BURNS M Fahud Khurram - PowerPoint Presentation

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BURNS

M

Fahud

Khurram

MS,

MCh

, DNB (Plastic Surgery) , MNAMS

Former fellow Stanford University, USA

Department of Plastic Surgery

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Important topics

History of

Tt

of burnsEpidemiologyPreventionCare of OPD PtsPre-hospital mgtPathophysiologyFluid resuscitationInhalational injuryNutritional injury

Pediatrics burns

Electrical burns

Chemical burns

Complications

Maltreatment by burning

Psychiatric disorders

PG entrance

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Burns are one of the most devastating conditions

encountered in

medicine.

The injury represents an assault on all aspects of the patient, from the physical to the psychological.

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all ages,developed and developing world.

scars

are long lasting and often lead to

chronic disability. global public health problem, 195 000 deaths annually, > low- and middle-income countries.

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Burns in the developing world

high risk:

High

population density,illiteracy, and poverty 700,000

to 800,000 burn admissions annually (>20,00,000 cases per year

).

175000 deaths every year

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In the United Kingdom about 250 000 people are burnt each year

.

Of

these, 175,000 attend accident and emergency departments, and 13,000 of these are admitted to hospital.In an average year 300 burn deaths occur.

Epidemiology

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The

great Boston fire 1872

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What are the causes of burns

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What are the causes of burns?

Thermal

injuries

Scalds —About 70% of burns in children are caused by scalds.They also often occur in elderly people. Flame —Flame burns comprise 50% of adult burns. Flame burns tend to be deep dermal or full thickness.

Contact

—

extremely hot object

Electrocution

and

C

hemical

injuries

.

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heat

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Daily life

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electricity

Chemical

materials

Radioactive

materials

laser

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lightning

explosive

BURN INJURY (5)

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Fire

is also

used in

homicides and suicides.

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Who gets burnt?

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Risk factors

Gender: F>M;

Open fire cooking

Inherently unsafe cook-stovesLoose clothingInter-personal violence/ domestic violenceAge: extreme of ageRegional factorsOthers: Occupation (exposure to fire)Poverty, over-crowding, lack of safety measuresUnskilled workers

Epilepsy, peripheral neuropathy, physical and cognitive disabilities

Alcohol abuse, smoking

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Pathophysiology of Acute Burns

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Pathophysiology

Understanding

the pathophysiology of a burn injury

is important for effective management. In addition, different causes lead to different injury patterns, which require different management.

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Burn injuries result in both local and systemic responses (>30% TBSA).

The body’s response to a burn

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Pathophysiology

The

underlying process involved is both a local and systemic inflammatory reaction,

shift of intravascular fluid into the surrounding interstitial space.

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Pathophysiology

This

occurs as a consequence of changes in vascular permeability as the normal capillary barrier is disrupted by a host of mediators, including

histamine, serotonin, prostaglandins,

platelet

products,

complement

components, and

members

of the

kinin

family.

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The three zones of a burn were described by Jackson in 1947.

Zone of

coagulation

—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.LOCAL RESPONSE

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The body’s response to a burn

Zone of stasis

—

The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The

main aim of

burns resuscitation

is to increase tissue perfusion here and

prevent any

damage becoming irreversible.

Additional

insults—such

as prolonged

hypotension, infection, or

oedema

—can convert

this zone

into an area of complete tissue loss

.

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Zone of

hyperaemia

—In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion.

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Pathophysiology of burn shock and burn edema

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Burn shock results from the interplay of

hypovolemia

and multiple mediators of inflammation with effects on both the microcirculation as well as function of heart, large vessels and lungs.

Increase in pulmonary and systemic vascular resistance (SVR) and myocardial depression occur despite adequate preload and volume support.

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Hypovolemia and rapid edema

formation

Extravasation

of plasma into burn wound and surrounding tissues.Similar to hemorrhagic shock except increase hematocrit.Fluid resuscitation complicated not only by burn wound edema but also by sequestrated fluid and protein in non- burned soft tissue.

Blood volume is restored after 24-36

hrs

Edema develops when the rate by which fluid is filtered out of the micro- vessels exceed the flow in the lymph vessels draining the same tissue

mass

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Hypovolemia and rapid edema

formation

Edema follows bi-phasic pattern

Immediate and rapid increase in the water content of burnt tissue in first hourSecond and gradual increase in fluid flux of both burned and non-burned soft tissues occurs in first 12-24

hrs

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Hypovolemia and rapid edema

formation

The

amount of edema formation in burned skin depends on Type and extent of injuryFluid resuscitationVolume of fluid administered

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Non- burned tissue edema

Severe

hypoproteinemia

Alteration in interstitial structureInterstitial protein washout increases the compliance of the interstitial space and that of water transport and hydraulic conductivity across the entire blood–tissue-lymph barrier increased with hypoproteinemia.

