrose
-atrophy of skin
-disappearance of hair follicles/sweat glands
Classification of frostbite: 2 systems
Orr/Fainer: stage 1-4

washburn: superficial/deep
Orr/Fainer Frostbite classification system
stage 1:
-erythema
-edema
-no bullae
stage 2:
-BULLAE
stage 3:
-FULL THICKNESS INJURY and GANGRENE
stage 4:
-COMPLETE NECROSIS and loss of part
signs of good prognosis for frostbite
-clear fluid in bullae
-intact sensation
-pink skin when thawed
bad prognosis in frostbite
-white/cyanotic
-insensate
-hemorrhagic blisters
-muscle necrosis
-gas gangrene
risk factors for frostbite
-low temperature
-long exposure
-moist environment (water conducts 25x faster than air)
-wind chill (temp-2xwind)
-alcohol: vasodilate, increase heat loss
-tight shoes: decrease O2
treatment for hypothermia
rewarm slowly: 1 degree C/hour

avoid rewarming shock- intense vasodilation
treatment of frozen extremity
rapid rewarming with pain meds

100-112F liquid
Treatment of frostbite
-fluids
-possibly abx
-leave hemorrhagic bullae intact
-drain clear bullae
-NWB
-let demarcate
-bone scan
-amputation
5 D's of frostbite
-Deroof bullae
-dressing changes
-debride
-demarcate
-definitive amputation
What is erythermalgia?
painful and erythematous skin without a cause
due to:
-myeloproliferative disorder
-ideopathic
-secondary
Primary or ideopathic erythermalgia
-no associate disease
-rare
-possibly the other disease is not diagnosed
secondary erythermalgia
erythermalgia associated with other disorder

myeloproliferative disords
-polycythemia vera
-thrombocytopenia
5 criteria for erythermalgia
1. burning
2. erethematous
3. pain is intensified with exposure to heat
4. cold relieves pain
5. no response to therapy
common traits of erythermalgia
-usually seen in summer
-middle age patients
treatment of erythermalgia
aspirin

NSAIDS
tourniquet
-arrest cirulation to limb to provide bloodless field
Tourniquet musts
-make sure tourniquet is properly padded (webril)
-exanguanate area first
ankle joint tourniquets
-ABOVE MALLEOLI
-inflate to 100mmHg above systolic BP (approx 250)
calf tourniquet
-risk of sliding down
-difficult to exanguanate
-use if unable to use thigh tourniquet
thigh tourniquet
-inflate 175mmHg above systolic
-apply as high as possible
Tourniquet pressures
ankle: 100mmHg over systolic

thich: 175mmHg over systolic
pneumatic tourniquets
looks like BP cuff, hooked to machine to measure pressure
esmark tourniquet
use to exanguate foot

max pressure 250mmHg
digital tournicot
toe tourniquet
how to exsanguanate
use esmark
elevate
inflate

elevate above heart for 2 minutes or use esmark

don't exanguanate if signs of infection
maximum time limit for tourniquet use
90-120 minutes

perfuse 5 minutes for every 1/2 hour over
risks associated with tourniquet use over 2 hours
mitochondrial damage

poor healing potential
complications of tourniquet use
if pressure is not high enough- only venous drainage will be blocked

calcified arteries cannot be blocked- take off tourniquet so venous drainage occurs

never use bilateral thigh tourniquets- overload heart

increase BP, HR

hypercoaguable state- DVT risk post-op

incresaes acidosis and increased K+ (when released affects heart)

blood vessel damage

thrombophelbitis

thigh tourniquet: damage to lateral femoral cutaneous nerve (myalgia paresthetica)

paralysis
contraindications to tourniquet use
1. hypercoaguability (hormone therapy, previous DVT
2. obese- unable to occlude artery
3. decreased vascularity
4. thrombophelbitis (don't further irritate veins)
5. sickle cell anemia- can cause crisis
vasculitis
inflammation of vessels leading to necrosis
polyarteritis nodosa
small/medium sized arteries

all layers inflamed

nodal aneurysms
allergic granulomatosis
small arteries and veins

lung involvement

eosinophilia
hypersensitivity angiitis
small arteries/veins
history of drug allergy- sulfa
all organs are in the same stage of disease
pathogenesis of vasculitis
unknown
with hepatitis
associated with antitrypsin deficiency
infectious
malignancy
Labs in vasculitis
WBC: increased, granulomatosis, eosinophilia

anemia: normochromic, cytic

increased ESR

increased CRP (c-reactive protein)

quantitative Ig
increased Ig: systemic necrotizing vasculitis
increased IgA: henoch-scholein purpura

renal function: proteinuria, hematuria, red cells

rheumatoid factor: SLE and sceroderma

angiography: saccular or fusiform aneurysms, vessel narrowing

TISSUE BIOPSY: HIGHEST DIAGNOSTIC DETERMINANT
polyarteritis nodosa
only seen on arteriogram

inflammation of small vessels

nodular thickening of vessels

walls of vessels are infiltrated by PMNs: lymphocytes, eosinophils

causes fibrinoid necrosis

vessels will eventually thrombose or form aneurysm

if arterial flow is stopped, necrosis occurs and lesions develop with gangrene

40-60YO, fever, malaise, may appear toxemic from infection

abrupt onset of peripheral neuropathy

cutaneous lesions: nodules, palpable purpura, ulcerations

hemoptysis

wheezing/cough

uclerations, neuropathy

transient arthritis

NECROTIC, FIBROUS ULCERATION, USUALLY NEAR ANKLES, LOOKS LIKE ISCHEMIC AREA
Polyarteritis lab findings
increased ESR
anemia
eosinophilia
proteinuria
arteriogram: aneurysms, narrowed/tapered vessels
EKG: tachycardia
Chest x-ray for possible mass
polyarteritis nodosum prognosis
treat with steroids and immunosuppressives

poor prognosis, but not fatal

lasts days to years
polyarteritis nodosum diagnosis
BIOPSY: SKIN, MUSCLE, NERVE

obscure illness
increased ESR
eosinophilia
allergic granulomatosis
CHURG STRAUSS SYNDROME

ADULT ONSET ASTHMA: seen prior to vasculitis, increased IgE

extravascular granulma

unknown etiology

palpable purpura/nodules
allergic granulomatosis pathology
lung, GI, skin involvment

granulomatosis infiltration of vessels

eosinic infiltration of vessels

small arteries and veins

lumen narrowing

usually die due to MI
allergic granulomatosis labs
EOSINOPHILIA
leukocyte count over 60,000
increased ESR
increased IgE
anemia
Allergic granulomatosis diagnosis
HISTORY OF ADULT ONSET ASTHMA
eosinophilia
biopsy of VESSEL: EOSINOPHILIC INFILTRATES and necrotizing vasculitis
Allergic granulomatosis treatment
steroids

immunosuppressants