Jv is the volume of fluid that crosses the microvasculature barrier.
Kf is the capil ary filtration coefficient, which is the product of the surface area
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and hydraulic conductivity of the capil ary wal
Pc is the capil ary hydrostatic pressure
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Pif is the interstitial fluid hydrostatic pressurep is the colloid osmotic pressure of plasma
if is the colloid osmotic pressure of interstitial fluid
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is the osmotic reflection coefficient.
Edema occurs when the lymphatic drainage (JL) does not keep pace with the
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increased JvLandis Starling Equation
Skin Biology & Response to Burns
Epidermis
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? Derived from ectoderm so is capable of
regenerative healing.
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? Keratinocytes proliferate from dermalappendages leading to re-epithelialization.
? Depleted melanocytes regenerate slowly
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leading to pigmentary changes
? Loss of anchoring collagen fibrils (type7) leads
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to blister formationSkin Biology & Response to Burns
Dermis
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? Superficial papil ary? Deep reticular
? Fibroblasts produce col agen fibrils and elastic
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fibers
? Dermal appendages lined by keratinocyte derived
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epidermal cel s? Contain capil ary plexus and sensory nerves
? Derived from mesoderm so heal by scarring
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Patho-phyisological changes
Jackson Zones
? Temperature and duration of contact have a
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synergestic effect
? 1s at 69OC / 1 hour at 45oC
? Zone of coagulation? Centre of the wound
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? Zone of stasis ? At risk area with mix of viableand non viable cel s along with vasoconstriction
? Zone of hyperemia- Viable cel s with vasodialtion
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? Protection of zone of stasis is achieved withadequate fluid resuscitation, avoidance of
vasoconstrictors and prevention of infection
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Depth of Burn
1st Degree
? Burns involving only the epidermis.
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? Erythematous and very painful but do notform blisters.
? Sunburns fit this category of superficial,
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epidermal injury.
? Within 3?4 days, the dead epidermis sloughs
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and is replaced by regenerating keratinocytes.2nd degree (Superficial dermal burns)
? Extend into the papil ary dermis and characteristical y
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form blisters.? Appearance is pink, wet and hypersensitive to touch.
? Painful as uncovering the wound al ows currents of air
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to pass over it.
? These wounds blanch with pressure as the blood flow
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to the dermis is increased due to vasodilation.? Superficial dermal burns usual y heal within 2?3 weeks
without risk of scarring and therefore do not require
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operation.
3rd degree (Deep Dermal Burns)
? Extend into the reticular dermis and general y wil take
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3 or more weeks to heal.
? They also blister, but the wound surface appears
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mottled pink and white? The patient complains of discomfort and pressure
rather than pain.
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? When pressure is applied to the burn, capil aries refil
slowly
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? Partial-thickness burns that are predicted not to healby 3 weeks should be excised and grafted.
4th Degree (Ful Thickness)
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? Ful -thickness burns involve the entire dermis andextend into subcutaneous tissue.
? Their appearance may be charred, leathery, firm, and
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depressed when compared to adjoining normal skin.
? These wounds are insensitive to light touch and
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pinprick.? Non-charred ful -thickness burns can be deceptive as
they may have a mottled appearance
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? Must be excised and grafted early
SCALD INJURY
Scald Injury
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? The depth of scald injury depends on the watertemperature, the skin thickness and the duration of
contact.
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? Boiling water often causes a deep dermal burn, unless
the duration of contact is very short.
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? Soups and sauces, which are thicker in consistency, wilremain in contact longer with the skin and invariably
cause deep dermal burns.
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? Exposed areas tend to be burned less deeply than
clothed areas.
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? Clothing retains the heat and keeps the liquid incontact with the skin longer.
Scalds are a mosaic of dermal burns
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? A common example is a toddler who reaches
above head level and spills hot water on
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himself. His face bears a superficial burn, histrunk burn is of indeterminate thickness, and
his skin under his diaper has a deep dermal
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burn.
Immersion Scalds
? Immersion scalds are often deep because of the
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prolonged skin exposure.
