Advanced Burn Life 632b67

Advanced Burn Life Manual Review

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Skin Anatomy Epidermis Dermis

Hypodermis

Function of Normal Skin • • • •

Protection from infection & injury Prevention of loss of body fluid Regulation of body temperature Sensory with environment

What is a Burn? • An injury to tissue from: –Exposure to flames or hot liquids – with hot objects –Exposure to caustic chemicals or radiation – with an electrical current

Pathophysiology of Burn Injury • Zone of Coagulation: – Irreversible damage

• Zone of Stasis: – Impairment of blood flow – Recovery variable

• Zone of Hyperemia: – Prominent vasodilation – Usually recovers

Pathophysiology of Burns • Get edema in burned & non-burned skin • Burns cause coagulative necrosis – Chemical/Electricity also cause direct injury to cell membranes, in addition to heat transfer

• Depth of burn depends on: – 1. Temperature – 2. Time exposed – 3. Specific heat (higher for grease)

Pathophysiology of Burns • Burns release of inflammatory mediators • Increased capillary permeability – Leak proteins into interstitium

• Large fluid loss due to fluid shifts & also losses from exposed burned skin • Characteristic “Ebb and Flow” of burns – Ebb: Low metabolism/cardiac output, ↓Temp – Flow: hypermetabolism, high cardiac output, hyperglycemia, increased heat produx

Burn Pathophysiology: Systemic Response • Accelerated intravascular volume depletion • Inadequate tissue perfusion • Risk of multiorgan dysfunction

Burn Pathophysiology: Metabolic Response • Hypermetabolism:  glucose metabolism, lipolysis, and proteolysis • Neuroendocrine response:  catecholamines,  thyroid hormones,  cortisol

Burn Pathophysiology: Tissue Repair • Initial hemostatic response = coagulation and microvascular constriction • Resuscitative phase = vasodilatation and capillary leak • Epithelialization = restoration of fluid maintenance, temperature regulation, and microbial barrier function • Fibrogenesis = wound appearance and strength

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Initial Assessment (primary survey) • Initial burn treatment: remove burn source • Always start with ABC – In trauma/burns, ABCDE (disability/exposure)

• Airway can be an issue with severe burns or inhalational injury (esp. with indoor fire) – Direct injury from heated air/smoke -> edema – Edema from inflammatory response to burns – Edema from the resuscitation fluids

Initial Assessment (primary survey) • Suspect airway injury if: – Facial burns, singed nasal hairs, wheezing, carbonaceous sputum, tachypnea

• Give pt oxygen & put on pulse oximetry • Progressive hoarseness is a sign of impending airway obstruction • Pre-emptively intubate anyone with: – Respiratory distress, inhalational injury, large burns (due to inevitable edema from resusc) – Bronchoscopy to help dx inhalational injury

Initial Assessment (primary survey) • Breathing (Breath sounds, chest rise, ET CO2) – Chest escharotomies if constrictive eschar

• Circulation: get vitals (HR & BP) – 2 large bore IV (unburned before burned skin) – Start burn resuscitation with Lactated Ringer’s – Place patient on continuous EKG / monitor – Palpate or doppler extremity signals with circumferential extremity burns

• Disability (GCS less than eight -> intubate) • Exposure: remove all clothing

Initial Assessment (secondary survey) • Complete heat-to-toe examination • AMPLE history – Allergies – Medications (also ask about last tetanus) – Past medical history (CHF – careful w fluids) – Last meal – Events regarding the injury (how did the fire start, how long was the exposure, what type of exposure – flame, grease)

Initial Assessment • Burn Resuscitation with Lactated Ringer’s • Figure out burn size by “rule of nines” or entire palmar surface of pt’s hand = 1% (palm rule) • Parkland formula – 4 x Wt(kg) x %TBSA = mL to give in 1 day – Half over 1st 8hrs (subtract what was given) – Give other Half over next 16 hours – In reality, titrate to UOP of 0.5mL/kg/hr in adults and 1mL/kg/hr in children • Do not give colloid in first 24 hrs

