Photodermatoses, Mucocutaneous Reactions, Cold Injuries Flashcards
Photosensitivity
- abnormal response to UV radiation or visible light
- diagnosis made primarily from history and physical exam
- skin biopsy may be useful in some cases
Sunburn Characteristics
- exposure to excessive UVA and UVB causes inflammatory response in the skin
- clinical manifestations include painful erythema and blistering
- erythema noted 3-5 hours post-exposure, peaks at 12-24 hours, subsides at 72 hours
Sunburn Prevention
- limit sun exposure in summer between 10 and 4 pm
- protective clothing like long sleeves and hats
- broad spectrum sunscreen with SPF 30+, reapply every 2 hours
- infants younger than 6 months avoid sun exposure
Sunburn Treatment
- self limiting condition
- may require hospitalization if pain and blistering severe
- topical agents like aloe vera and cool compresses may help discomfort
- oral OTC analgesics (tylenol/ibup)
Polymorphous Light Eruption (PMLE)
- sun poisoning or sun allergy
- papulonodular lesions symmetrically distributed on sun-exposed skin
- pruritic
- angular chelitis is a distinguishing characteristic
- there is a genetic component
- treat: sun avoidance, topical/oral corticosteroids, phototherapy
Phototoxicity
- results from cellular damage following sun exposure when taking a precipitating compound (including sulfonamides, NSAIDS, tar compounds)
- endogenous causes: lupus, porphyria (rare blood disorder), dermatomyositis
Stevens Johnson Syndrome
- dermatologic emergency
- skin detachment is < 10% of BSA
- mucous membranes affected in > 90% of patients
- usually 2 different mucous membranes at one time (ocular, oral, genital)
Toxic Epidermal Necrolysis
- dermatologic emergency
- same as Stevens Johnson, but more severe
- detachment of >30% of BSA
Stevens Johnson/Toxic Epidermal Necrolysis Clinical Appearance
- prodrome of fever and flu like symptoms 1-3 days
- coalescing erythematous macules
- vesicles and bullae on skin and mucous membranes then skin sloughing
- lesions begin on face and trunk then spread rapidly
- palms and soles become erythematous, painful and swollen
- positive Nikolsky sign: gentle pressure on skin results in blister formation
Stevens Johnson/Toxic Epidermal Necrolysis Triggers
- medications: allopurinol (gout), anticonvulsants, sulfonamides, NSAIDS
- infections: mycoplasma, CMV (cytomegalovirus)
Stevens Johnson/Toxic Epidermal Necrolysis Complications
- shock
- hypotension
- renal and respiratory failure
- corneal ulcerations, ocular scarring, blindness
- vulvovaginitis or balanitis
Stevens Johnson/Toxic Epidermal Necrolysis Treatment
- discontinue the causative agent (if a medicine)
- referral to burn center is necessary
- treatment similar to major burn: fluid resuscitation, wound care, prevention/treatment of infection
Populations Most At Risk of Cold Injuries
- winter athletes
- mountaineers
- military personnel
- elderly
- homeless
- employed in the cold
What can cause frostbite?
- environmental exposure to cold
- direct exposure to freezing materials, eg ice packs applied to musculoskeletal injuries
- inhalation of hydrocarbons (frostbite of upper airway)
What areas of the body are most sensitive to cold injuries?
-hands, feet, face (nose and cheeks), ears
- Frostnip
2. Immersion Foot/Trench Foot
- pre-frostbite; cold-induced, local paresthesias that resolve with rewarming; no ice crystals formed in the cells
- injury to sympathetic nerves and vasculature of the feet; feet are red, edematous, numb or painful and covered with hemorrhagic bullae
Pernio (Chilblain)
- results from acute or repetitive exposure to damp cold above the freezing point
- lesions are edematous, red/purple, and may be painful or pruritic
- exposure to cold causes vasoconstriction of small blood vessels
Frostbite
- tissue cooling with vasoconstriction and ischemia; cooling of nerves causes paresthesia or hyperesthesia
- ice crystals form in ICF and ECF; causes abnormal electrolyte balance, cell dehydration, lysis and death
- thawing process initiates an inflammatory response which causes progressive tissue ischemia, emboli within microvessels and thrombi in larger vessels
Clinical Appearance of Frostbite
- patients complain of cold, numbness, and clumsiness of the area
- skin is insensate, white or gray in color and hard or waxy to the touch
- bullae may develop upon rewarming
Frostbite Diagnosis
- largely clinical
- look for other co-morbidities
- diagnostic studies not needed, but do help later when considering surgical options
1st Degree Frostbite
- superficial
- central area of pallor and anesthesia of the skin surrounded by erythema
- no tissue infarction
2nd Degree Frostbite
- large blisters containing clear fluid surrounded by edema and erythema
- develops w/in 24 hours of rewarming
- extends to the tips of digits
- no tissue loss
3rd Degree Frostbite
- injury deeper than 2nd degree
- blister are hemorrhagic and more proximal
- skin forms a black eschar in one week+
4th Degree Frostbite
- extends to muscle and bone
