Diff Diag exam 1

  1. Burns- definition
    thermal destruction of skin from direct contact or exposure to a source

    Depth is function of temperature or source of energy and duration of exposure
  2. type of burns
    • thermal
    • chemical
    • electrical
    • radiation
  3. Thermal
    flame, hot liquids, hot object, steam, semisolids(tar)

    • severity depends on location of the
    • burn, temperature of the burn source, duration of contact
  4. chemical
    tissue contact or ingestion, inhalation, or injection of strong acids, alkalis or organic compounds-household cleaning agents, military, industry, agriculture
  5. electrical
    heat generated by resistance of the body tissue to the current

    Electrical burns are really damaging b/c they can affect the nerves and damage the organs and stuff that you cannot see on the inside besides just what you can see on the outside. 
  6. radiation
    least common, except sunburn
  7. Epidemiology
    Highest for children< 4 y.o. and adults>65y.o.

    Peak incidence children 1-5 y.o.- scald burns--pull something off a high surface and it lands on them

    Adults- men ages 16-40---flammable liquids

    house fires 85% of deaths-- more due to smoke exposure
  8. Severity of burns assessed with:
    Risk of infection

    Risk of mortality

    • Risk of cosmetic or functional
    • disability
  9. Factors affecting severity:
    Burn depth

    Burn size


    Age of patient

    General health

    Mechanism of injury
  10. Burn depth
    • Divided by elements of the skin
    • that are damaged

    New terminology is:


    -Superficial partial thickness

    -Deep partial thickness

    -Full thickness
  11. Rule of 9's
    Can give an over estimate of burn wound size

    its how to determine size of wound and used in ED b/c fast and easily recognized and tends to over estimates the size of the wound and determines if the pts needs to sends pts to burn center
  12. Lund-Brower
    modification of Rule of Nines- and makes modification for body size for kids and tends to be done after debridement
  13. Pathogensis- small burns
    localized response
  14. Pathogenesis- extensive burn
    • Cardiovascular- 
    • BP drops- capillary permeability so fluid leaks out– the thin stuff leaks out so only thick stuff is left so more likely to gets clots since its so viscous
    • -Shock sets in
    • -Edema
    • -HR increases
    • -Organ death due to clot that can form
    • Metabolic
    • -Loosing protein from fluid loss but you need protein to rebuild muscles, skin and tissues
    • Renal System
    • Rhabdo
    • GI system
    • Immune System
    • Respiratory System
  15. Scald Burns
    Scald burns tend to be deep partial or full thickness because with immersion it is harder to get out of the hot liquid harder so you are exposed longer so increase contact time
  16. Thermal- Flame Burns
    occur due to flame exposure from fire or flammable liquids, or ignition of clothing

    often causes superficial and deep partial-thickness burns

    may also result in carbon monoxide poisoning
  17. Thermal- Flash Burns
    Damage to upper airway b/c tend to gasp when you are exposed 

    occur due to the explosion of flammable liquid such as gasoline or propane

    often results in partial-thickness burns or superficial

    burns distributed over all exposed skin
  18. Electrical Burns
    type of current

    AC more dangerous than DC

    • -DC causes convulsive contraction that
    • forces the victim away from the source

    -AC produces tetany which holds the victim to the source

    entrance wound-often small, necrotic, and depressed area

    • exit wound-single wound or multiple wounds
    • located where the victim was grounded during injury-may be explosive and necrotic
  19. Chemical burns
    pulmonary complications

    • bronchospasm
    • -airway obstruction
    • -pulmonaryedema

    • metabolic complications
    • -liver necrosis, renal dysfunction

    • tissue death can progress slowly for
    • many hours after the burn
    • -may take 72 hours to determine full
    • extent of the damage
  20. Superficial Burns
    Sun burn or minor flash burn

    Minor exposure

    Epidermis effected only

    Dry, bright red or pink skin, blanches under pressure, no edema, no blisters, generally heals in 3-5 days s scarring,