They occur in individuals who
? Cannot perceive the discomfort of prolonged
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immersion (i.e. a diabetic patient soaking his foot
in hot water)
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? Those who are not able to escape from the hotwater (i.e. young children, the elderly, or people
with physical and cognitive disabilities).
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Atypical Scalds? Grease and cooking oils cause deep dermal and
full thickness injuries
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? Tar and asphalt are `special scald' injuries
because they have to be first removed before the
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depth of wound can be assessed? Tar can be removed by application of petroleum-
based ointment under a dressing.
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? The dressing is changed and ointment reapplied
every 2?4 h until the tar has dissolved
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RADIATION BURNRadiation Injuries
? Damage to biological tissue by ionizing
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radiation is due to1) Electromagnetic radiation (e.g. X-rays and
gamma rays)
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2) Particulate radiation (e.g. alpha and beta
particles or neutrons).
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? The severity of tissue damage is determinedby the energy deposited per unit track length,
known as Linear Energy Transfer (LET).
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How to measure Radiation Injury
? Electromagnetic radiation passes through tissue
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almost unimpeded by the skin and are cal ed lowLET since little energy is left behind.
? Neutron exposure has high-LET, resulting in
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significant energy absorption within the first few
centimeters of the body.
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? Alpha and low-energy beta particles do notpenetrate the skin, and represent a hazard only
when internalized by inhalation, ingestion or
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absorption through a wound.
How to measure Radiation Injury
? The biological effect of radiation is measured by rad
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( Radiation Absorbed Dose)
? 1 Gy= 100 rad
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? Is 1Gy of X Ray = 1 Gy of Neutron?? rem(Roentgen Equivalent Man)= dose in
rads*Quality Factor(QF)
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? QF takes into account linear energy transfer so
QF for X ray=1 & neutron=10
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? 1 (Sv) Seivert= 100 rem? So now 1Sv of X ray= 1Sv of neutron
Incidence of radiation injury
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The majority of radiation accidents are from
1) Radiation devices such as accelerator
2) Highly radioactive sources used for industrial
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radiography.3) Radioisotope accidents involving radioactive
materials which are unsealed, such as tritium,
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fission products, radium and free isotopes
used for diagnosis and therapy.
How does Radiation Injury Occur?
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Radiation accident is defined as
? Whole body doses >25 rem (0.25 Sv)
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? Skin doses > 600 rem (6 Sv)? Absorbed dose > 75 rem (0.75 Sv) to other tissues
or organs from an external source
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? Internal contamination >one-half the maximum
permissible body burden (MPBB) as defined by
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the International Commission on Radiological Protection( different for each radionuclide)
Radiation Effect
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? Ionizing radiation causes formation of free
radicles which injure DNA, nuclear and cel ular
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membrane? Cel s are most sensitive when undergoing mitosis
so that those that divide rapidly such as bone
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marrow, skin and the gastrointestinal tract are
more susceptible to radiation damage.
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? Radiation to an organ such as brain or liver, whichhas parenchymal cel s with a slow turnover rate,
results in damage to the more sensitive
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connective tissue and microcirculation.
Localized Injury-Skin
? Erythema is equivalent to a first-degree thermal
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burn and occurs in two stages.
1) Mild erythema appears within minutes or hours
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fol owing the initial exposure and subsides in 2?3 days.
2) The second onset of erythema occurs 2?3 weeks
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after exposure and is accompanied by dry
desquamation of the epidermal keratinocytes.
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? Epilation may occur as soon as 7 days post injury.? It is usual y temporary with doses less than 5 Gy
but may be permanent with higher doses.
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Localized Injury-Skin
? Moist desquamation is equivalent to a second-
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degree thermal burn and develops after a latentperiod of about 3 weeks with a dose of 12?20 Gy.
? The latency period may be shorter with higher
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doses.
? Blisters form, which are susceptible to infection if
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not treated.? Full-thickness skin ulceration and necrosis are
caused by doses in excess of about 25 Gy
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ARS? Physiological effects of whole-body radiation are
described as the acute radiation syndrome (ARS).
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? Prodromal symptoms include nausea, vomiting,
diarrhea, fatigue, fever and headache.
