Unit 5 : Burns

RECONSTRUCTIVE SURGERY

Burns

•Burns are injuries to tissues caused by heat, friction, electricity, radiation, or chemicals.

•Burn is the damage to skin due to extreme heat source such as chemical, electricity, and radiation.

•Burn occurs where is injury to the tissue of the body caused by heat, chemical, electrical current or radiation.

Incidence of burn

•In USA  2 milion people require medical attention for burn injury, 51,000 require acute hospital admission, 4500 people die from burn and related inhalation injuries.

•Young children and elderly people are at particularly high risk for burn injury

•Most burn injuries occur in the home, in the kitchen, in the bath room – scald or impropr use of electrical appliances around water sources

•Narses can play an active role in preventing fires and burns by teaching prevention concept and promoting legislation related to fire safety

Promoting the use of smoke alarms has had the greatest impacton decreasing fire deaths

Causes of Burn Injuries

•Thermal

•Flame

•Steam

•Scald

•Electrical

•Chemical

•Inhalation

•Radiation

Electrical Burns

•Similar to thermal burns

•True extent of the damage is often hidden

–Entry / exit wound

•best à worst conductors = nerve, blood, muscle, skin, tendon, fat, bone

•Clinical Findings

•Hyperkalemia

•Acidosis

•Myoglobinuria is common

–Maintain high u/o to avoid renal damage

•Peripheral neuropathies or spinal cord deficits

•Cataract formation

•Cardiac dysrhythmias up to 48o post injury

Chemical Burns

•Caused by strong acid or alkaline solution

•Damage continues until the substance is removed or neutralized

•May take time to take effect & may continue to penetrate 24-48hrs

•Full-thickness burns appear superficial

•Flush with copious amounts of water

•Specific Antidotes;

•Hydrofluoric Acid à 10% Calcium Gluconate

•Phenols à polyethylene glycol & methylated spirits

Phosphorus à 1% copper sulfate identifies residual phosphorus

Inhalation Burns

•Smoke inhalation

•Heat inhalation injury

•Asphyxiation

•Carbon monoxide

(CO) poisoning

•Toxic gas inhalation

Carbon Monoxide Poisoning

•CO combines w/ Hgb à Carboxyhemoglobin (COHb)

–200 x’s more affinity for Hgb

–Direct myocardial depression

–

•S & S

–Headache, irritibility

–Respiratory failure, myocardial ischemia

–Seizures, coma, death

–

•Treatment = 100% O2 (reduces CO half-life from 4hrs to 40min)

•SpO2 will read “falsely high”

•ABGs must have co-oximetry to determine true O2 saturation

Frostbite

•Local freezing of tissue

–Ice formation in the extracellular space

–Appears waxy / white

–Extent of damage may be hidden for days to weeks

•Numbness & Pain (upon thawing)

•Upon thawing

–Severe hyperemia, edema, blistering

–RBC & Platelet dumping = circulatory stasis / ischemia (gangrene)

•Treatment

–Rapid re-warming decreases extent of the damage

•Emersion in warm water

Pathophysiology of burns

Systemic Responses

•Fluid Balance- increased capillary permeability leads to the leakage of plasma and proteins into the tissue.

•Cardiac- decrease in cardiac output

•Metabolic- demands are very high in patients with burns

•Gastrointestinal- gastric dilation, peptic ulcers, and paralytic ileus

•Renal-Acute renal insufficiency can occur as a result of hypovolemia and decreased cardiac output

•Pulmonary- Pulmonary effects are mostly related to smoke inhalation.

•Immune- With the skin destroyed, the body loses its first line of defense against infection.

Stages of Burn Injuries

1st Stage – Edema 

2nd Stage – Diuresis

1st Stage:  Edema

•First 24 hours

•Fluid leak: vascular space Ù interstitial space

•Û osmotic pressure

•Û capillary permeability

•Vasoactive substances released

•

•Û interstitial edema and intravascular hypovolemia occurs

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

–Burned tissue edema

•Direct thermal injury to endothelial cells

and Û burn tissue osmolarity

–Non-burn tissue edema

•Severe hypoproteinemia

•

•Small wound

–Edema greatest 8-12 hrs post injury

–

•Large wound

–Edema greatest 18-24 hrs post injury

2nd Stage:  Diuresis

•24-36 hours after burn, fluid and electrolytes begin to remobilize back into intravascular space