    Redness  from underlying blood vessels might not appear until next day

    Nerves are not damaged so painful
  21. Superficial Partial-Thickness Burn
    Epidermis and top layer (papillary layer) of dermis is affected

    Severe sun burn, long duration sun burn, brief contact burns c dilute chemicals or brief contact burns c surfaces

    Blisters, leaking skin, moist, edema, and localized erythema, blanched under pressure, rapid capillary refill, extremely painful due to exposed nerve endings, drainage, tend to heal in 10-14 days with minimal to no scarring, slight pigment changes
  22. Deep Partial-Thickness Burn
    Deeper layer of dermis damaged

    Exposure to hot liquids or objects, flash burns, chemical burns,

    Damage to dermal vessels, modeled areas of white and red skin (eschar), no blisters ( no skin to blisters)

    Some nerve ending maybe intact

    Blanching but sluggish capillary refill

    Decreased pin prick sensation but deep pressure might be intact

    If not managed appropriately can become full thickness wound

    Heals in 3-8 weeks, scarring and pigment changes, hypertrophic scarring is likely and contractures is possible
  23. Full Thickness Burn
    Everything is damaged to sub-dermal tissue

    Initially red- but then changes to model white, grey or black


    Takes a long time to heal

    Likely take surgical debridement- likely makes hypertrophic scarring and contractures (decrease ROM- due to contracting of skin)

    Not painful- because there is no nerves left but can be itchy afterwards
  24. Zone of Coagulation
    worse part of the burn

    located in the center of the burn

    area of greatest damage contains non-viable tissue(eschar)
  25. Zone of stasis
    can be turned into zone of coagulation if not treated correctly (splint to tight, gait belt to tight etc)

    surrounds the zone of coagulation and contains marginally viable tissue
  26. Who goes automatically to a burn center
    Kids- under 10

    Elderly (over 50)

    Everyone over 20% TBSA

    Full think burn over 5% TBSA

    people complicated cases
  27. Hormones affecting glucose metabolism
    • epinephrine- adrenal medulla- part of ANS- fight or flight

    • glucocrticoids- cortisol- surge in the morning- precursor is cholesterol
    • aldosterone- sodium reabsorption into kidneys

    progesterone, HCS

    Growth hormone
  28. Clinical syndrome of diabetes
    no insulin- late stage of type 1

    too little insulin- beginning of type 1

    unable to use insulin- type 2
  29. metabolic challenge of diabetes
    • -Cells unable to use glucose for energy.
    • -Protein and fat metabolism also affected.
    • -Blood glucose levels go up.
  30. Etiology of type 1
    • -Autoimmune (most common)
    • (viral influences)
    • -Idiopathic (increased in African
    • American and Asian pop.)
    • - Requires INSULIN injections to live
    • -Ketones
    • -Greatest risk for siblings and children of
    • people with Type 1
  31. Symptoms of type 1
    • Polyuria
    • Polydipsia
    • Polyphagia
    • Weight loss
    • Vision changes
    • Dry skin
  32. characteristics of type 2
    • -Family members with Type 2 diabetes
    • -Greatest risk at 45*
    • -Overweight (80% of patients)
    • -Previous GDM
    • -Drug induced (secondary)
    • -Insulin resistance
    • -Ketones rare
    • *Incidence increasing in children
  33. symptoms of type 2
    • Any of the symptoms of Type 1
    • Frequent and/or recurring infections
    • Blurred vision
    • Slow healing of cuts and bruises
    • Tingling and numbness in hands or feet
    • Muscle cramps
    • Ketones are rare
  34. Diagnosis of diabetes
    Two fasting blood sugar levels > 126

    One random blood sugar level > 200
  35. hyperglycemia
    BG > 140 fasting, > 180 pp

