Electrical & Chemical Flashcards
How do you classify electrical burns?
- Voltage
- High (> 1000V, assoc’d w/ deep tissue injury/rhabdo/AKI) vs. low (< 1000V)
- Current
- AC vs. DC
- Mechanism
- Flash (thermal burn), arc (usu high voltage, assoc deep tissues injured), conduction (injury to deep tissues between contact points)
What is the pathophysiology of injury in electrical injuries?
3 mechanisms of injury:
- Direct cellular damage due to change to cellular membrane potential, electroporation (formation of acqeuous pores in lipid cellular bilayer –> coagulation necrosis)
- Transfer of electrical energy into heat energy - deep tissue thermal destruction, coagulative necrosis
- Mechanical injury - electrical injury often associated wiht some form of trauma - ie fall or fracture
define electroporation
Electroporation is a concept relevent to electrical burns
Process by which the lipid bilayer of cells is disrupted and aqueous pores form, causing direct cellular necrosis
What are the factors that determine the severity and distribution of electrical injury?
Kouwenhaven’s 7 factors
- Amount of Voltage: high worse than low
- Type of current: AC worse than DC at low voltage
- Amount of current: Higher current worse (esp for cardiac injury)
- Pathway of current: arm to arm contact points worse than arm to leg (more cardiac, sci)
- Resistance: greater resistance worse severity; resistance is inversely proportioal to cross-sectional area (ie wrist, ankle, extremity > trunk)
- Duration of contact: longer = worse
- Area of contact: greater area = worse
Discuss immediate management of patient with electrical injury
Follow ATLS protocol
- Primary survey
- ABCS, consider intubation, assess/identify other sites of life/limb threatening injury, palpate distal pulses, ECG & cardiac monitor, give tetanus prophylaxis
- Secondary survey
- Measure TBSA, identify circumferential injury, identify “contact points”, palpate compartments +/- measure compartment pressure & distal pulses, neurologic injury
- Initiate fluid resuscitation
- Complete history: TAMPLE
- Type of injury (voltage, current, flash/arc/conduction), duration of contact, area of contact, witnessed mechanical/associated injury, loss of vital signs/consciousness
- First aid +/- CPR performed at scene, on transfer
- Initial workup
- Labs
- Cardiac monitoring and ECG
- Any required imaging (injury, rule in/out SCI)
- Early surgical debridement
- Escharotomy/fasciotomy
- Debridement of non-viable tissue
Discuss resuscitation of electrical injuries
Parkland often underestimates fluid requirement bc underlying injury isn’t manifested superficially with TBSA
General rule of thumb is 2x parkland (ie ~ 7-9cc/kg/%TBSA) and titrate to urine output of ~ 1cc/kg/hr
Identify and treat “pigmenturia” / (urine myoglobin) / rhabdomyolysis by aiming for clear urine, urine output of 1-2cc/kg/hr, adding mannitol 5% IV (25g bolus, 12.5g/hr rate) and alkinalizing urine (bicarb of 200-400mEq / hr x 4-6 hrs target arterial pH 7.35)
Discuss cardiac monitoring in electrical injury
Electrically injured patients can have almost any type of cardiac injury from arrest, arrhythmia, non-specific ST-T changes, contusion; v.tach can be delayed 12hr
Who needs cardiac monitoring x 24-48hrs?
- History of CAD; witnessed loss of consciousness or VS at scene or in transfer; abnormal ECG on transfer / in ED (besides sinus brady/tachy); arrhythmia; TBSA/burn injury that requires monitoring
Who does not need cardiac monitoring (can be discharged after 6 hrs observation):
- No h/o CAD; no LOC or cardiac arrest; normal ECG on transfer / in ED; low voltage injury; no neurologic abnormalities; no burn
Discuss wound management in electrical injury
- Immediate
- Escharotomy, fasciotomy: for tight compartments, signs of compartment syndrome (if possible to assess: pain out of proportion, non-responder to fluid resuscitation ) or compartment pressures measured > 30-35mmHg
- Debridement of clinically non-viable tissue
- Dress and splint
- Early
- Plan always for multiple debridements at 24-48h+
- Consider amputation vs. salvage
- Dress w/ sulfamylon (vs SSD for eschar penetration)
- Ensure vital structures are apporpriately covered with (local)/regional/distant flaps if required
- Late
- Reconstruction / rehab / scar management as indicated
Discuss systems invilved and potential complications of electrical injury
- Pschological: PTSD, failure to return to work
- CNS: SCI, paralysis, CHI
- PNS: direct nerve injury / peripheral neuropathy
- CVS: any injury possible - ECG changes, ischemia, contusion, arrhythmia, arrest
- vascular: thrombosis, vasculitis
- GI: ileus , peptic ulcer disease
- GU/renal: AKI, rhabdomyolysis
- MSK: muscle injury, compartment syndrome, fracture, contractures, heterotopic ossification
- H&N: TM rupture, corneal burn, optic nerve atrophy
- Resp: arrest, PTX
What factors determine extent of tissue destruction with chemical injury?