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Systemic Response

Occurs when burn reaches 30

% of total body surface area

.

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Systemic effects of burn injury

Respiratory system

Cardiovascular system

Renal system

Haematological system

Immune system

Psychological system

Gastrointestinal system

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Systemic response

Increased vascular permeability and oedema

Altered

haemodynamics Decreased renal perfusionDecreased cardiac outputIncreased gut mucosal permeabilityImmunosuppressionhyper metabolism

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Systemic Response

Associated

massive release of inflammatory mediators leads to SIRS MODS and then death.

Early adequate resuscitation and prevention of wound sepsis attenuates the SIRS response.

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CARDIOVASCULAR CHANGES

Capillary

permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment.

Peripheral and splanchnic vasoconstriction occurs.Myocardial contractility is decreased, possibly due to release of tumour necrosis factor . These

changes

, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ

hypoperfusion

.

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PULMONARY RESPONSE

Inhalation injury is the leading cause of death in fire victims.

caused mainly by carbon monoxide.

Deterioration results from bronchoconstriction and chest constriction secondary to circumferential full-thickness chest burns.

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15-30% of burn admissions have inhalation injuryIndependent predictor of mortality, ↑ by 20%

Increases pneumonia risk

Leading diagnosis of those hospitalized and treated on 9/11, World Trade Center attack

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Anatomic ClassificationUpper airwayLower airway

Systemic toxicity

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Tissue hypoxia, a result of carbon monoxide combining with

hemoglobin

to form

carboxyhemoglobin, which competes with oxygen for available hemoglobin binding sites.

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Diagnosis

Clinical findings:

Facial burns (96%)

Wheezing (47%)Carbonaceous sputum (39%)Rales (35%)Dyspnea (27%)Hoarsness (26%)Tachypnea (26%)Cough (26%)Cough and hypersecretion (26%)

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Diagnosis of inhalation injury is a priority.

Serum

carboxyhemoglobin

levels and arterial blood gas levels are frequently used to assess for inhalation injuries.Bronchoscopy and xenon-133 (133Xe) ventilation-perfusion scans.45

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Grading of inhalational injury

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SmokeCO poisoning

CO from incomplete combustion

CO +

Hb → COHb (affinity 200-250x)LEFT shift of oxy-Hb curve (Haldane effect)CO binding to intracellular cytochromes and metalloproteins

(myoglobin)

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Symptoms of CO poisoning

“Cherry-red lips, cyanosis, retinal hemorrhage”-

rare

CNS and Cardiovascular ↑ RR, ↑HR, dysrhythmias, MI, ↓BP, coma, seizuresDelayed neuropsychiatric syndrome (3-240d)Cognitive/personality changes/parkinsonianism

COHb

%

Symptoms

0-5

Normal

15-20

Headache, confusion, fatigue

20-40

Hallucination, vision

Δ

’s

40-60

Combative, coma

60 +

Cardiopulmonary arrest

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METABOLIC CHANGES

The

basal metabolic rate increases up

to three times its original rate. This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity.

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IMMUNOLOGICAL CHANGES

Non-specific

down regulation of the immune response occurs, affecting both cell mediated and

humoral pathways.

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Immunosuppression

Loss

of barriers

Dose dependent damage to chemotaxis, phagocytosis, intracellular killing powerImpaired complement activationB cell function compromisedLoss of immunoglobulins

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Gastrointestinal

Stress ulcers

(curling`s ulcer)

Gastrointestinal bleeding 48hAcute gastric dilatationMotility disorders

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Effects on Fluids, Electrolytes, and Blood Volume

Serum sodium levels vary in response to fluid resuscitation.

Usually

hyponatremia is present, as water shifts from the interstitial to the vascular space.

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Effects on Fluids, Electrolytes, and Blood Volume

Hyperkalemia

results from massive cell destruction.

Hypokalemia may occur later with fluid shifts and inadequate potassium replacement.Destruction of red blood cells, blood loss during surgical procedures, wound care, and diagnostic studies result in anemia. Coagulation abnormalities, including a decrease in platelets and prolonged clotting and

prothrombin

times also occur.