Severity of a Burn Depends on: • Depth of burn • Extent of burn • Location of injury • Patient’s age • Presence of associated injury or diseases

Depth of a burn Superficial (1°): epidermis (sunburn) Partial-thickness (2°): Superficial partial-thickness: papillary dermis Blisters with fluid collection at the interface of the epidermis and dermis. Tissue pink & wet. Deep partial-thickness: reticular dermis Blisters. Tissue molted, dry, decreased sensation. Full-thickness (3°): dermis Leathery, firm, insensate. 4th degree: skin, subcutaneous fat, muscle, bone

Classification of Burn Depth

Third degree

Depth of a Burn • First Degree – Epidermis only – Erythematous – Hypersensitive – Classic sunburn – Heals without scar

Depth of a Burn • Second Degree – Epidermis + part of dermis • Superficial • Deep – Blisters – Edematous and red – Very painful – Scaring variable

Depth of a Burn • Third Degree – Full thickness burn – Can involve underlying muscle, tendon, bone – Waxy white, leathery brown or charred black – Painless – Heals with scar

Extent of a Burn • “Rule of Nines” – Most universal guide for initial estimate – Deviates in children due to larger head surface area – Palm rule

The Rule of Nines and Lund–Browder Charts

Orgill D. N Engl J Med 2009;360:893-901

“Robyn’s Rule of 4s”

Criteria for Referral to a Burn Center

(Orgill D. NEJM 2009;360:893-901)

ABA Burn Referral Criteria (addition) • 2nd & 3rd degree burns of greater than 10% BSA in patients under 10 or over 50 yrs old • 2nd & 3rd degree burns of greater than 20% BSA in other age groups • 2nd & 3rd degree burns with functional or cosmetic implications • 3rd degree burn of greater then 5% BSA • Circumferential burn of chest or extremity

Management Principles • • • • • • •

Stop the Burning Process Universal Precautions Airway Management Breathing Management Circulatory Management Insertion of a Nasogastric Tube Insertion of a Foley Catheter

Management Principles • • • • •

Relieve Pain Assess Extremity Pulses Regularly Assess for Ventilatory Limitation Provide Emotional Suicide Management

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Airway Management

Inhalation Injury • Important determinant of morbidity & mortality • Manifests within the first 5 days after injury • Present in 20-50% of pts itted to burn centers • Present in 60-70% of pts who die in burn centers

Indicators of Inhalation Injury • • • • • • •

Burned in closed space Facial or intra-oral burns Singed nasal hairs Soot in mouth, nostrils, larynx Hoarseness or stridor Respiratory distress Signs of hypoxemia

History of Event • Is there a history of unconsciousness? • Were there noxious chemicals involved? • Did injury occur in closed space?

Types of Inhalation Injury • Carbon Monoxide Poisoning • Inhalation Injury Above the Glottis • Inhalation Below the Glottis

Carbon Monoxide Poisoning • • • •

Colorless, odorless gas Binds to hemoglobin 200 times more than oxygen Most immediate threat to life in survivors with severe inhalation injury Toxicity related directly to percentage of hemoglobin it saturates

Carbon Monoxide Poisoning Signs & Symptoms of Carbon Monoxide Toxicity

Carboxyhemoglobin (%)

Signs/Symptoms

0-10

None

10-30

Headache

30-50

Headache, nausea, dizziness, tachycardia

50-60

CNS dysfunction, coma

60+

Death

Signs of CO Poisoning • • • • •

Cherry red coloration Normal or pale skin with lip coloration Hypoxic with no apparent cyanosis PaO2 is unaffected Essential to determine carboxyhemoglobin levels !

CO Poisoning: Treatment • 100% oxygen until carboxyhemoglobin levels less than 15 – Increases rate of CO diffusion from 4 hours to 45 minutes

• Hyperbaric oxygen is of unproven value – May be useful in isolated CO intoxication but complicates wound care

Inhalation Injury Above the Glottis • Most common inhalation injury • Results from heat dissipation into tissues • Commonly leads to obstruction • Edema lasts for 2-4 days • Dx by visualization of upper airways

Inhalation Injury Above the Glottis: Treatment

Intubate!!!

