Advanced Burn Life Support 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 contact with environment
What is a Burn?
An injury to tissue from:
Exposure to flames or hot liquids Contact with hot objects Exposure to caustic chemicals or radiation Contact 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 Ringers 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 Ringers Figure out burn size by rule of nines or entire palmar surface of pts 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 Patients 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 LundBrowder Charts
Orgill D. N Engl J Med 2009;360:893-901
Robyns 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 Support 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 admitted 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 (%)
0-10 10-30 30-50 50-60 60+
Signs/Symptoms
None Headache Headache, nausea, dizziness, tachycardia CNS dysfunction, coma 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
Prior to transfer to burn center Intubation
to clear secretions relieve dyspnea deliver PEEP Improve oxygenation
Inhalation Injury Below the Glottis: Treatment
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 Ps
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 joints 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
Contact 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 Pass 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 contact 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 passage 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
ABCs 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 admission Continuous cardiac monitoring for first 24 hours
Management of Electrical Injury: Fluid Resuscitation
Administer Ringers 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 CPK & urine myoglobin due to possibility of rhabdomyolysis
Management of Electrical Injury: Peripheral Circulation
Hourly monitoring of skin color, sensation, capillary refill and peripheral pulses Remember 6Ps 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 Contact chemical burns & systemic effects
Chemical Burns
Factors That Determine Severity:
Agent Concentration Volume Duration of contact (delay in treatment) Alkalis generally cause worse damage
Treatment of Chemical Burns
Speed is essential, ABCDE, Eremove clothing The clinical signs of severe chemical injury : altered mental status, respiratory insufficiency, cardiovascular instability, and a period of unconsciousness or convulsions. Initial supportive 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
Contact 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 Ringers Lactate is administered 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)
20-100 200-400
Response
Change in # of leukocytes 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
2 000+
GI ulceration, death within 2 weeks
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) 300 1000-2000 2000 Epilation Erythema Transdermal Injury 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 administer warm air Central administration of warm Ringers solution
Cold Injuries: Hypothermia
Monitor for systemic acidosis with serial ABGs
Treat with sodium bicarbonate
Cardiopulmonary bypass Cardiac monitoring
Ventricular dysrhythmia
Patients not to be declared dead until rewarmed
Continue CPR 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 yes yes yes no no no no no Tetanus-Prone Wounds TD1 TIG yes yes yes no yes yes no no
Uncertain 0-1 2 3 or more
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!