BURN

นร. สทุธพิงษ์ นาวาจะร.ท. หญิง ฝนทิพย์จนัทรณ์รงค์

อาจารยท่ี์ปรกึษา อาจารย์ พ.ท. ธรีวฒัน์ ภจูิญญาณ์

Structure of the skin

Structure of the skin

BURN DEPTH

Classification of Burn Depth

“First-Degree”a. Involves injury to epidermal layer

b. Erythema (pink to red) c. Skin blanches absence

of blistersd. Painful with tingling

sensation, pain is eased by

coolinge. Discomfort lasts 48 hrs healing occurs 3 to 5

daysf. No scarring; intact skin

Classification of Burn Depth

“First-Degree”

2. Superficial partial-thickness burna. Involves injury to the epidermis

and the superficial layers of the dermis

b. Large blisters may cover an extensive area

c. Pink to red base and broken epidermis, with wet,

shiny and weeping surface d. Excruciating Pain e. Heals in 10 to 21 days f. Some scarring and minor pigment changes may occur

2 degree BURN DEPTHSuperficial partial – thckness burn

2 degree BURN DEPTHSuperficial partial – thckness burn

2 degree BURN DEPTHDeep partial – thckness burn

3. Deep partial-thickness burn

a. Involves injury of most of the dermal layer

b. Pain is reduced

c. Wound surface is red and dry with white areas in deeper parts, no blisters

d. Generally heals in 3-6 weeks

e. Scar formation

2 degree BURN DEPTHDeep partial – thckness burn

Second degree BURN DEPTH

Superficial partial-thickness:•Usually quite painful •Erythemetous with blebs and bullae

•Even air motion across skin hurts

Deep partial-thickness:• Sensation impaired to a variable degree

Second degree BURN DEPTH

Classification of Burn Depth“third-Degree”

4. Full -thickness burna. Involves injury and destruction of the epidermis and the dermis, the wound will not heal by re-epithelialization and grafting may be requiredb. Appears dry, hard, leathery eschar c. Appears as a waxy white, deep red, yellow, brown, or blackd. Absence of sensation because of nerve ending destructione. Scarring and wound contractures are likely to develop without preventive measures

Classification of Burn Depth“fourth-Degree”

5. Deep full-thickness burn (subcutaneous)

a. Extends beyond the skin into underlying fascia and tissues and damage to the muscle, bone, and tendons occurs

b. Injured area appears black and sensation is completely absent

c. Eschar is hard and inelastic

d. Healing time takes months and grafts are required

Severity of burn

1.Minor Burn Injury

2.Moderate Burn Injury

3.Major Burn Injury

Minor Burn Injury

Minor Burn Injury• Second-degree burn of less than 15% total body surface area (TBSA) in adults 10% TBSA in children• Third-degree burn of less than 2% TBSA not involving special care areas (eyes, ears, face, hands, feet, perineum, joints)

Moderate Burn Injury

Moderate, Uncomplicated Burn Injury• Second-degree burns of 15%–25% TBSA in adults or 10%–20% in children• Third-degree burns of less than 10% TBSA not involving special care areas

Major Burn Injury

Major Burn Injury• Second-degree burns exceeding 25% TBSA in adults or 20% in children• All third-degree burns exceeding 10% TBSA• All burns involving eyes, ears, face, hands, feet, perineum, joints• All inhalation injury, electrical injury

Adult Rule of Nines Chart

Child Rule of Nines Chart

Infant Rule of Nines Chart

Lund & Browder Chart 5yrs - Adult

Lund & Browder Chart Infant - 5yrs

Berkow Chart

BURN LOCATION1. Burns of the head, neck, and

chest are associated with pulmonary

complications2. Burns of the face are associated with corneal abrasion3. Burns of the ear are associated with auricular chondritis4. Hands and joints require intensive therapy to prevent disability5. The perineal area is prone to autocontamination by urine and feces6. Circumferential burns of the extremities can produce a tourniquet-like effect and lead to vascular compromise (compartment syndrome)7. Circumferential thorax burns lead to inadequate chest wall expansion and pulmonary sufficiency