Inhalation Injury Below the Glottis • Chemical pneumonitis caused by toxic products of combustion – Ammonia, chlorine, hydrogen chloride, phosgene, aldehydes, sulfur & nitrogen oxides – Related to amount and type of volatile substances inhaled

• Onset of symptoms is unpredictable – Close monitoring for first 24 hours

Inhalation Injury Below the Glottis: Treatment

Prior to transfer to burn center • Intubation – – – –

to clear secretions relieve dyspnea deliver PEEP Improve oxygenation

• Steroids not indicated • Prophylactic antibiotics unjustified • Circumferential chest burns: escharotomies

Inhalation Injury in the Pediatric Patient • Small airways: rapid onset of obstruction – Well secured, appropriately sized, uncuffed tube

• Rib cage is not ossified – More pliable – Pt exhausts rapidly due to decrease in compliance with circumferential chest burns – Escharotomies performed with first evidence of ventilatory impairment

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Shock & Fluid Resuscitation Goal: • To maintain vital organ function while avoiding the complications of inadequate or excessive therapy

Systemic Effects of Burn Injury • Magnitude & duration of response proportional to extent of surface burned • Hypovolemia – Decreased perfusion & oxygen delivery

• Initial increase in PVR & decrease in CO – Neurogenic & humoral effects

• Corrected with adequate fluid resuscitation – Prevent shock & organ failure

Cellular Response to Burn Injury • Severity dependant on temperature exposed and duration of exposure • “Zone of Stasis”: recovery of injured cells dependant on prompt resuscitation

Resuscitation Fluid Needs • Related to: – extent of burn (rule of nines) – body size (pre-injury weight estimate)

• Delivered through large bore peripheral IV – Attempt to avoid overlying burned skin – Can use venous cut down or central line

Resuscitation Fluid Needs: First 24 Hours • Parkland Formula: – Adults: 2-4 ml RL x Kg body weight x % burn – Children: 3-4 ml RL x Kg body weight x % burn

• First half of volume over first 8 hours, second half over following 16 hours – Hypovolemia, decreased CO – Increased capillary permeability – Crystalloid fluid is keystone, colloid not useful

Resuscitation Fluid Needs: Second 24 Hours • Capillary permeability gradually returns to normal • Colloid fluids started to minimize volume – Only necessary in patients with large burns (greater than 30% TBSA) – 0.5 ml of 5% albumin x Kg body weight x % burn

Monitoring of Resuscitation • Actual volume infused with vary from calculates according to physiologic monitoring • Optimal regimen: – minimizes volume & salt loading – prevents acute renal failure – low incidence of pulmonary & cerebral edema

Monitoring of Resuscitation • Urinary output is a reliable guide to end organ perfusion – Adults: 30-50 ml per hour – Children (less than 30 Kg): 1 ml/Kg per hour

• Infusion rate should be increased or decreased by 1/3 if u/o falls or exceeds limits by more than 1/3 for 2-3 hours

Fluid Resuscitation Complications • Overresuscitation complications: Poor tissue perfusion Compartment syndrome Pulmonary edema Pleural effusion Electrolyte abnormalities

Management of Myoglobinuria & Hemoglobinuria • High voltage electrical injury and mechanical trauma • Maintain urine output of 75-100 ml per hour • Add 12.5 gm of Mannitol to each liter of fluid – Urine output not sustained – Urine pigment does not clear

• Sodium bicarbonate 1 amp (50 meq) per liter of fluid – Heme pigments more soluble in alkaline urine

Monitoring Resuscitation • Blood pressure: – Can be misleading due to progressive edema & vasoconstriction

• Heart Rate: – Tachycardia commonly observed

• Hemaglobin & hematocrit: – Not a reliable guide – Transfusion not to be used for resuscitation

• Baseline serum chemistries & arterial blood gases – Baseline to be obtained in burns of >30% BSA

Monitoring Resuscitation • CXR: daily for first 5-7 days – Normal study in first 24 hours does not r/o inhalation injury