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? There then fol ows a latent period, the durationof which is related to the dose.
? Hematopoietic and gastrointestinal complications
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fol ow this.
ARS
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Three Sub Syndromes of ARS-? Hematopoietic syndrome
Opportunistic infections result from the granulocytopenia and
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spontaneous bleeding results from thrombocytopenia.
? Gastrointestinal syndrome
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Epithelial damage results in loss of transport capability, bacterialtranslocation with sepsis, bowel ischemia and bloody diarrhea.
? Neurovascular syndrome
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Due to endothelial injury there is release of NO and other vasodilator
mediators.
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This leads to neurological symptoms, respiratory distress,cardiovascular collapse and death.
Treatment
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? First aid (airway, breathing , circulation)? Irrigation with running water until Geiger Muller
counter shows minimum radiation count
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? Exposures >100 rem require full evaluation inhospital.
? Patients with exposures >200 rem or who have
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symptoms of ARS should preferably be sent to
specialist centers with facilities to treat bone
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marrow failure.Treatment..
? Burn wound is managed as per the depth of
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wound
? Pain is severe and can be treated by opiates
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? Radiation injury causes severe nausea andvomiting which can be managed by
ondensetaron ( safe in children)
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? Diethylene triamine pentaacetic acid (DTPA)
and intravenous administration of DTPA for
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workers exposed to plutoniumFROSTBITE
Frostbite
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? Traumatic injury caused by the failure of normalprotective mechanisms against the thermal
environment, resulting in local tissue
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temperatures fal ing below freezing
? At risk populations are
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Mental y ilHomeless
Alcohol and Drug Intoxications
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Wilderness activities( Treking /Camping)
? Acral areas are typical y affected
Pathophysiology
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Direct Cellular Damage
? Intracel ular formation of Ice crystals
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D/t rapid cooling and leads to severe cel injuryHistamine release occurs which causes flushing and
formation of blisters
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? Extracel ular formation of Ice crystals
D/t slow cooling and leads to injury to cel
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membraneLeads to gradual dehydration of cel as osmotic
imbalance occurs
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Pathophysiology
Microvascular Occlusion
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? Cold injury causes vasoconstriction? With rewarming capil ary blood flow resumes but
with presence of microemboli
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? Certain areas close to injury wil have complete
cessation of blood flow within 20 min
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? The remaining area is at risk due to endothelialinjury and accumulation of inflamatory mediators
similar to Jackson Model
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Classification? First-degree injury
It is superficial, without formation of vesicles or blebs.
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There may initial y be an area of pal or with surrounding erythema.
? Second-degree
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Partial dermal involvement with general y favourable prognosisAssociated with light-colored blisters and subsequent epidermal
sloughings.
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? Third-degree
Has dark or hemorrhagic blisters that evolve into thick, black eschar
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over 1?2 weeks.? Fourth-degree
Injury involves bone, tendon or muscle and uniformly results in tissue
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loss.
Management
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? Rewarming in the field should not be pursuedunless the ability to maintain the affected tissue
in a thawed state is certain
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? Injured areas should be mechanical y protected
from trauma because they are typical y insensate
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and are at high risk for further injury? Management of Hypothermia (Temp<32) should
be started before Management of frostbite
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Management? Rewarming is done with the help of water
bath at temperatures of 40- 42oC
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? Duration of rewarming is usually 30 min
? Clinically until sensation returns and flushing
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in the most distal part of tissue? Blisters may be debrided as they help in
assessment of the deeper tissue
--- Content provided by FirstRanker.com ---
? Blisters contain high amount of PGF2Aalpha
&TXA2
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Non Surgical Management? Systemic NSAIDs and topical aloe vera to
address the inflammatory chemokines
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coupled with systemic penicillin as prophylaxis
against Gram-positive infection
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? Pentoxifylline improves red blood cellflexibility, which may limit microvascular
sludging and thereby diminish thrombus
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formation in small vessels.
Role of Thrombolytics
? Use of Thrombolytic therapy can enhance survival
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of digits
? t-PA only appears to be efficacious within 24
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hours of thaw, meaning that this may not be anoption for patients who are injured in extremely
remote environments.