- Agent: what was the agent, form of agent, concentration of agent, how much of agent
- Injury: site of injury, surface area exposed, duration of contact
Damage continues until: agent is washed off, neutralized, or tissue reaction has been exhausted
How do you classify type of chemical injury?
- Oxidation (by oxidizing protein) and reducing (by using free electron) agents cause protein denaturation, partial/full thickness burn, +/- hepatorenal failure
- Corrosives - denature protein on contact
- Acids: coagulation necrosis - protein denaturation - eschar - limited penetration
- Bases: liquefaction necrosis - protein denaturation and fat saponification - deeply and rapidly penetrating - local bone decalcification & erosion
- (excpetion HF is an acid that causes liquefaction necrosis)
- Protoplasmic Protein - form salts w/ protein or inhibit metabolism
- Dessicants - dehydration or exothermic reactions
- Vessicants - ischemic injury to cells
What are the principles of emergency treatment of chemical burns?
- Remove particles
- if solid, brush off
- Irrigate / dilute
- copious irrigation for > 30 mins (for > 2 - 24 hrs for many bases)
- Exception: Metals Li,
- Apply antidotes or special scenarios
- HF = CaGluc
- Phenol = polyethylene glycol wipe
- Sodium, lithium metal - cover burn w/ oil, excise particles
- White phosphorus = lavage w/ 1-2% Copper Sulfate, excise particles then immerse in water
- Assess TBSA
- Address systemic toxicity: serologic and monitoring, call WHMIS / poison control
- Identify ocular contact: H20 lavage at scene / hosp; call ophtho
- Identify inhalational injury: if aerosolized - low threshold for intubation/bronch
- Initiate early hospital care
- Investigations: CBC (hemolytic anemia), lytes/extended lytes, Cr, LFT, ECG, cardiac monitor
- Resuscitation
- Dressings & debridements: as per thermal injury; depth usually declare in ~ 48 hrs
- Consultations: ophtho, ENT, GI / gen surg, resp
Discuss HF burn
- HF is an acid, produces local and systemic injury
- Locally HF causes tissue injury through corrosive action of free H+, but primarily through liquifaction necrosis, protein denaturation and saponification of fat, where free F- rapidly and deeply penetrates all underlying tissue including bone,
- the hallmark of local injury is excrutiating pain
- Systemically the free Fluoride ion forms insoluble salt w Ca and Mg, depleting stores, causing secondary hyperkalemia, acidosis and inciting cardiac risk for arrythmia or arrest, renal and liver dysfx
- Treatment consists of full serologic evaluation, ECG and cardiac monitoring
- Local treatment is firstline
- start with ensuring at least 30 mins of copious water/saline irrigation (as first aid at site and continue at emerg)
- topical application of 2.5% calcium gluconate jelly in glove and massage for 30 mins; response measured by reduction in pain; if no response reasonable to have a second try
- failure of 1 or 2 trials of topical jelly proceed to subcutaneous injection of 10% calcium gluconate, 0.5cc (5g) per cm2, 5mm past affected area; failure / non-response reasonable for a second trial and consider removing nail plate to improve penetration and reduce load
- failure of this or if severely burned hand then consider intra-arterial infusion (controversial) - cannulate brachial or radial artery (or interventional guidance) slowly infuse 10cc of 10% calcium gluconate in 50cc of D5W
- systemic therapy with intravenous calcium 2g over 20-30 minutes for patients with high risk injuries (50% HF any TBSA; 5% TBSA any HF; inhalation) or profound hypocalcemia or malignant cardiac arrhythmia
Discuss general treatment of chemical burns, and exceptions
- General treatment of chemical burns includes removing particles if present, irrigation / dilution of chemical (> 30 mins acid; > 2+++ hrs alkali [until alkali isn’t soapy]), serologic workup including hepatorenal work up
- Then await for tissue injury and depth to demarcate/declare itself, manage with supportive dressings, ultimately excision and grafting and/or reconstructive procedures as necessary
- Exceptions:
- HF - use calcium gluconate antidote
- Li or Na metal - do not irrigate as first step; instead cover with oil, remove particles, then immerse
- Phenol - wipe with polyethylene glycol
- Tar - use Tween 80 (or neosporin) to remove/emulsify
- Phosphorus - immerse (not irrigate) in water; irrigate with 1% copper sulfate (will precipate/turn black any remaining particles) then debride particles
Describe commisuroplasty
- 4 approaches
- Use 2 rhomboid flaps from buccal mucosa
- Use tongue flap, cheek rhomboid or nasolabial/mental transposition flaps w/ tongue flap
- Converse: excise triangle of skin to new commissure, labial/buccal mucosal flaps turned over and sutured in place
- Gilles: excise skin and open commissure; rotate inferior lip mucosa to new commissure for uppler lip, advance lower lip labial mucosa for lower lip