• ECG: – All electrical injuries – Pre-existing cardiovascular disease

Fluid Resuscitation in the Pediatric Patient • Require greater amounts of fluid – Greater surface area per unit body mass

• More sensitive to fluid overload – Lesser intravascular volume per unit surface area burned

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Wound Management: General • Clean & debride wound • Prophylactic systemic abx unnecessary (no data for oral or IV abx) • Topical abx delay wound colonization and infection • Give tetanus toxoid if not up to date • Escharotomy/fasciotomy may be required (circumferential burns, deep burns, compartment syndrome)

Initial Burn Wound Management • Circumferential deep 2nd or 3rd degree extremity burn can compromise circulation • Assess for the 6 P’s – Pain, – pallor, – pulselessness (check Doppler), – paresthesias, – paralysis, – poikilothermia

Initial Burn Wound Management Extremity Escharotomy Chest Escharotomy • Circumferential burn of • Circumferential chest the extremity wall burns • Remove rings, watches • Performed in the anterior • Elevation of limb axillary line • Hourly monitoring: • Extend to abdominal wall – Skin color, Temperature if involved – Sensation, Pain – Capillary refill • Divide eschar completely – Electric cautery – Sharp division

– Peripheral pulses – Ultrasonic flowmeter

Initial Burn Wound Management Finger Escharotomy • Seldom required • Performed after consultation with burn center physician • Extend through full thickness of skin only • Avoid tactile areas

Performing an Escharotomy • Bedside procedure • Sterile technique (sharp division or electrocautery) • Local anesthesia not required – Control anxiety

• • • •

Avoid major nerves & vessels Extend incision into subcutaneous fat Incision to be carried across involved ts 2nd incision on contralateral aspect of limb may be required

Wound Management: Topical Antibiotics • Mafenide acetate (Sulfamylon) for ears – Good at penetrating eschar & is painful – Broad spectrum – Side effect: metabolic acidosis via carbonic anhydrase inhibition

• Bacitracin for face – Gram-positive bacteria

• Silver sulfadiazine (Silvadene) for trunk & extremities – Broad spectrum, esp. Pseudomonas – Does not penetrate eschar very well – Side effects: neutropenia/thrombocytopenia

Excision and Grafting • 3rd & (most) deep 2nd need early excision & grafting, • Except – palm, – soles, – face, – Genitals Perform 3-7 days post-burn

Orgill D. N Engl J Med 2009;360:893-901

Wound Management: Burn Excision & Grafting • Early excision & grafting improved burn patient mortality & functional outcome • Initial excision should occur soon after resuscitation • Full-thickness skin grafts (FTSG) • Split-thickness skin grafts (STSG) • Human allograft • Porcine xenograft • Dermal substitutes: Integra

Specific Anatomical Burns • Facial Burns

– Require hospital care – Possibility of respiratory damage

– Elevate HOB 30 degrees – Use water or NS to clean to avoid

chemical conjunctivitis

Specific Anatomical Burns • Burns of the Eyes – Examine ASAP – Use fluorescein to identify corneal injury – Chemical burns to be rinsed with copious NS – Opthalmic antibiotic drops if corneal injury present – Solutions with steroids dangerous – Tarsorrhaphy is never indicated in acute phase

Specific Anatomical Burns • Burns of the Ears – Examine external canal & drum early – Determine if OM/OE present – Avoid pressure dressings & additional trauma

Specific Anatomical Burns • Burns of the Hands – Determine vascular status & need for escharatomy – Presence of radial pulse does not exclude compartment syndrome – Monitor with Doppler U/S – Elevate hand above heart – Dressings impair ability to monitor

• Burns of the Feet – Assess circulation on scheduled basis – Elevate limb – Dressings to be avoided to not interfere with monitoring

Specific Anatomical Burns • Burns of the Genitalia & Perineum – Burn to the penis requires immediate insertion of Foley catheter – With circumferential burns, a dorsal escharotomy may be indicated – Scrotal swelling does not require treatment – Diverting colostomy not indicated in perineal burns

Tar Burns • burns • Bitumen is non-toxic • Immediate cooling of molten with cold H20 • Removal of tar not an emergency • Cover with petroleum based product & dressed to emulsify tar

Please the Mayo!

