BURNS

MR. Prasanth.K

MSc cardiothoracic nursing

ANATOMY OF SKIN

The Skin Membrane that covers entire

body Largest, most dynamic

organ

Epidermis

Dermis

Subcutaneous layer (superficial fascia)

Deep fascia

Definition Injury to the tissues of the body caused by

heat, chemicals, electric current, or radiation.

Incidence Domestic cases – 93-95% India – 0.4million / year Women are more affected than men – 1.6:1 Overall mortality – 3.5/100000 popu

Burn wound healing Inflammation Proliferation Remodeling

Inflammation Platelet adhesion Fibrin deposit Thrombus + vasoconstriction Hemostasis Local vasodilatation and increase of capillary permeability Neutrophil (24 hrs) Monocyte Macrophages Consume pathogens and dead tissue Secrete various growth factors Proliferation of fibroblasts + deposited of a provisional wound matrix

Proliferation (2-3 days post burn) Number of fibroblasts at peak Granulation Reepithelialization

Remodeling (lasts for years) Collagen fibers are reorganized Scars contract and fade in color

When burn extends to dermal tissue scars developed are

- hypertrophic- overgrowth of dermal tissue remains in the boundaries

- Colloid – extends beyond boundaries

ETIOLOGY

TYPES

Thermal

Caused by – flash , flame , scaled, contact with hot objects

Management – extinguish flame

Flush with cool water

Chemical Agent Forms Management

Acid House hold cleanersHCL, oxalic,

Water irrigation Irrigate skin with soup solution

Remove the person or agent away. Take self precaution and remove the cloth which contain chemical.

Alkali Drain cleaners Fertilizers

Adhere to tissue and protein hydrolysis

Irrigate skin with slightly acidic solutions like lemon water

Dry chemical –

Brush away from skin

Irrigate skin

Smoke and inhalation injury Agent Injury signs and

symptomsManagement

Carbon monoxide poisoning -Incomplete combustion of burning material

Cherry red skin color 10-20% - head ach , dizziness , nausea, abdominal pain

21-41%- irritability , confusion , stupor, hypotension , bradycardia, pale to dark red skin color

41-60%- convulsion , coma, hypotension, tachycardia

>60%- death

100% o2

Injury above glottis –Usually thermally produced Inhalation f hot air , steam , or smoke Especially .- burn in enclosed space

Mucosal burning of larynx and oropharynxRedness Blistering Edema Quick mechanical obstruction Singed nasal hair Hoarseness painful swallowing Darkened oral and nasal membrane Carbonaceous sputum

Medical emergency

Injury below glottis – Chemically produced

Pulmonary edema ARDS

Close observation for ARDS

Electrical burns Damage to the nerves and vessels Factors related to severity

voltage

Tissue resistance

Current pathways

Surface area of contact

Length of time

S/S

Ice berg effect

Chance of cervical spine injury (fall)

Muscle contraction – fracture

Dyarrhythmias- AF, VF

Cardiac arrest

Metabolic acidosis

Myoglobinuria lead to – acute renal tubular necrosis

Management Disconnect source of current CPR

Cold thermal injuries Frostbite – gangrene

Radiation Source – solar, X ray , radioactive agent Management

Shield

Move client away

PATHOPHYSIOLOGY

AMERICAN BURN ASSOCIATION - burn unit referral criteria

Burn injuries that should be referred to a burn unit include the following \

1. Partial thickness burns more than 10% TBSA

2. Burns that involve s the face hands feet genitalia perineum or major joints

3. Third degree burns in any age group

4. Electrical burns including lightning injury

5. Chemical burns

6. Inhalation injury

7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality

8. Any patients with burns and concomitant trauma (fractures) in which the burn injury poses the greatest risk of morbidity or mortality.

