Diff Diag exam 1

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

• thermal
• chemical
• electrical
• radiation

flame, hot liquids, hot object, steam, semisolids(tar)

• severity depends on location of the
• burn, temperature of the burn source, duration of contact

tissue contact or ingestion, inhalation, or injection of strong acids, alkalis or organic compounds-household cleaning agents, military, industry, agriculture

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. 

least common, except sunburn

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

Risk of infection

Risk of mortality

• Risk of cosmetic or functional
• disability

Burn depth

Burn size

Location

Age of patient

General health

Mechanism of injury

• Divided by elements of the skin
• that are damaged

New terminology is:

-Superficial

-Superficial partial thickness

-Deep partial thickness

-Full thickness

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

modification of Rule of Nines- and makes modification for body size for kids and tends to be done after debridement

localized response

• 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

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

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

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

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

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

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

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

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

Everything is damaged to sub-dermal tissue

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

White-ischemia

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

worse part of the burn

located in the center of the burn

area of greatest damage contains non-viable tissue(eschar)

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

Kids- under 10

Elderly (over 50)

Everyone over 20% TBSA

Full think burn over 5% TBSA

people complicated cases

• ALL INCREASE GLUCOSE LEVELS
• 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

no insulin- late stage of type 1

too little insulin- beginning of type 1

unable to use insulin- type 2

• -Cells unable to use glucose for energy.
• -Protein and fat metabolism also affected.
• -Blood glucose levels go up.

• -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

• Polyuria
• Polydipsia
• Polyphagia
• Weight loss
• Vision changes
• Dry skin

• -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

• 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

Two fasting blood sugar levels > 126

One random blood sugar level > 200

BG > 140 fasting, > 180 pp

• Untreated, leads to :
• -DKA (Type 1)
• -Hyperosmolar Non-ketotic Syndrome (Type 2)

• TYPE 1 ONLY 
• Slow Onset
• Thirst
• Excessive Urine
• Acetone In Urine
• Acetone Breath (sweet smelling breath)
• Dry Skin
• Vomiting
• Abdominal Pain
• BG>240 + ketones

85% of lower extremity amputations preceded by foot ulcers

sensory loss + mechanical stress +/- PAD = 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 

most common complication of diabetes

symmetrical-- affects distal nerves first

• ➢ Sensory loss occurs gradually and is
• painless
• ➢ Patients may be unaware
• ➢ Paresthesias
• ➢ 5.07 Semmes-Weinstein
• monofilament=10 grams of pressure
• =protective sensation

• 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

• Alterations in
• ● Sweating mechanisms (hydration)
• ● Callus formation
• ● Blood flow (vasomotor regulation)

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

• 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

• 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

• •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

Usually starts where the arteries bifurcate 

affects ELASTIC and muscular vessel

Progressive

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

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

• too much blood supply
• valve failure
• varicosity
• peripheral edema