CLASSIFICATION OF BURNS

- According to burn depth- According to extent of body response- According to area injured- According to mechanism of injury- Others

o Age, presence of inhalation injuryo Injury in special areas: face, perineum, hands and feeto Past medical history

BURN DEPTH p. 1720

- Superficial partial- thickness injury- Deep partial

SUPERFICIAL- PARTIAL THICKNESS

- Causeo Sunburno Low intensity flash

- Skin involvement o Epidermis

- Sxo Tingling, hypersensitivity, round appearance o Reddened, blanches with pressure, dry minimal/ no edema, possible

blisters- Recuperative course

o Complete recovery within a weeko No scarring

DEEP- PARTIAL THICKNESS

- Causeo Scalds, flash flames

- Skin involvemento Epidermis, upper dermis, portion of

Systemic response, physiologic changes during a major burn

- Renal response- Renal function may be altered as a result of decrease blood volume- During a major burn, the body responds initially by shunting blood from the kidneys and

decreasing glumerular filtration rate causing oliguria- Destruction of RBC at the injury site results in free Hgb in the urine - When muscle damage occurs, myoglobulins are released from the muscle cells and

excreted by the kidney- If there is inadequate blood flow through the kidneys, the Hgb and myoglobin occlude

the renal tubules, resulting in a acute tubular necrosis and renal failure- GI response- Blood flow to the mesenteric bed is also diminished leading to the development of

intestinal ileus and GI dysfunction in clients with severe burns- May cause 2 potential GI complications: Paralytic ileus (absence of instestinal persitalsis)

and Curling’s ulcer (ulceration and perforation of the GI mucosa)- Manifestations of paralytic ileus due to burn trauma:

o Decreased peristalsiso Decreased bowel soundso There will be abd distention later on manifested as nausea and vomiting

- Gastric distention and nausea may occur leading to vomiting unless gastric compression is initiated

- Gastric bleeding secondary to massive physiologic stress may be signaled, by occult blood in the stool, regurgitation of the coffee ground material from the stomach or bloody vomitus. These signs suggest gastric or duodenal erosion (Curling’s ulcer)

- METABOLIC RESPONSE- Inability to regulate body temperature due to loss of skin- Burn patients may therefore exhibit low body temperature in early burns after injury- Then, hypermetabolism resets core temp, burn pxs become hyperthermic for much of

the post burn period, even in the absence of infection- Burn injury triggers a hypermetabolic state which is manifested by a negative nitrogen

balance with increased protein degradation and urea excretion, hyperglycemia and hyperlactatemia

- Due to enhanced post-burn metabolic rate, there is an increase in the generation of toxic by-products such as reactive oxygen ospecies and dicarbonyls such as methylglyoxal which can cause cell damage.

PATHOPHYSIOLOGIC CHANGES

Different phases of burn

1. Emergent/ Resuscitative Phase- Begins at the time of injury and concludes with the restoration of capillary permeability,

usually at 48-72 hours following the injury

2. Acute/ Intermediate Phase- From beginning of dieresis to near completion of wound closure3. Rehabilitation Phase- Usually starts from the closure of the wound to return to individual’s optimal level of

physical and psychosocial adjustment

During the emergent/ resuscitative phase, there are:

- Fluid accumulation phase (shock phase- Plasma to interstitial fluid (edema at burn site)

OBSERVATION EXPLANATIONGeneralized dehydration Plasma leaks through damaged capillariesReduction of blood volume Secondary to plasma loss, fall of blood

pressure, and diminished cardiac outputDecreased urinary output Secondary to: decreased renal blood flow, Na

and H20 retention caused by increased arenocortical activity

Potassium excess Massive cellular trauma causes relase of potassium ions into extracellular fluid

Sodium deficit Large amounts of Na is lost in trapped edema fluid and exudates and by shift into cells as potassium is released from cells

Metabolic acidosis (base-bicarbonate deficit) Loss of bicarbonate ions accompanies sodium loss

Hemoconcentration (elevated Hct) Liquid blood component is lost into extravascular space

During acute/ intermediate phase of burn care

- Fluid and electrolyte changes in the acute phaseo Fluid remobilization phase (state of dieresis)o Interstitial fluid to plasma

OBSERVATION EXPLANATIONHemodilution (decreased Hct) Blood cell concentration is diluted as fluid enters

the intravascular compartment; loss of RBC destroyed at burn site

Increased urinary output Fluid shift intravascular compartment

During the emergent phase

- Acute respi failiure- Distributive shock- Acute renal failure- Compartment syndrome – managed by escarotomy- Conditions need to address:

o Heart failure and pulmonary edemao Sepsiso Acute respi failure (hypoxemia and hypo…)o Acute respi distress syndrome (condition not responsive to oxygen

supplementation)o Visceral damage (electrical burns)