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Electrical Injury • Occurs when electricity is converted to heat as it travels through tissue • Divided into: – High voltage – greater than 1000 V • Local injury, deep injury, fractures, blunt injuries • Risk of rhabdomyolysis, compartment syndrome, cardiac injury

– Low voltage – less than 1000 • Local injury

• Hands & wrists are common entrance wounds • Feet are common exit wounds

Electrical Burns • Extremely difficult to evaluate clinically • Greatest tissue damage occurs under and adjacent to points, • Most significant injury is within deep tissue • Edema can compromise circulation • Explore & debride necrotic tissue • May have to re-explore questionable areas • Late complications: cataracts, progressive demyelinating neurologic loss

Types of Tissue Injury • Cutaneous Burn with no underlying tissue damage – No age of current through patient

• Cutaneous Burn plus deep tissue damage – Involving fat, fascia, muscle and/or bone

• Muscle damage associated with myoglobin release – Urine may be light red to “port wine” color – Risk of kidney damage

Lightning Injury • Direct current of >100 000 000 volts and up to 200 000 amps • Injury results from: – Direct strike – Side flash • Flow of current between person & nearby object

• Often travels on surface of body – Burns typically superficial – “splashed on” spidery pattern

Management of Electrical Injury • ABC’s • Assess Injury – History • LOC, cardiac arrythmia, other trauma – Physical Exam • neuro exam, long bone #, dislocations, cervical spine

• Maintain Patency of Airway • Cardiac Monitoring: – Standard 12 lead EKG on ission – Continuous cardiac monitoring for first 24 hours

Management of Electrical Injury: Fluid Resuscitation • ister Ringer’s Lactate in amounts estimated with Parkland Formula – Will underestimate required volume due to underlying tissue damage – Increase fluids as per urine output

• Examine urine for pigment – Maintain urine output 75-100 ml/hr until clear – Add 1 amp (50 meq) per liter of RL to alkalize urine – Mannitol 12.5 mg/liter to maintain urine output

• Follow serial K & urine myoglobin due to possibility of rhabdomyolysis

Management of Electrical Injury: Peripheral Circulation • Hourly monitoring of skin color, sensation, capillary refill and peripheral pulses • 6P’s • Remove all rings, watches, jewelry • Surgical correction of vascular compromise – Decompression by escharotomy or fasciotomy – Upper limb-volar & dorsal incisions with protection of ulnar nerve – Lower limb-medial & lateral incisions

Electrical Burns in the Pediatric Patient • Low voltage accidents most common – Generally household (faulty insulation, frayed cords, insertion of metal object into wall socket) – Cutaneous injury, no muscle damage

• Oral commisure injury – Look worse than they are

– No initial debridement

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Chemical Burns: Classification • Alkalis – Hydroxides, carbonates and caustic sodas of sodium, ammonium, lithium, barium & calcium – Oven & drain cleaners, fertilizers, industrial cleaners

• Acids – HCl, oxalic, muriatic & sulfuric acids – Common in household & swimming pool cleaners

• Organic Compounds – Phenols, creosote, petroleum products – chemical burns & systemic effects

Chemical Burns • Factors That Determine Severity: – Agent – Concentration – Volume – Duration of (delay in treatment) – Alkalis generally cause worse damage

Treatment of Chemical Burns • Speed is essential, ABCDE, “E”remove clothing • The clinical signs of severe chemical injury : – altered mental status, – respiratory insufficiency, – cardiovascular instability, and – a period of unconsciousness or convulsions. • Initial ive therapy should be focused on airway patency, ventilation, and circulation, at the same time that patients are examined for burns, trauma, and other injuries.

