Electrical & Chemical Flashcards
1
Q
How do you classify electrical burns?
A
- 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)
2
Q
What is the pathophysiology of injury in electrical injuries?
A
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
3
Q
define electroporation
A
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
4
Q
What are the factors that determine the severity and distribution of electrical injury?
A
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
5
Q
Discuss immediate management of patient with electrical injury
A
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
6
Q
Discuss resuscitation of electrical injuries
A
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)
7
Q
Discuss cardiac monitoring in electrical injury
A
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
8
Q
Discuss wound management in electrical injury
A
- 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
9
Q
Discuss systems invilved and potential complications of electrical injury
A
- 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
10
Q
What factors determine extent of tissue destruction with chemical injury?
A
- 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
11
Q
How do you classify type of chemical injury?
A
- 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
12
Q
What are the principles of emergency treatment of chemical burns?
A
- 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
13
Q
Discuss HF burn
A
- 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
14
Q
Discuss general treatment of chemical burns, and exceptions
A
- 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
15
Q
Describe commisuroplasty
A
- 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