•

•Capillary seal reestablishes

•

•Diuresis occurs due to Û GFR in response to Û intravascular volume

•

•May see hypernatremia and hypokalemia

•

•Cardiac output may Û 200-300% normal

•

•Û O2 consumption

Impact on Systems

•Immune System

–Alters immune cells ability to function

–Ü killing power of neutrophils

–Macrophages and lymphocytes do not work well

–

•Hematologic System

–Destruction of RBCs

–Hemoglobinuria

–Û Hgb level  Ù viscosity

–Û WBC level

Coagulation altered

Impact on Systems

•Cellular Response

–Ü tissue oxygen tension

–Na and H2O shift into cell Ù intracellular swelling

–Possible cell death

–Û K+ level intravascularly

–Ü O2 level

–Anaerobic metabolism begins

–Û Lactic acid levels

Metabolic acidosis occurs

•Endocrine System

–Massive release of catecholamines, glucagon, ACTH, ADH, Renin, Angiotensin, & Aldosterone

•Hyperglycemia

•

•Neurological System

–Ü cerebral perfusion

–Cerebral edema occurs from Na shifts

–Carbon monoxide or associated head injury may cause neuro changes

•GI System

–Slow peristalsis and possible ileus

–Û HCL acid secretion from stress response

–Narcotics for pain management further slow peristalsis

–

•Hepatic System

–Decreased hepatic synthesis

–Decreased metabolic function

•Renal System

–ÜRBF & GFR

–Activation of RAS

–Release of ADH

–retain water & Na

–lose 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

•CV System (first 24 hrs)

–Activation of CNS system and catecholamine release:

•Tachycardia

•Vasoconstriction

–During early phase:

•Classic S/S of compensated shock

•Dramatic decrease in cardiac output

–Volume loss and decreased venous return:

•Ü preload

•Ü cardiac filling pressure

•Ü CVP and PCWP

–After 24hrs = increased blood flow to tissues, HTN

•Respiratory System

–Upper airway injury

•Involves all of airway to level of true vocal cords

•Initially due to inflammation from heat of inspired smoke

•Exacerbated by accumulation of excess interstitial fluid

–Major airway injuries

•Involves trachea and bronchi

–Parenchymal injury

•Involves entire respiratory tract down to,

and including, alveolar membrane

•Commonly lethal within first few hours after injury

due to profound bronchospasms and hypoxia

•Respiratory System Con’t

–0-24hrs

•Edema

•Obstruction

•Carbon Monoxide Poisoning

•

–2-5 Days

•May develop ARDS

•

–Signs & Symptoms

•Stridor  /  Hoarseness  /  Facial burns  /  Singed nasal hairs  /  Carbonaceous sputum  /  Impaired level of consciousness

•S/S of deteriorating ABGs & increasing respiratory distress

Classification of Burn Injury

•1. Based on the extent of injury

–Lund and Browder chart

–Rule of 9

–Palm method

•2. Based on the depth of the injury

–1st degree/superficial – epidermis(heal in 5-10days)

–2nd degree/partial – epidermis and varying degree of dermis (papillae) (heal in 7-14 days)

–3rd degree/ deep – involve sebaseous gland, sweat gland, hair follicle. Pain (heal in14-21 days)

–4th degree/full thickness – involve sebaseous gland, fat & muscle & bone. No pain because the nerve root are destroyed. (need skin grafting)

Rule of 9’s

•Head and neck…9%

•Each arm………..9%

•Each leg………..18%

•Anterior trunk…..18%

•Posterior trunk…18%

•Perineum………...1%

•

Lund and Browder

•Designed

for children

•Larger heads

•Adjustments

based on growth

Palm method

•In patient with scattered burns, a method to estimate the percantage of burn is the palm method

•The size of the patient´s palm is approximately 1% of TBSA

Classification of Burn Depth

“First-Degree”

•First–degree

•Superficial (sunburn)

•Erythema, pain, absence of blisters

•Consists of epidermal damage alone

–1st degree/superficial – epidermis(heal in 5-10days)

•Heals within 3 to 6 days

“Second-Degree”

•Second-degree

•Involves:

•Entire epidermal layer

•Part of underlying dermis

•Mottled and red, painful, swelling and blisters

–2nd degree/partial – epidermis and varying degree of dermis (papillae) (heal in 7-14 days)

•Healing in 10 to 21 days

Third-Degree

•Third-degree /deep

•Destruction of all epidermal and dermal elements

•Burn into subcutaneous fat or deeper

•Skin is charred and leathery (woody)