Type of BURN

A. Thermal burns are caused by exposure to flames, hot liquids, steam, or hot objects Inhalation Injury ???

B. Chemical burns1. Burns are caused by

tissue contact with strong acids, alkalis, or organic compounds

2. Systemic toxicity from cutaneous absorption can occur

3. Deep partial-thickness injuries

Type of BURN C. Electrical burns1. Burns are caused by heat generated by electrical energy as it passes through the body 2. Electrical burns result in internal tissue damage3. Cutaneous burns cause muscle and soft tissue damage that may be extensive, particularly in high-voltage electric injuries 4. The voltage, type of current, contact site, and duration of contact are important to identify5. Alternating current is more dangerous than direct current because it is associated with cardiopulmonary arrest, ventricular fibrillation, tetenic muscle contrations, and long bone or vertebral fractures6. Subcutaneous (Fourth Degree)

D. Radiation burns are caused by exposure to ultraviolet light, x-rays or radioactivity (superficial burn = sunburn )

INHALATION INJURIES

Smoke inhalation injury1. Description: Injury results when the

victim is trapped in an enclosed, hot, smoke-filled space.

2. Assessment:a. Facial burnsb. Erythemac. Swelling of oropharynx and nasopharynxd. Singed nasal hairse. Flaring nostrilsf. Stridor, wheezing, and dyspneag. Hoarse voiceh. Sooty (carbonaceous) sputum and coughi. Tachycardiaj. Agitation and anxiety

Carbon monoxide poisoning1. Desciptiona. Carbon monoxide is colorless, odorless, and tasteless gas that has an affinity for hemoglobin 200 times than that of oxygenb. Oxygen molecules are displace and carbon monoxide reversibly binds to hemoglobin to form carboxyhemoglobinc. Tissue hypoxia occurs

Mild: headache, nauseaModerate: dizziness, confusion,

ataxia, visual changes, pallorSevere: dysrhythmias, coma,

cherry red buccal membrane, cherry-red cast to skin

Signs of Carboxyhaemoglobinaemia

COHb levels Symptoms

0-10% Minimal (normal level in heavy smokers)

10-20% Nausea, headache

20-30% Drowsiness, lethargy

30-40% Confusion, agitation

40 -50% Coma, respiratory depression

>50% Death

QUESTIONS ?

What assessment of the patient would you make?

Discuss airway assessment, The significance of perform SaO2

and other investigations you would perform (COHb).

What are the indications for intubations.

What fluid requirements will patients have ?

What fluid would you give, when you give, and why ?

Discuss analgesia, are burns painful ?

Where should the patient be looked after ?

Step 1: Initial Assessment

Airway: does the patient have a patent airway?Breathing: is the patient breathing adequately?Circulation: Is the patient’s circulatory and cardiac status stable?Neurological status: EVMNote: burns do NOT alter mentation—if the patient is un-alert or disoriented, something else is going on! Expose the patient, and treat for hypothermia

Step 2: Determining Burn Severity

•Burn severity is determined primarily by assessing the extent of the burn as percentage of total body surface area, and its depth•‘Partial/full thickness’ and ‘1st/2nd/3rd degree’ are acceptable terminology•First and second degree burns are partial thickness burns•Third degree burns are full thickness burns

Fluid Resuscitation• Parkland formula

– 4cc X weight X % burn– ½ volume in first 8 hours– Second ½ over last 16 hours

• Brooke formula– 2cc X weight X % burn– ½ volume in first 8 hours– Second ½ over last 16 hours

• Daily maintenance fluids

Fluid Resuscitation

End point Urine outputin adults 0.5-1.0 ml/kg/hour

in children 1.0-1.5 ml/kg/hour

Stages of Thermal Injuries

1st Stage – Edema

2nd Stage – Diuresis

1st Stage – Edema

First 24 hoursFluid leak: vascular space interstitial space

osmotic pressure capillary permeabilityVasoactive substances released

interstitial edema and intravascular hypovolemia occurs

1st Stage – Edema

Burns >30% BSA cause capillary changes in both burned and non-burned tissue

Burned tissue edemaDirect thermal injury to endothelial cells and burn tissue osmolarity