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Pathophysiology

The

peak of

third-space loss occurs at some point 6-12 hours postburn as the capillary barrier begins to regain its integrity, hence the reduction in fluid requirements observed in resuscitation formulas around this point. At this point, the theoretic benefits of adjuvant colloid therapy during the resuscitation allow the careful downward titration of fluid administration to reduce the obligatory edema.

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Hematologic response

Red blood cells and erythropoiesis

Almost all hematologic parameters are significantly affected in a biphasic manner

Anemia is present– directly proportional to TBSA burn15-40% full thickness burn lose 12% rbc in first 6hrs and 18% in 18 hrsThen 1-2 % everyday till wound healsCause of rbc destruction: direct thermal

inj

, thrombus in blood vessels d/t activation of complement and coagulation cascades; oxygen free radicals.

Paradox: initial increase in hematocrit d/t loss of fluid

Thrombocytopenia, leukopenia, increase in acute phase proteins

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Acute Renal FailureHypovolemia

Depressed myocardium

Extrinsic compression (ACS)

Denatured proteins

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Classification of burns

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Classification of burns

Traditional Classification

1

st degree2nd degree3rd degree

Current Classification

Superficial partial thickness

Deep partial thickness

Full Thickness

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Anatomy of skin

Epidermis

Dermis

The skin is made up of two layers, the outer layer (

epidermis

) and inner layer (

dermis

). Between the epidermis and dermis is the

basement membrane

which is semi permeable and

acellular

. It provides support, flexibility and regulates the transfer of substances across the dermal-epidermal junction.

Under the skin is the

subcutaneous layer

which allows the skin to be loosely attached to the underlying fascia. It increases mobility and is especially important over joints.

basement membrane

Subcutaneous layer

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A protective barrier of stratified

squamous epithelium consisting of 5 layers

Stratum

corneum: 20-30 rows of dead cells continually shed

Stratum

lucidum

:

3-4 layers clear flat dead cells

Stratum

granulosum

:

Cells degenerating with production of keratin

Stratum

spinosum

:

8-10 rows of cells that produce protein but can not duplicate

Stratum

basale

:

Columnar cells continually dividing, gradually migrating to surface

EPIDERMIS

There are three other cell types within the epidermis:

melanocyte

,

Langerhan

and

Merkel

cells

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Dermis

The dermis consists of 2 layers:

Papiliary

dermis: The upper layer of dermis. It has extensions protruding into the epidermis called Rete pegs which also contain small capillary loopsReticular dermis: The lower layer of dermis. It is made up of collagen, elastin and ground substance as well as hair follicles, sweat and sebaceous glands

Fibroblasts are the predominant cell type in the dermis and produce collagen and elastin which provide strength and flexibility to the skin.

In addition, there are blood vessels, sebaceous glands, sweat glands, hair follicles, sensory receptors and fat cells.

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Functions of the skin

P

hysical barrier

T

emperature control

I

mmunity

S

ensation

V

itamin D production

I

dentity

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Classification of Burns

Burn depth

Superficial partial-thickness

burn: the epidermis is destroyed or injured and a portion of the dermis may be injured. The damaged skin may be painful and appear red and dry, or it may blister.Deep partial-thickness burn: involves destruction of the epidermis and upper layers of the dermis and injury to deeper portions of the dermis.Full-thickness burns

(painless): involves total destruction of epidermis and dermis and, in some cases, underlying tissue as well.

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Estimation

of burn depth

On

direct examination, there are four elements that should be assessed— bleeding on needle prick, sensation, appearance, and

blanching

to pressure

.

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Cleland H. Thermal burns - assessment and acute management in the general practice setting.

Aust Fam Physician

. 2012;41(6):372–375.

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Ⅰ

0

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superficial

Ⅱ

0

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superficial

Ⅱ

0

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Ⅲ

0

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Electrical injuries

3-4

%

An electric current will travel through the body from one point to another, creating “entry” and “exit” points (or source contact point and ground contact point). The tissue between these two points can be damaged by the current.

Slide78

Electrical injuries

The voltage is

the

main determinant High voltage (>1000v) Low voltage(<1000v)

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Domestic

electricity —

Low voltages tend to cause small, deep contact burns at the exit and entry sites. The alternating nature of domestic current can interfere with the cardiac cycle, giving rise to arrhythmias.

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High tension electric burns

There

is extensive tissue damage and often limb loss.

Muscle damage gives rise to rhabdomyolysis, and renal failure may occur with these injuries. This injury pattern needs more aggressive resuscitation and debridement than other burns.