During the rehab phase

- Contractures- Inadequate psychological adaptation to burn injury

MGT OF PXS ACCORDING TO PHASES OF BURN INJURY

a. Emergent/ resuscitative phase on the care scene- “pre-hospital care” should begin with removing the victim from the source of burn

and/or eliminating cause of burn- On the scene care:

o Preventing injury to the rescuer (1st priority)o Fire and emergency medical serviceso Cover the wounds, establish airways, oxygen, IV local effects (most

evident) systemic effects (life threatening)- Primary survey: ABC (cervical immobilization/ cardiac monitoring)- Secondary survey: Total body assessment including mechanism of injury, inhalation

injury, corneal injury- Identify other life threatening injuries- If with major burn (20-25%)

o NGT with low intermittent suction machine MOST COMMON: gravity drain

o Assessment of TBSA and deptho Tetanus prophylaxiso Psychologic needs (px and family)

o Transfer to burn unit Partial thickness >10% Full thickness burn; all age group Special burn areas including joints Chemical, electrical, inhalation Pre-existing medical problems Special social, emotional or rehabilitation needs

o Prior to transfer to a burn unit Ensure adequate airway Peripheral circulation is established IVF Adequate IO (0.5 – 1 cc/kg/hour) Indwelling catheter Analgesic Covering with clean, dry sheet Keep comfortably warm

- Primary goal: prevent hypovolemic (burn) shock and to prevent vital organ functioning bu:1. Establishing airway and breathing2. Fluids replacement therapy3. Burn wound care4. Infection control5. Prevention of complications

For airway and breathing:

- Immediate therapy: establishing an airway and administering humidified 100% oxygen- Mild pulmonary injury: inspired air humidified, patient encouraged to cough- Severe pulmonary injury: bronchial suctioning, administration of bronchodilators and

mucolytic agents- Edema of airway: endotracheal intubation- Continuous positive airway pressure and mechanical ventilation (Contraindication of

PEEP: decreased cardiac output)

Fluid replacement therapy:

- Prevent irreversible shocks by replacing lost fluids and electrolytes- PARAMETERS: weight, lab test results: Hgb, Hct, serum Na- UO 0.5 – 1.0 ml/kghr- IV and catheter must be in place- Factors associated with increased fluid requirement:

o Delayed resuscitation, full thickness, inhalation injury- Indicators of adequate fluid replacement:

o Output of 30-50ml/houro Systolic BP >100mmHgo PR <110bpm

GUIDELINES AND FORMULAR FOR FLUID REPLACEMENT

Consensus formula Evans formula Brooke Army formula Parkland/ Baxter formula Hypertonic saline solution

Consensus formula

- LRS or other balanced saline solution- 2-4 ml x KBS x %TBSA burned

o Half given in first 8 hrso Half given over next 16hrs

Evans formula

1. Colloids: 1 ml x KBS x %TBSA burned2. Electrolytes (saline) : 1 ml x BW x %TBSA burned3. Glucose (5% in water): 2000ml for insensible loss

o Day 1: half given in first 8 hrs, half given over next 16 hrso Day 2: half of previous’ day’s colloids and electrolytes; all of insensible

fluid replacemento Maximum of 10,000 ml over 24 hours

Brooke Army formula

1. Colloids: 0.5ml x KBW x %TBSA burned2. Electrolytes (LRS): 1.5ml x KBS x %TBSA burned3. Glucose (5% in water): 2000ml for insensible loss

o Day 1: half given in first 8 hrs, half given over next 16 hrso Day 2: half colloids, half electrolytes; all of insensible fluid replacement

Parkland/ Baxter formula

- LRS: 4ml x BW x %TBSA burned- Day 1: half given un first 8 hrs, half given over next 16 hrs- Day 2: varies. Colloid is added

NRG MGT DURING FLUID RESUSCITATION

- Accurate monitoring of VS and UO- Maintain body temp, infection control - Adequate titration of IVF - Daily head-toe assessment- Ensure understanding of the case- Geriatric consideration

CASE!

- 40% TBA in a patient with burn injurt- BW 8 kgs- Compute using IVF using consensus formula- Infusion rate first 8 hrs then 16 hrs- Adequate UO

ANSWERS!