Non-burn tissue edema Severe hypoproteinemia

Small woundEdema greatest 8-12 hrs post injury

Large woundEdema greatest 18-24 hrs post injury

2nd Stage – Diuresis

24-36 hours after burn, fluid and electrolytes begin to remobilize back into intravascular spaceCapillary seal reestablishesDiuresis occurs due to GFR in response to intravascular volumeMay see hypernatremia and hypokalemiaCardiac output may 200-300% normal

O2 consumption

burn effect

1.Localized Effect

2.Systemic Effect

Localized Effect

Systemic Effect

CardiovascularBloodElectrolyte, Acid & BaseRespiratoryEndocrineImmuneGastrointestinalMuscls & Skeleton

cardiovascular system

CardioVascular System (first 24 hrs)

Activation of CNS system and catecholamine release:

TachycardiaVasoconstriction

During early phase:Classic S/S of compensated shockDramatic decrease in cardiac output

Volume loss and decreased venous return:

preload cardiac filling pressure CVP and PCWP

After 24hrs = increased blood flow to tissues, HTN

Immune and hemtolpgic system

Immune SystemAlters immune cells ability to function killing power of neutrophilsMacrophages and lymphocytes do not work well

Hematologic SystemDestruction of RBCsHemoglobinuria Hgb level viscosity WBC level Coagulation altered

Endocrine and neurological system

Endocrine SystemMassive release of catecholamines, glucagon, ACTH, ADH, Renin, Angiotensin, & Aldosterone

Hyperglycemia

Neurological System cerebral perfusionCerebral edema occurs from Na shiftsCarbon monoxide or associated head injury may cause neuro changes

Respiratory System

Upper airway injuryInvolves all of airway to level of true vocal cordsInitially due to inflammation from heat of inspired smokeExacerbated by accumulation of excess interstitial fluid

Major airway injuriesInvolves trachea and bronchi

Parenchymal injuryInvolves entire respiratory tract down to, and including, alveolar membraneCommonly lethal within first few hours after injury due to profound bronchospasms and hypoxia

Respiratory System

Respiratory System Con’t0-24hrs

EdemaObstructionCarbon Monoxide Poisoning

2-5 DaysMay develop ARDS

Signs & SymptomsStridor / Hoarseness / Facial burns / Singed nasal hairs / Carbonaceous sputum / Impaired level of consciousness S/S of deteriorating ABGs & increasing respiratory distress

Renal System

Renal SystemRBF & GFRActivation of RASRelease of ADH

retain water & Nalose of K, Ca, & Mg

ARF Acute Tubular Necrosis 2o hemoglobinuria & myoglobinuria d/t hemolysis & tissue necrosis

Maintain high u/o (2ml/kg/hr) w/ fluids / osmotic diuretics

GI and hepatic System

GI SystemSlow peristalsis and possible ileus HCL acid secretion from stress responseNarcotics for pain management further slow peristalsis

Hepatic SystemDecreased hepatic synthesisDecreased metabolic function

Induction Medications

- Burn patients require higher than normal doses of non depolarizing muscle relaxants dueto altered protein binding and increase in extrajunctional acetylcholine receptors.

Muscle Relaxants

Depolarizers– safe in the 1st 24hrs (afterwhich hyperkalemia may be a problem up to a year or the burn is healed)

Non-depolarizers – burn patient’s tend to be resistant to the effects of non-depolarizing muscle relaxants

May need 2-5 x’s the normal dose!!!

Common Operations

- Decompression procedures

escharotomies & fasciotomies

- Burn excision & skin grafting- Reconstruction operations- Supportive procedures

tracheostomy, gastrostomy, vascular access

Review – Anesthetic Management

Preop MedsProvide adequate analgesiaFluids

Establish Adequate Vascular Access

Consider Invasive Monitoring

Airway ManagementConsider Alternatives to Direct Laryngoscopy

Awake FOBVentilation

Increased minute ventilation

increased metabolic rate

Fluids & BloodAnticipate rapid, large blood lossParkland Formula

Temperature Regulation

Increase ambient temperatureWarm IV fluids

Anesthetic DrugsInclude opioidsConsider effects of increased circulating catecholamines

Muscle RelaxantsAvoid SuccinylAnticipate resistance to nondepolarizing muscle relaxants

PostoperativeAnticipate increased analgesic requirements

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