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)
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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
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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

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4
Q

What are the factors that determine the severity and distribution of electrical injury?

A

Kouwenhaven’s 7 factors

  1. Amount of Voltage: high worse than low
  2. Type of current: AC worse than DC at low voltage
  3. Amount of current: Higher current worse (esp for cardiac injury)
  4. Pathway of current: arm to arm contact points worse than arm to leg (more cardiac, sci)
  5. Resistance: greater resistance worse severity; resistance is inversely proportioal to cross-sectional area (ie wrist, ankle, extremity > trunk)
  6. Duration of contact: longer = worse
  7. Area of contact: greater area = worse
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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
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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)

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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
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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
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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
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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

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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
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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
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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
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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
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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
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16
Q

In what products is HF usually found

A

Used in

  • industrial cleaning agent, fertilizer manufacturing
  • glass manufacturing/glass etching
  • household (rust remover, tire/tile cleaners)
17
Q

In what products are alkali products found?

A
  • Household cleanign agents, drain cleaners (Drano)
  • industrial processing cement, lime, lye
18
Q

In what products are phosphorus found?

A
  • Manufacturing of Insecticides and fertilizers, rodent poisons, fireworks