9. Patients who will require special social, emotional, or long term rehabilitation intervention

CLASSIFICATION OF BURN INJURY

Severity determined by –

Depth of burn

Extent of burn – calculated by TBSA

Location of burn

Patient risk factors

Classification based on depth Superficial Partial thickness

superficial partial thickness

deep partial thickness Full thickness

Superficial burns Involves epidermis ---- UV rays, sun burn, minor flash injury,

mild radiation s/s

Skin color – pink – bright red

Slight edema

Chills, nausea, vomiting – in extensive burns

Management – I/V fluid treatment

Partial thickness Superficial partial thickness Deep partial thickness

Affected - Dermis and papillae of dermis Bright red color + moist + glistening appearance + blisters + blanching on pressure + pain response to temperature and air is severe Heal with in 21 days + minimal or no scaring Management – analgesics Skin substitutes for large disrupted blisters

Dermis +more deeper Pale + waxy+ moist / dry large blisters + decreased capillary refill + less painful Heal – more than 21 daysComplication Necrosis may lead to full thickness injury , contractures Management – excision and grafting

Full thickness burn Epidermis + dermis + epidermal

appendages + subcutaneous fat+ connective tissue + muscle + bone

Pale ,waxy ,brown ,mottled ,leathery ,firm to touch

No sensation of pain

Management –

Skin grafting

Classification by extent of burn Lund- Browder chart According to Rule of nine

( not accurate for estimating the percentage TBSA for adults who are short, obese or very thin. )

Sage burn diagram – computerized burn estimation tool.

(www.sagediagram.com)

Classification according to ABA Minor burn injury Moderate burn injury Major burn injury

Excludes electrical injury, inhalation injury, and all clients at high risk Partial thickness burns of less than 15 % of TBSA in adults Full thickness burns of less than 2% of TBSA not involving special care areas.( eye ,ear, hand , feet, face , joints , perineum )

Excludes electrical injury, inhalation injury, and all clients at high risk Partial thickness burns of less than 15 %- 25 % of TBSA in adults Full thickness burns of less than 10 % of TBSA not involving special care areas.( eye ,ear, hand , feet, face , joints , perineum )

Includes electrical injury, inhalation injury, and all clients at high risk involving special care areas.( eye ,ear, hand , feet, face , joints , perineum

Partial thickness burns of more than 25 % of TBSA in adults Full thickness burns of 10 % or greater of the TBSA

DIAGNOSTIC EVALUATION Sodium

hyponatreamea - dilutional Hyponatreamea

Water intoxication

Potassium – hyperkalemea – renal failure

Adrenocortical insufficiancy

Massive deep muscle injury

Hypokalemea- dilution / GI wash…

MANAGEMENT Pre hospital care Emergent phase

Air way management

Fluid therapy

Wound care

PRE HOSPITAL CARE Remove person from the source of burn Self shield – by rescuers Small burns <=10% TBSA – covered with

clean, cool, tap water-dampened towel. Assesement and Management of ABC

EMERGENT PHASE (resuscitative phase)

Air way management Early Endotracheal / orotracheal intubation Ventilatory assistance – with PEEP assess ABG values Extubation- when edema resolves Escharotomies - to relive respiratory

distress secondary to circumferential, fulthickness burns to the neck and trunk

Assess lower respiratoty tract by – fiberoptic bronchoscopy

For inhalation injury – no intubation perfornmed

Humidified Oxygen

Position – high fowler’s position (not for pts with spinal injury)

If spinal injury – reverse tendelberg position Deep breathing and coughing exercise Reposition every 1-2 hrs Bronchodilators O2 therapy until carboxyhemoglobin

become normal .

Fluid therapy Pt >15% TBSA – large bore I/V access >30% TBSA – central and arterial line Crystalloid solutions – RL Colloids – albumin Calculate fluid requirement brooke’s and

(baxter) parkland formula

Formula First 24 hrs Second 24 hrs

Brooke (modified)

Crystalloid colloids Glucose in water

4ml RL X Kgbody wt X%TBSA burn= total fluid repalcement for 1st 24 hrs Application ½ of total in 1st 8hrs ¼ of total in second 8 hr ¼ of total in third 8 hr

0.3-0.5ml/kg/% TBSA

Amount to replace estimated evaporative losses

Parkland formula (baxter)

RL 4ml X kgX %TBSA burn, ½ given first 8hr¼ given each next 8 hr

20-60% of calculated plasma volume

Amount to replace estimated evaporative losses

Wound care Start until airway patency maintained Cleansing and gentle debridement

Necrotic skin removed

Escharotomies ( removal of dry scab)

Fasciotomies Hydrotherapy / cart shower

Once daily shower and dressing

Control of infection Open method Multiple dressing change method

Burn covered with cover with topical antimicrobial solution with out dressing

Sterile dressing impregnated with topical antimicrobial medication changed every 12 / 24 hrs or once in every 3 days.