    • Untreated, leads to :
    • -DKA (Type 1)
    • -Hyperosmolar Non-ketotic Syndrome (Type 2)
  36. DKA ( diabetic ketoacidosis)
    • TYPE 1 ONLY 
    • Slow Onset
    • Thirst
    • Excessive Urine
    • Acetone In Urine
    • Acetone Breath (sweet smelling breath)
    • Dry Skin
    • Vomiting
    • Abdominal Pain
    • BG>240 + ketones
  37. Diabetic Foot Disease Epidemiology
    85% of lower extremity amputations preceded by foot ulcers
  38. Etiology
    sensory loss + mechanical stress +/- PAD = Ulceration
  39. mechanical stress that leads to ulceration
    Low pressure ischemia- squeezing toes into high heels-- cuts off circulation but they dont feel the pain and leave shoes on 

    Shear- internal forces causing rubbing on wound

    Direct injury- injury caused by something going directly into foot

    Moderate repetitive stress- walking

    never walk barefoot if you dont have sensation of the foot 
  40. Neuropathy
    most common complication of diabetes

    symmetrical-- affects distal nerves first
  41. sensory neuropathy
    • ➢ Sensory loss occurs gradually and is
    • painless
    • ➢ Patients may be unaware
    • ➢ Paresthesias
    • ➢ 5.07 Semmes-Weinstein
    • monofilament=10 grams of pressure
    • =protective sensation
  42. motor neuropathy
    • Paralysis of intrinsic muscles= muscle
    • imbalances
    • ➢ Decreased ROM and deformity
    • ➢ Increases plantar pressures and shear
    • forces
    • ➢ Loss of intrinsic function-foot less stable
    • during stance

    • hallux valgus (bunion), claw toe deformities
    • met head more prominent--more pressure in WTB
  43. Autonomic Neuropathy
    • Alterations in
    • ● Sweating mechanisms (hydration)
    • ● Callus formation
    • ● Blood flow (vasomotor regulation)
  44. Wagner Classification of Diabetic Foot Ulcers
    Grade 0-5

    • 0- no ulcer in a high risk foot
    • 1- superficial ulcer
    • 2-3--increasing sevrity
    • 4- localized gangrene
    • 5- gangrene of whole foot
  45. 5PT method
    • Pain
    • Position- where on foot
    • Presentation- rim of callus, eschar, drainage
    • Periwound- dry cracked skin, callus build up plantar aspect, structural deformities, vasodilation
    • Pulses-
    • Temperature- local area of increase temp may signal future ulceration or deep space infection
  46. DFU risk categories for PT
    • 0 - no loss of protective sensation
    • 1-loss of protective sensation
    • 2-loss of protective sensation + deformity or decrease circulation
    • 3- all of above +history of or/ active DFU or charcot foot

    • 1- go in 3-6 months
    • 2- go in every 1-3 month and recommend modified shoes and orthotics
    • 3- go in weekly for foot checkds
  47. Arterial Ulcers
    • •decrease in arterial blood supply
    • •Causes:
    • –Trauma
    • –Acute embolism
    • –Thromboangitis (Beurger’s
    • disease)•Seen in young adults who smoke heavily
    • –Arteriosclerosis (thickening and hardening of arterial
    • walls) •Main cause

    • more common distally
    • not much drainage
  48. Atherosclerosis
    Usually starts where the arteries bifurcate 

    affects ELASTIC and muscular vessel


    Intermittent claudication
  49. Intermittent claudication
    –Activity specific discomfort

    –Local ischemia

    –Stops within 1-5 min of ceasing the activity

    –Usually have at least 50 % occlusion

    –Cramping burning or fatigue
  50. Ischemic Rest Pain
    Progression from IC

    Exacerbated at night with elevation (even in neutral)

    circulation is so poor that gravity has effect on tissue perfusion

    revascular surgery is best option

    hot pack proximally in femoral triangle to increase distal circulation then they can participate in PT
  51. Venous Ulcer
    • too much blood supply
    • valve failure
    • varicosity
    • peripheral edema
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Diff Diag exam 1
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