- Total fluid: 6800ml- 3400 ml (1st 8 hrs): 425ml/hr- 3400ml (16 hours): 212 ml/hr- UO: 42-85 ml/hr

WOUND CARE

- Aseptic mgt- All clothing and jewelry removed- Elevate affected area

During acute/ intermediate phase

- Infection prevention- Burn wound care

o Wound cleaning, topical antibacterial therapy, wound dressing, dressing changes, wound debridement, wound grafting

- Pain mgt- Nutritional support- Hydrotherapy

o Limited to 20-30 mins to prevent chillso Temperate of water: 37.8 ⁰Co Temperature of room: 26.6⁰C – 29.4⁰C dailyo Goal: protect wound against bacterial proliferation

- Topical antibacterial therapyo Promotes conversion of open, dirty wound to a clean oneo Silver silfadiazine : GOLD STANDARD SINCE BACTERICIDALo Criteria for choosing topical agent

Effective against P. aeruginosa (44%), S. aureus and even fungi (candida)

Staph and Enterococcus (50% nosocomial) Intestinal tract (primary source) Clinically effective Penetrates eschar but not systemically toxic Maintains effectiveness Cost effective, available, acceptable to patient Easy to apply (minimize nursing time)

- Wound dressingo Adequate wound dressingo Occlusive dressing for 3-5 dayso Circumferential: applied distal – proximal o Check for the discharge of the dressingo If excessive amount of discharges, change

- Dressing changeso Wound and surrounding skin are carefully inspectedo Dressing change procedure

- Wound debridemento Two goals:

Remove tissue contaminated with bacteria and foreign bodies →to protect patient from bacterial invasion

Remove devitalized tissue in preparation for grafting and wound healing

o Types Natural Mechanical Surgical

- Wound graftingo Autografts

graft derived from one part of the px’s body and used on another part

Ideal since no rejection can happeno Biologic dressings

Homografts (Allografts) Graft transferred from one human (living or

cadaveric) to another human Most expensive but provide best infection

control Heterografts (Xenografts)

Graft obtained from an animal of a specia (eg.: pig skin)

o Biosysnthetic and synthetic dressings Biobrane

Most widely used Less costly than homograft or pigskin Semitransparent and sterile

o Nylon, syslastic membrane combined with a collagen derivative

BCG matrix Beta glucan with collagen, stimulate

macrophages (partial thickness, donor) Dermal susbsitutes

Autologous donors are unavailable Integra

o Newest type of dermal substitute

o Composed of 2 layers Epidermal

later – silastic Bacterial barrier and prevents water loss from dermis

Dermal later – animal collagen

Alloderm- Care of the graft site

o Protectiono Replace dressing after 2-5 dayso Infection, bleeding beneath the graft, shearing force: most common

reason for graft losso Position and turning: elevated to minimize edemao Exercise 5-7 days post grafting

- Care of donor siteo Pain and infection controlo Heals 7-14 days with proper care

- Pain mgto Pain is inevitable during recovery from any burn injuryo 3 types of pain:

Background/ resting pain – exists 24 hours Procedural pain – during procedures such as wound care

or range of motion exercises Breakthrough pain – occurs when blood vessels of

analgesic agents fall below level required to control background pain

o Opoid administration (IV route) Morphine sulfate Fentayl

o Non- pharmacologic measures: relaxation techniques, deep breathing exercises, distraction, guided imagery, hypnosis, therapeutic touch, humor, information giving

D/O OF WOUND HEALING

- Scarso Hypertrophic scars

More common in children, dark-skinned, areas of stretch or motion

- Keloidso Large, heaped up mass of scar tissue

- Failure to heal- Contraptures- NRG MGT

o Restore normal fluid balance Monitor IV and OFI Use IV infusion pumps to minimize risk of rapid infusion Obtain intake, output and daily weights

o Preventing infection Detect and prevent infection Provide clean and safe environment

Clean technique used for wound care procedures Fresh fruits, flowers, and plants are not permitted in the

px’s room (risk for microbial growth) Change linens regularly

o Maintaining adequate nutrition Provide pleasant surroundings during meal time

o Promoting skin integrity Wound care

o Relieving pain and discomfort Administer meds as ordered Work quickly but efficiently during wound care to reduce

discomforto Promoting physical mobility

Monitor splinted areas Deep breathing, turning, proper repositioning

o Supporting px and family Address the spoken and unspoken concerns

o Strengthening coping strategies Include px in making decisions regarding care

Rehab phase – from wound closer to return of px to optimal functioning

- Prioritieso Prevention of scars and contractures

Require to wear pressure garment Instruct px about the need for lubrication and protection

of the healing skino Functional and cosmetic reconstructiono Promote activity tolerance

Nurse incorporates physical therapy exercises in px’s care Provide divertional activites

The exact causes of nontoxic goiter are not known. In general, goiters may be caused by too much or too little thyroid hormones. There is often normal thyroid function with a nontoxic goiter. Some possible causes of nontoxic goiter include:

Heredity (family history of goiters) Regular use of medications such as :: lithium , ::

propylthiouracil , phenylbutazone, or aminoglutethimide

Regular intake of substances (goitrogens) that inhibit production of thyroid hormone—common goitrogens include foods such as cabbage, turnips, brussel sprouts, seaweed, and millet

Iodine deficiency—Iodine deficiency is very rare in the US and other developed countries, due to the use of iodized table salt; this is a primary cause of goiter in other parts of the world, particularly in mountainous areas, or areas that experience heavy rainfall or flooding