Moist wound healing method

Skin graft Porcine skin – hetero graft or xenograft

(different spicies)

Cadaveri skin – homograft or allograft (same spicies)

Cultured epithelial autograft

Autograft – own skin

Porcine collagen bonded to silicone memberane – Biobrane

Bovine collagen and glycosaminoglycan bonded to silicone memberane

Acellular dermal matrix derived from donated human skin ( Alloderm )

Care of facial burn Open dressing Ophthalmological examination – corneal

burns and edema Periorbital edema – reassurece

DRUG THERAPY

Analgesics I/v medications Mrphine Fentanyle Morphine NSAIDs Oxycodone

Sedatives Haloperidol Lorazepam Midazolam

Other medications Ranitidine Nystatin Antacids

Tetanus immunization

If not had active immunization in 10 years – go for tetanus immunoglobulin

Antimicrobial agents

Silver sulfadiazine Mafenide acetate

Oral infection – nystatin mouth wash

NUTRITIONAL THERAPY TPN High protein high cal – diet

ACUTE PHASE Wound care

Debridment of necrotic tissue

Enzymatic debridement

Use meshed dressing with paraffine oil

Moist dressing for donor site

Skin grafting Pain management Other pain management techniques

Guided imaginary

Relaxation therapy

Hypnosis

Physical and occupational therapy

ROM

Nutritional care

Psychosocial care

REHABILITATION PHASE Manage emotions

Fear

Anger

Anxiety

Guilt

Depression

COMPLICATIONS Contractures – abnormal condition of a joint

characterized by flexion and fixation

NURSING DIAGNOSIS Impaired gas exchange related to carbon

monoxide poisoning as evidenced by labored breathing

Ineffective air way clearance related to edema and effects of smoke inhalation and evidenced by ventilatory support

Disturbed body image related to disfigurement secondary to burn as evidenced by verbalized negative comments about appearance.

Fluid volume deficit related to fluid loss as manifested by decreased serum electrolyte level and dry skin

Acute pain related to impaired skin integrity as manifested by facial expression and crying.

Impaired skin integrity related to thermal injury as manifested by blisters and lesions.

Activity intolerance related to weakness, as manifested by verbalization.

Anxiety related to prognosis of disease condition and disturbed body image.

Risk for infection related to impaired skin integrity and suppressed immune response

Risk for contractures related to the burn injury

Ineffective individual coping related to fear and emotional impact of burn injury as evidenced by increased questioning

Imbalanced nutrition less than body requirement related to inability to intake as evidenced by weight loss.

Hyperthermia, related to infection, as manifested by rise in body temperature..

Research studies

The treatment of pain produced during the management of burn injury has been an ongoing problem for physicians caring for these patients. The main therapeutic option for analgesia has been the repeated and prolonged use of opioids.

The adverse effects of opioids are well known but the long term use of opioids which produces tolerance with accompanying dose escalation and dependence is most problematic. Another potentially important consequence of opioid exposure that sometimes masks as tolerance is that of opioid induced hyperalgesia.

This syndrome is manifest as enhanced pain, sensitivity and loss of analgesic efficacy in patients treated with opioids who actually become sensitized to painful stimuli. This article focuses on the treatment of burn pain and how current analgesic therapies with opioids may cause hyperalgesia and affect the adequacy of treatment for burn pain. This article also provides possible modalities to help therapeutically manage these patients and considers future analgesic strategies which may help to improve pain management in this complicated patient population.