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“

Flash

” injury

can occur when there has been an arc of current from a high tension voltage source. The heat from this arc can cause superficial flash burns to exposed body parts, typically the face and hands. However, clothing can also be set alight, giving rise to deeper burns.

No

current actually

passes through

the victim’s body

.

Slide84

A

particular concern after an electrical injury is the need

for cardiac

monitoring. If there are electrocardiographic abnormalities or a loss of consciousness, 24 hours of monitoring is advised.

Slide85

Usually, for both AC and DC, the higher the voltage (V) and amperage, the greater the ensuing electrical injury (for the same duration of exposure).

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Amount of dissipated heat energy equals amperage

2

× resistance × time; thus, for any given current and duration, tissue with the highest resistance tends to suffer the most damage.

Body resistance (measured in ohms/cm2) is provided primarily by the skin. Skin thickness and dryness increase resistance; dry, well-keratinized, intact skin averages 20,000 to 30,000 ohms/cm2.For a thickly calloused palm or sole, resistance may be 2 to 3 million ohms/cm

2

; for moist, thin skin, resistance is about 500 ohms/cm

2

.

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Resistance

for punctured skin (

eg

, cut, abrasion, needle puncture) or moist mucous membranes (eg, mouth, rectum, vagina) may be as low as 200 to 300 ohms/cm2. If skin resistance is high, much electrical energy may be dissipated at the skin, resulting in large skin burns where the energy contacts the skin but less internal damage.

Slide88

If

skin resistance is low, skin burns are less extensive or absent, with more electrical energy transmitted to internal structures.

Thus

, the absence of external burns does not predict the absence of electrical injury, and the severity of external burns does not predict the severity of electrical injury.

Slide89

Nerves

, designed to carry electrical signals, and

muscle

and blood vessels, because of their high electrolyte and water content, have a low resistance and are good conductors. Bone, tendon, and fat, which all contain a large amount of inert matrix, have a very high resistance and tend to heat up and coagulate rather than transmit current.

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Damage to internal tissues depends also on their resistance and additionally on current density (current per unit area; energy is concentrated when the same current flows through a smaller area).

For

example, as electrical energy flows in an arm (primarily through lower-resistance tissues,

eg, muscle, vessels, nerves), current density increases at joints because a significant proportion of the joint's cross-sectional area consists of higher-resistance tissues (eg, bone, tendon), which decreases the area of lower-resistance tissue; thus, damage to the lower-resistance tissues tends to be most severe at joints.

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Myoglobinuria

,

hypovolemia

, and hypotension increase risk of acute renal failure.

Slide93

CHEMICAL INJURIES

Slide94

Chemical injuries are usually as a result of industrial accidents but

may occur with household chemical products.

These burns tend

to be deep, as the corrosive agent continues to cause coagulative necrosis until completely removed.

Slide95

Chemical Burns

Both acids and bases can be defined as caustics, which cause significant tissue damage on contact.

ACIDS

produce a coagulation necrosis by denaturing proteins, forming a coagulum (eg. eschar) that limits the penetration of the acid.

BASES

typically produce a more severe injury known as liquefaction necrosis

Slide96

Chemical Burns

Acids

Toilet bowl cleaners, drain cleaners, metal cleaners, automobile battery fluid, fertilizer manufacturing, rust removers, tire cleaners, tile cleaners, glass etching, dental work, refrigerant, and hair wave neutralizers

BasesDrain cleaners, bleach, oven cleaners, mortar, plaster, and cement

Slide97

Chemical injuries

Alkalis

tend

to penetrate deeper and cause worse burns than acids.

Slide98

Key points

Burns

are a major cause of injury and death worldwide

Flame burns are the most common typeDeath is more likely with increasing age, increasing burn size, and presence of inhalational injury90% of burns are preventable

Slide99

Key points

A

burn results in three distinct zones—coagulation, stasis,

and hyperaemiaThe aim of burns resuscitation is to maintain perfusion of the zone of stasisSystemic response occurs once a burn is greater than 30% of total body surface areaDifferent

burn mechanisms lead to different injury patterns

Identification

of

non-accidental

burn injury is important

Slide100

When to Transfer to a Burn Center

>10% TBSA partial thickness burns

Any size full-thickness burns

Burns to special areas of function or cosmesisInhalation injurySerious chemical injuryElectrical injuryBurns with trauma where burns are the major problemPediatric burnsSmaller burns in patients with multiple comorbidities

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