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? Additional y, although digit salvage has been
improved with thrombolytics, the actual long-
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term functional results of this salvage have notbeen documented.
HBO
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? Studies of hyperbaric oxygen are limited but
have some of the most promising functional
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results of an adjunctive therapy for frostbite.? One of the early documented uses of HBO for
therapy in frostbite involved four Alpine
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mountaineers, all of whom presented 10 or
more days following injury and all of whom
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demonstrated good tissue preservation withHBO
Management
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? Prevalent clinical practice remains to timesurgery anywhere from 4 weeks to 3 months
following injury, once tissues have clearly
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demarcated to an experienced clinical eye.
CHEMICAL BURNS
Chemical Burns
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? The 3D structure of biological proteins depends
on hydrogen bonding and weak Van der wal s
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forces? Chemicals substances can destabilize a protein
and alter its function by changing the pH or
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dissolving the lipids thus altering the hydrogen
bonding
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? Thermal injury also occurs by breaking thehydrogen bonds and causing protein
denaturation
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Severity of Chemical Burn
? Quantity of Chemical Agent
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? Concentration of Chemicals? Manner and Duration of skin contact
? Extent of penetration
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? Mechanism of action
Mechanism Of Action
1.Reduction: Act by binding free electrons in tissue proteins, causing
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denaturation.
Eg Alkyl mercuric compounds, Ferrous iron, and Sulphite compounds.
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2. Oxidation: Oxidizing agents are oxidized on contact with tissueproteins. Byproducts are often toxic and continue to react with the
surrounding tissue.
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Eg Sodium hypochlorite, Potassium permanganate, Peroxide.
3. Corrosive agents: Corrosive substances denature tissue proteins on
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contact and form eschar and a shal ow ulcer.Eg. Phenols, Cresols, White phosphorus, sodium metals, lyes,
sulphuric acid, and hydrochloric acid, Alkalis .
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Mechanism Of Action
4. Protoplasmic poisons: These agents produce their
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effects by binding or inhibiting calcium or other organic ions necessaryfor tissue viability and function.
Eg. Acetic acid, Formic acid, Oxalic, Hydrofluoric, and hydrazoic acid.
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5. Vesicants: Vesicant agents produce ischemia with necrosis at the
site of contact.
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Eg. Mustard gas (sulphur and nitrogen), and Lewisite.6. Desiccants: cause damage by dehydrating tissues and exothermic
reactions causing the release of heat into the tissue.
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Eg. Calcium sulphate , Silica gel
Alkalis more dangerous than Acids
? Acids cause coagulation necrosis with
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precipitation of protein, whereas the reaction
to alkali is `liquefaction' necrosis allowing the
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alkali to penetrate deeper into the injuredtissue.
? The presence of hydroxyl ions within these
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tissues increases their solubility, allowing
alkaline proteinates to form when the alkalis
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dissolve the proteins of the tissues.Treatment
Removal of the Chemical
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? This requires removal of al contaminated
clothing and copious irrigation.
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? Irrigation of chemical burns requires protectionof healthcare providers to prevent additional
injuries.
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? Wounds should not be irrigated by placing the
patient into a tub, thereby containing the
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chemical and spreading the injurious material.? Irrigation should be large volume and drained `to
the floor,' or out of an appropriate drain
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Treatment? Do not use neutralizing agents
? They cause exothermic reactions causing
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further thermal damage? Protect from hypothermia as unwarmed
lavage fluid is being used
--- Content provided by FirstRanker.com ---
? Most of these patients require excision with
grafting as the chemical burn wound tend to
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be deeper than they appearManagement of Hydrofluoric Acid
Burn
--- Content provided by FirstRanker.com ---
? HF is used as cleaning agent in petroleum
industry, for glass etching and removal of rust
--- Content provided by FirstRanker.com ---
? Acid component causes coagulation necrosis? Fluoride ion then gains a portal of entry that
chelates calcium and magnesium, resulting in
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hypocalcemia and hypomagnesemia.