- complete tissue necrosis
Pre-Hospital Frostbite Treatment
- do not walk on frostbitten feet if possible; walk on frozen feet
- splint or pad frozen extremities
- do not rewarm frostbitten tissue if there is a chance of freezing again (increases tissue damage)
- do not rub areas to rewarm (increases tissue damage)
Hospital Frostbite Treatment
- rewarming by placing affected area in water 37-39C; it is painful; higher temps will not warm it faster
- rewarming by ambient heat (fire, oven) less consistent and may cause a burn
- air dry the tissues or gently blot dry to prevent further damage
- thawing is usually complete when tissue is red or purple and soft to the touch
Frostbite Wound Care
- apply nonstick gauze to area covered with sterile fluff dressing
- elevation of extremity to reduce edema
- blisters: management is controversial; debride nonhemorrhagic; drain hemorrhagic but do not debride
- tetanus prophylaxis
- topical antibiotics increase maceration and should be avoided
Frostbite: Thrombolytic Therapy
- goal is to save tissue from microvascular thrombus
- tissue plasminogen activator use w/in 24 hours of thaw may benefit
- for use in deep injuries with potential for serious morbidity
Complications of Frostbite
- infection, gangrene, autoamputation
- ischemic neuritis - very painful
- long term hypersensitivity to cold: cold exposure contraindicated for 6 months after minor, 12 months after major injury
Amputation with Frostbite
- complete demarcation of tissue injury may take 1-3 months
- angiography, MRI, technetium-99 bone scan may be used to determine surgical margins
- amputation may take place after definitive demarcation if no signs of sepsis
List the 5 mechanisms by which body heat is lost to the environment.
- radiation
- conduction
- convection
- evaporation
- respiration
Hypothermia - General Info
- normal set point for human core temp is 37C
- body, in response to cold stress, stimulates heat production through shivering and increased catecholamines
- body also vasoconstricts vessels in the peripheral tissues to prevent conductive heat loss
Hypothermia Causes
- dermal diseases: burns, exfoliative dermatitis
- drug induced: ethanol, sedatives
- environmental
- iatrogenic: aggressive fluid resus, heat stroke Tx
- metabolic: hypothyroid, hypoadrenal
- neurologic: acute spinal cord transection, head trauma
- neuromuscular inefficiency: extreme age, impaired shivering, lack of acclimatization
- sepsis
Mild Hypothermia
- initial excitation phase to combat cold: HTN, shivering, tachycardia and tachypnea, vasoconstriction
- with time and onset of fatigue: apathy, ataxia, cold diuresis, impaired judgment
Moderate Hypothermia
- atrial dysrhythmias
- decreased HR, RR, BP
- decreased LOC
- dilated pupils
- no shivering
- hyporeflexia, decreased gag reflex
- J wave on EKG
- paradoxical undressing
EKG Changes with Hypothermia
- baseline artifact from shivering
- J waves (Osborne waves): a positive deflection at the J point; height of J point is roughly proportional to degree of hypothermia
- bradycardia
Severe Hypothermia
- apnea
- coma
- nonreactive pupils
- oliguria
- pulmonary edema
- minimal to no activity on EEG
- ventricular dysrhythmias/asystole
Temperature Monitoring for Frostbite Patients
- accurate temp monitoring essential
- rectal probe thermometer
- temporal therms are not accurate for hypothermia
- esophageal is most accurate
- bladder and rectal not accurate b/c they lag behind core temp
Passive External Rewarming
- used for mild hypothermia
- patient’s cold/wet clothing is removed and pt is covered with blankets or other types of insulation
- reduction in heat loss combined with pt’s intrinsic heat production produces rewarming
- pt must have intact thermoregulatory mechanisms, normal endocrine function, and adequate energy store to create endogenous heat
- warm the trunk before extremities
Active External Rewarming
- used for moderate to severe or those who fail passive external rewarming
- application of heat directly to the skin
- effective only if there is intact circulation that can return peripherally rewarmed blood to the core
Risks of Active External Rewarming
- afterdrop: cold peripheral blood rapidly returns to the heart; minimize the risk by also using minimally invasive core rewarming
- rewarming acidosis: cold, acidemic blood in extremities moves into the trunk, dropping core temp and pH
Active Internal/Core Rewarming
- most aggressive strategy
- for patients with severe hypothermia
- warm IV fluids: saline with dextrose heated to 40-45C
- warmed humidified oxygen: warmed to 40C
- extracorporeal blood warming: accomplished by cardiopulmonary bypass; most effective method; increase core temp 1-2C every 3-5 minutes
Hypothermia-Associated Abnormalities
effects on other conditions, normal physiology
- cardiac arrhythmias (v fib)
- insulin ineffective below 30C
- hematocrit increases 2% for each 1C drop
- rewarming associated w/ unpredictable changes in electrolytes
- inhibition of clotting factors