Treatment of Chemical Burns • • • •

Wear gloves and protective clothing Remove saturated clothing Brush skin if agent is a powder End the exposure, Irrigate, irrigate, irrigate! – Copious amounts of water – Continued until pain or burning has decreased

• Neutralization of agent contraindicated – Generation of heat may lead to further injury

Specific Chemical Burns: Treatment • Alkali Injury to the Eye – Bond to tissue proteins leading to liquefaction necrosis – Require prolonged irrigation • Water or saline

– Likely to present with swelling & lid spasm – Place catheter in lateral sulcus to irrigate

Specific Chemical Burns: Treatment • Petroleum Injuries – with gasoline or diesel fuel – Delipidation: causes an initial partial thickness burn become a full-thickness burn – Systemic toxicity evident within 6 to 24 hours • • • •

Pulmonary insufficiency Hepatic failure Renal failure CNS narcosis

– No specific antidote

Specific Chemical Burns: Treatment • Hydrofluric Acid – Most tissue reactive inorganic acid – Fluoride ion penetrates & binds tissue • Ceases when it combines with Ca or Mg • Burns greater than 5%TBSA – can be life threatening

– Acute Tx: copious irrigation with H2O or Zephiran (benzalkonium chloride) – Topical calcium gluconate gel or Epsom salts – If pain persists, inject 10% Ca gluconate into site – Intraarterial and IV infusions with Bier block – Hydrofluoric acid: can cause severe hypoCa

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Pediatric Burns • Scald burns most common burn in < 3 years • Flame burns most common in children > 3 years • Always consider child abuse

Pediatric Burns: Pathophysiology • Greater surface area per pound of body weight – Greater fluid needs – Greater evaporative water loss – Greater heat loss

• Disproportionately thin skin – Burns may be deeper than initially assessed – Requires less exposure time to result in burn

Pediatric Burns: Airway • Intubation performed by someone experienced • Larynx more cephalad – More acute angulation of the glottis

• Incuffed tube always used • Cricothyroidotomy is never indicated • Large bore needle placed through cricothyroid membrane may be used in emergency cases

Pediatric Burns: Circulatory Status • Burn > 10% BSA should be hospitalized • IV Ringer’s Lactate is istered as per formula – Must also add maintenance fluid (4-2-1 rule)

• NG tube • Urinary catheter to monitor urine output: – <30 Kg: 1ml/Kg per hour – >30 Kg: 30-50 ml per hour

• If hypoglycemic, add 5% glucose to RL solution

Pediatric Patient: Wound Care • Stop burning process • Remove all clothing • Topical antibiotics not indicated before transfer • Conserve heat with thermal blankets • Escharotomy – Chest: ventilatory impairment – Limb: vascular compromise

Overview • • • • • • • • •

Burn Pathophysiology Initial Assessment & Management Airway Management & Inhalation Injury Shock & Fluid Resuscitation Burn Wound Management Electrical Injuries Chemical Burns Pediatric Burns Other Topics

Radiation Injury • Effects reproductive mechanism of certain tissue cells • Mature cells suffer less damage • Stem cells are more vulnerable to injury • Large doses of radiation (> 2000 RAD) may lead to acute mortality

Outcomes Associated with Ranges of Whole Body Radiation Whole Body Dose(RAD)

Response

20-100

Change in # of leukocytes

200-400

Severe reduction in leuks, N/V, hair loss, death due to infection

600- 1 000 Destruction of mone marrow, diarrhea, 50% mortality within 1 month

1 000-2 000

GI ulceration, death within 2 weeks

2 000+

Death within hours due to severe damage to CNS

Types of Ionizing Radiation • Alpha particles – Large, highly charged particles – Associated with decay of natural radioactive elements – Penetrate only a few microns of tissue

• Beta particles – Positive electrons or negatively charged particles – Penetrate approximately 1 cm of tissue

Types of Ionizing Radiation • Gamma and X-rays – Radioactive decay or x-ray machines – Penetrate deeply – Once removed from source, no further radiation injury occurs – Poses no threat to attendants

• Protons, Deuterons, Neutrons, Mesons and Heavy Nuclei – Produced by equipment for medical and industrial use

Radiation Burns • Identical in appearance to thermal burns – Treat as you would a non-contaminated burn