? Efflux of intracellular calcium down
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concentration gradient occurs with resultantcell death.
HF Burn Management.....
--- Content provided by FirstRanker.com ---
? Death is mostly due to systemic toxicity? When concentration of exposure is >20% or
duration of exposure is prolonged Calcium
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gluconate injections are to be given topically,subcutaneously and intra Arterially
? 10% Calcium Gluconate 0.5ml/cm2
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? 10 ml of 10% Calcium Gluconate in D5 to beinfused over 2-4 hrs
Vesicant Chemical Warfare agents
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? Lewisite, Mustard gas ? Affect all epithelial
tissue including eyes and respiratory
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epithelium? Cause burning in eyes & throat along with
blister formation on skin
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? Dimercaprol is used as Cheliating agent for
Lewisite
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? Sodium thiosulfate & N-Acetylcysteine formanagement of Mustard gas poisoning
ELECTRIC BURN
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Electric BurnPathophysiology
? High Voltage burns (>1000V) are associated
--- Content provided by FirstRanker.com ---
with deep extension and tissue damage likecrush injury
? Low Voltage(<1000V) cause injury mostly
--- Content provided by FirstRanker.com ---
around the area of contact point
? Current = Voltage / Resistance
Pathophysiology
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Burn severity is determined by
? voltage
? current (amperage),
? type of current (alternating or direct),
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? path of current flow,? duration of contact,
? resistance at the point of contact
Pathophysiology...
--- Content provided by FirstRanker.com ---
? Alternating current causes tetanic muscle
contractions, which may either throw victims
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away from the contact or draw them intocontinued contact with the electrical source ? the
`no-let-go' phenomenon
--- Content provided by FirstRanker.com ---
? This phenomenon occurs because both flexors
and extensors of the forearm are stimulated by
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current flow.? However, the muscles of flexion are stronger,
making the person unable to let go voluntarily
--- Content provided by FirstRanker.com ---
Pathophysiology...Electrical Injury is divided into
1) Joule Heating (J) =I2(Current)?R(Resistance)
--- Content provided by FirstRanker.com ---
? Tissue resistance is from lowest to highest in
nerves<blood vessels< muscle< skin< tendon< fat
--- Content provided by FirstRanker.com ---
< bone? Severity of injury is inversely proportional to the
cross-sectional area of the body part involved.
--- Content provided by FirstRanker.com ---
? Thus the most severe injuries are often seen at
the wrist and ankle
--- Content provided by FirstRanker.com ---
Pathophysiology...2) Electroporation
? It is the formation of aqueous pores in lipid
--- Content provided by FirstRanker.com ---
bilayers exposed to a supraphysiologicelectrical field.
? The formation of these pores allows calcium
--- Content provided by FirstRanker.com ---
influx into the cytoplasm and triggers a
subsequent cascade leading to apoptosis
Pathophysiology...
--- Content provided by FirstRanker.com ---
3) Electroconformational denaturation
? The transmembrane proteins change in
polarity of amino acids in response to
--- Content provided by FirstRanker.com ---
exposure to electrical fields.
? Voltage-gated channel proteins were found to
--- Content provided by FirstRanker.com ---
change their conductance and ion specificityafter exposure to a powerful pulsed field
Pathophysiology...
--- Content provided by FirstRanker.com ---
? Low voltage alternating current injury is
usually localized to the points of contact,
--- Content provided by FirstRanker.com ---
? On prolonged contact, tissue damage mayextend into deep tissues with little lateral
extension, as seen in high-voltage wounds.