•Pearly-white sheen / waxy

•Generally not painful (nerve endings are dead)

–3rd degree/ deep – involve sebaseous gland, sweat gland, hair follicle. Pain (heal in14-21 days)

•

Fourth-Degree

•Fourth-degree/Full thickness burn

•Full-thickness

•Extending into muscle, tendons or bones

•Typically involves appendage

•Black and dry

•No pain

–4th degree/full thickness – involve sebaseous gland, fat & muscle & bone. No pain because the nerve root are destroyed. (need skin grafting)

•

•

ABA Classification

•Minor – outpatient management

– <10% in adult

– <  5% <10 yo  >50 yo

– <  2% full thickness

•Moderate – admit

– 10 - 20 % in adult

–   5 - 10 %  <10 yo  >50 yo

– High voltage, suspected inhalation,

   circumferential or susceptibility to infection

•Major – admit to burn center

– > 20% adult

– > 10% <10 yo  >50 yo

– >   5% full thickness

– Any significant burn to face, eyes, ears,

   genitalia or joints

– Significant associated injuries

   (e.g. fractures)

Clinical manifestations

•Signs of a burn are localized redness, swelling, and pain.

•A severe burn will also blister. The skin may peel, appear white or charred, and feel numb.

•A burn may trigger a headache and fever.

•Extensive burns may induce shock, the symptoms of which are faintness, weakness, rapid pulse and breathing, pale and clammy skin, and bluish lips and fingernails.

DIAGNOSTIC TESTS

•Various diagnostic tests are performed for systemic reactions, infection, and other complications.

•Complete blood cell count (CBC) show eleveted hematocrit due to hemoconcentration and later decreased hematocrit, and differential count,

•WBC count may increase (30,000 mm3) due to inflammatory response

•Blood urea nitrogen (BUN),

•Serum glucose and electrolytes,

•Arterial blood gases,

•Serum protein and albumin,

•Urine cultures, urinalysis, clotting studies,

•Cervical spine series, electrocardiogram, wound cultures, and,

•If there is a suspected inhalation injury, arterial blood gases, bronchoscopy, and carboxyhemoglobin levels.

•Carboxyhemoglobin may be done to identify carbon monoxide poisining with inhalation injury

•Radiography: chest x-ray used to identify complications that may occur as a result of inhalation injury or with fluid shifting from rapid replacement

•Arterial blood gases: used to identify hypoxia or acid base imbalances, acidosis may be noted because of decreased renal perfusion.

•Lung scan:to identifymagnitude of lung damage from inhalation injury

•Electrocdiogram: used to identify myocardial ischemia or dysrhythmias that may occur with burns or electrolyte imbalances

•

TREATMENT

•Management of the acute burn injury includes

–hemodynamic stabilization,

–metabolic support,

–wound debridement,

–use of topical antibacterial therapy,

–biologic dressings, and

–wound closure.

–Prevention and treatment of complications, including infection and pulmonary damage, and rehabilitation are also of major importance. The patient will also require physical and occupational therapy and psychiatric and nutritional support.

Medical care

•Analgesics: required to reduce pain associated with tissue damage and nerve injury

•Tetanus toxiod: required to provide immunity against infective organisms

•Antimicrobials:required to treat infection

•surgery: required for skin grafting, fasciotomy, debridement, or repair of other injuries

•IV fluid: massive amount of IV fluids may be required for fluid resuscitation immediately post burn and will be required for maintenance of fluid balance as shifting occurs

Muscle Relaxants

•Anectine – 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

DRUG THERAPY

Tetanus Immunization.

Antimicrobial Agents.

Silver-impregnated dressings (Acticoat, Silverlon, Aquacel Ag)

Preoperative Evaluation & Testing

•Initial evaluation of the burn patient

•Diagnostic Testing

Anesthetic Technique & Management

•Preop Meds

•Temperature Regulation

•Anesthetic Drugs

•Muscle Relaxants

•Postoperative

Management of Complications

General Concerns

•Compromised Airway

•Hypovolemia

•Compromised Vascular Access

•Interaction of Anesthetic Agents

•Pain

•

Thermal Injuries

•General Management

Inhalation Injury

•Supportive Care

•Low volume, high PEEP

Fluid Resuscitation

•Parkland formula

•Brooke formula

•Daily maintenance fluids