• Differ from thermal burns from time between exposure and clinical manifestation SKIN RESPONSE TO RADIATION 200-300 (RADS)

Epilation

300

Erythema

1000-2000

Transdermal Injury

2000

Radionecrosis

Toxic Epidermal Necrolysis (TEN) • Exfoliative deramatitis – Begins with target lesions, develop into papules & bullae – Injury identical to partial thickness burn – Mucosal involvement of conjunctiva & GI tract

• Multiple eitiologies – Drugs (penicillins, sulfas, anti-inflammatories) – Infection: (staph toxin, HSV, menigococcus, septicemia) – Often unknown

Toxic Epidermal Necrolysis • TEN Type I – (Staph scalded skin syndrome) – Only stratum corneum denuded – Frequently in children – Excellent prognosis – 5% mortality

• TEN Type II – ( Stevens-Johnson syndrome) – Separation is at the dermal/epidermal junction – Adult population – High mortality (25-50%)

Initial Management of TEN • • • • • •

Steroids not indicated Systemic antibiotics limited to specific infection Fluid replacement Biologic dressing Maintain nutrition Prevent complications

Cold Injuries: Frostbite • Formation of ice crystals in the tissue fluids • Occurs in areas that lose heat rapidly • Three degrees of frostbite: – First degree: painful white or yellow firm plaque – Second degree: painful superficial clear or milky blisters – Third degree: deep red or purple blisters or skin color that is markedly changed

• Severity influenced by both patient & environment factors

Cold Injuries: Treatment of Frostbite • Rapid re-warming in 4O degree water bath • Avoid mechanical trauma - No massaging! • Tetanus prophylaxis • Escharotomy if vascularity compromised • Tissue injury is often underestimated

Cold Injuries: Hypothermia • Defined as a core temperature < 34 degrees C • Signs are vague & non-specific – May mimic other disease states

• Treatment: – Limit stimulation of patient –V.Fib easily induced – Rapid re-warming i9n warm water bath – Intubation to ister warm air – Central istration of warm Ringer’s solution

Cold Injuries: Hypothermia – Monitor for systemic acidosis with serial ABGs • Treat with sodium bicarbonate

– Cardiopulmonary by – Cardiac monitoring • Ventricular dysrhythmia

– Patients not to be declared dead until rewarmed • Continue R until core temperature> 36 degrees C.

– Secondary assessment for contributing diseases

Hyperthermia: Clinical Syndromes • Heat Cramps – Result from excessive loss of salt by evaporation – Experiences severe pain & cramping in muscles – Tx: oral replacement of salt & water

Hyperthermia: Clinical Syndromes • Heat Exhaustion – Consequence of inappropriate cardiovascular response to stress of heat – Diversion of blood to skin is not accompanied by vasoconstriction to other areas or by volume expansion – Present with postural hypotension, profuse sweating, pallor, nausea, light-headedness – Tx: oral replacement or IV normal saline if severe

Hyperthermia: Clinical Syndromes • Heat Stroke – Failure of body cooling mechanism • severe hyperpyrexia

– Setting of physical exercise w/o acclimatization – Present with temperature>103, no sweating, decreased LOC – Tx: rapid cooling until temperature <102 deg – If shivering develops, slowly give IV Thorazine – DIC frequently reported

Tetanus Immunization CLINICAL TETANUS-PRONE CLEAN FEATURES WOUNDS WOUNDS Age of wound > 6 Hours <6 Hours Configuration Stellate, avulsion Linear, abrasion Mechanism Missile,crush,heat, Sharp surface cold Signs of Infection Present Absent Devitalized Tissue Present Absent Contaminants Present Absent

Tetanus Immunization History Of Tetanus

Clean Wounds TD1 TIG

Uncertain 0-1 2 3 or more

yes yes yes no

Tetanus-Prone Wounds TD1 TIG

no no no no

yes yes yes no

yes yes no no

Consider patient partially immunized if: **For a clean wound, if last Td given > 1O years ago **For a dirty wound, if last Td given > 5 years ago

The End!