--- Content provided by FirstRanker.com ---
? These wounds are treated by excision to viable
tissue and appropriate coverage based on
--- Content provided by FirstRanker.com ---
wound depth and location.Management
? Besides the ATLS guidelines 3 points are to be
--- Content provided by FirstRanker.com ---
considered1) Identify patients who wil require ECG
monitoring
--- Content provided by FirstRanker.com ---
2) Fluid therapy for Myoglobinurea
3) Identify patients at risk for compartment
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syndromeECG Abnormality
? Due to skeletal muscle injury along with injury
--- Content provided by FirstRanker.com ---
to myocardium it is problematic to use cardiac
biomarkers such as CK-MB
--- Content provided by FirstRanker.com ---
? Non-specific ST-T changes are the mostcommon ECG abnormality and atrial
fibrillation is the most common dysrhythmia
--- Content provided by FirstRanker.com ---
? Low voltage injury patients normally do no not
require ECG monitoring
Criteria for 24 ECG monitoring
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(1) Loss of consciousness
(2) ECG abnormality
--- Content provided by FirstRanker.com ---
(3) Documented dysrhythmia either before orafter admission to the emergency room
(4) CPR in the field.
--- Content provided by FirstRanker.com ---
Myoglobinurea
? Light pink urine indicates myogloninurea
? Recussitation with RL to maintain urine
--- Content provided by FirstRanker.com ---
output>100ml/hr
? Alkalinization of the urine with a sodium
--- Content provided by FirstRanker.com ---
bicarbonate? Osmotic Diuresis with Mannitol
Compartment Syndrome
--- Content provided by FirstRanker.com ---
? Damaged muscle, and swel ing in the investing fascia ofthe extremity, may increase pressures to the point
where muscle blood flow is compromised.
--- Content provided by FirstRanker.com ---
? Loss of pulses is one of the last signs of a compartment
syndrome, unlike the early loss of pulses occurring in a
--- Content provided by FirstRanker.com ---
circumferential y burned extremity requiringescharotomy.
? A high index of suspicion is paramount for an early
--- Content provided by FirstRanker.com ---
diagnosis, usual y by serial examinations.
? Compartment pressure measurement is general y not
--- Content provided by FirstRanker.com ---
necessary and may even be misleadingCompartment Syndrome
? Four compartment fasciotomies of the lower
--- Content provided by FirstRanker.com ---
leg
? Anterior as well as posterior fasciotomies of
--- Content provided by FirstRanker.com ---
the upper extremity are performed in theoperating room under general anesthesia.
? Upper extremity decompression will generally
--- Content provided by FirstRanker.com ---
always include a carpal tunnel release, as this
is usually the location of the most severe
--- Content provided by FirstRanker.com ---
injury.Low Voltage Injuries
? Burns of the oral cavity are the most common
--- Content provided by FirstRanker.com ---
type of serious electrical burn in young children.? Injuries involving only the oral commissure are
almost never excised, as the extent of injury is
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difficult to predict
? Gentle stretching and the use of oral splints gives
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good cosmetic and functional results in mostpatients, with reconstructive surgery being
reserved for the remainder
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Low Voltage Injuries? Most cases require excision and grafting at the
point of contact only
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? Burns to the fingers are also mostly seen in
children as they insert their fingers in power
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socketsProblem Areas
? Scalp Injury where loss of outer table has occurred
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? Costal chondritis is the most frequent complication of
deep chest wal burns, often becoming a source of long
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-term morbidity, requiring multiple debridements.? Abdominal wounds provide the potential for internal
injuries, both directly under contact points and
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remotely as the result of late ischemic necrosis.
? Changes in their abdominal examination and/or
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feeding tolerance mandates investigation &laparotomy.
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Lightning Strike..
? Neurologic complications are relatively common
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and include unconsciousness, seizures,paresthesias and paralysis, which may develop
over several days after injury
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? Surgical y treatable lesions, including epidural,
subdural and intracerebral hematomas, may
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occur, mandating a high index of suspicion foraltered levels of consciousness.
? Prognosis of many lightning-caused neurologic
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injuries is general y better than for other types of
traumatic cause
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Lightning Strike? The pathognomonic sign of a lightning strike is a dendritic,
fern-like branching erythematous pattern on the skin.
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? Lichtenberg figures (also known as keraunographic
markings), consist of extravasation of blood in the
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subcutaneous tissue which appears within an hour of injuryand fades rapidly, much like a wheal and flare reaction.
? Full-thickness isolated burns on the tips of the toes have
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also been reported as characteristic.
? Lightning may cause both respiratory and cardiac stand-
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still, for which CPR is especially effective when promptlyinitiated.
Thank You
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