Conference 09/28/22

Conference 09/28/22

Lightning Lectures

Carbon Monoxide poisoning

  • Binds to Hgb, inhibits oxidative phosphorylation, decreased oxygen binding and delivery. 
  • 137 cases per-million a year in US. Low SES, those without adequate heating/housing 

Clinically evaluate for risk of exposure to CO. based on presentation,  if concerned initiate 100% O2, especially if AMS is present. 

Indications for Hyperbaric

  • decreased GCS/AMS
  • any pregnant patient with >15% COHb 
  • any patient with >25% regardless of presentation 

Clinical Pearl: The FiO2 delivered via NC is NOT adequate for CO toxicity. Consider NRB or other O2 delivery devices. 

Electrical Injuries

  • Lightning strikes rare, but approx injuries in the US do occur yearly.
  • 4 different mechanisms of injury by lighting strike depending on route of entry of electrical current. 
  • Shockwave from rapidly heated air can cause concussive injuries. 

Injuries

  • Neurological
    • Keraunoparalysis, Anisocoria/mydriasis, Seizures, increased risk of ICH
  • HEENT: TM rupture is very common 
  • CV: Any arrhythmia is possible, Coronary vasospasm, myocardial necrosis. 
  • Resp: Apnea due to resp muscle paralysis. 
  • Renal: rhabdo
  • MSK: compartment syndrome/fractures
  • Skin: any visible burn = high voltage, no correlation to surface injury with severity. Lichtenberg figures can be seen on skin. 

Treatment

  • ABCs, c-spine immobilization if evidence of trauma, CBC, CMP, CK, troponin, EKG. 
  • Dispo: Likely admission for observation/telemetry. 

Prolonged CPR/resuscitation may be required for lightning strike injuries as they may recover from Asystole arrest. 

Temperature related illnesses

4 types of thermoregulation 

  • evaporation, radiation, convection, conduction. 
  • evaporation is the human body’s primary means of heat dissipation

Thermoregulation failure

  • high humidity >75%
  • ambient temp > core body temp
  • dehydration: for every 1% of body mass lost to dehydration, core temp increases 0.22 degrees C

Who is at risk? 

  • athletes, firefighters, military, laborers, endurance athletes.

Still thousands of cases yearly in the US in young athletes. 

 Acclimatization 

  • greatest risk of heat illness occurs during first 2 weeks of activity. 
  • Body undergoes many physiologic changes to acclimatize to higher temperatures. (increased plasma volume, increased blood flow to skin, increased sweat production etc.) 

Categorizing heat illness

  • Heat cramps
    • cramping of muscles associated with exercise. Does not require correlation with heat. 
    • Intense muscle pain and spasm. Rehydrate, treat symptomatically, rest. Consider further work up if unable to alleviate. 
  • Heat Syncope  
    • Exercise associated syncope. 
    • Commonly occurs at the end of an event. Muscle contracture during exercise keeps blood pressure adequately elevated, end of exercise leads to drop. 
    • Benign/self limited. 
    • Clinical presentation similar to vasovagal syncope. 
    • Keep cardiac arrhythmia in differential 
    • Supportive care, hydrate and move to shade. 
  • Heat exhaustion 
    • inability to maintain adequate CO due to physical activity and heat stress. 
    • temp often 101-104, but can occur without hyperthermia. 
    • Inability to continue with exertion
    • NO CNS dysfunction. 
    • symptomatic treatment, cool patient, if symptoms do not resolve in 1-2 hours, requires ED Evaluation 
  • Heat Stroke
    • CNS dysfunction is the primary symptom. 
    • Core temp classically greater that 104. 
    • Cerebellar findings are usually the first notable symptoms. Other signs include disorientation/confusion, Seizures, coma. 
  • Prognosis
    • worst when immediate cooling is not initiated, direct correlation with morbidity and mortality with duration of hyperthermia. 
  • Cooling measures
    • ice water immersion is the quickest method for lowering core temperature. 
    • if ice water not available, room temperature water is adequate. 
    • When immersion not an option, douse with water as often as possible, put wet sheets around the patient with frequent rotation. ice directly to exposed skin.
    • Cool patient until they begin to shiver. 
  • Cooling in the ED
    • ice packs to axilla/groin. 
    • douse water
    • fans
    • Continue to assess temp, vitals, mental state, administer fluids. 
    • Lab evaluation: all organ systems are sensitive to injury. CBC, CMP, CK, Coags, lactic acid. 
    • Treat other complications that arise: AMS/Seizures, Rhabdo, DIC, ARDS, Enteric ischemia/GI Bleed, MI
    • Medications will not treat hyperthermia (NSAIDS etc.) 
    • Dispo: admission for all heat strokes. 

Toxic Alcohols

Ethanol 

  • AMS, hypoglycemia. 
  • ethanol levels usually correlate with symptoms
  • Hemodialysis is possible for severe ethanol toxicity. 

Isopropanol

  • rubbing alcohol
  • intoxication, GI irritation, NO metabolic acidosis. 
  • converts to acetone 
  • requires GC for actual identification of isopropanol, methanol and ethylene glycol. 
  • treat supportively. 
  • Can technically be dialyzed. 

Methanol

  • windshield washer fluid, solid cooking fuel, embalming fluid, tainted beverages, tainted beverages. 
  • toxic metabolite is formate/formic acid. 
  • Clinical manifestations: CNS effects (not always), multiple hours until symptom onset due to toxic metabolite. 
    • metabolic acidosis with high anion gap. 
    • ocular toxicity (formate toxic to optic nerve)
    • pancreatitis
    • basal ganglia toxicity/effect. 

Ethylene Glycol

  • sweet taste
  • 4 metabolites of concern: oxalate, glycoaldehyde, glycolic acid, glyoxylic acid
  • Clinical manifestations:  CNS effects, metabolic acidosis with AG, renal toxicity/failure, hypocalcemia from oxalate crystalizing into calcium oxalate crystals, basal ganglia toxicity. 
  • if not at U of L consider getting lab samples transported ASAP. 
  • Surrogate markers: calcium oxalate crystals, woods lamp (some antifreeze has fluorescein) elevated osmol gap (normal gap is around 10)
  • Many factors affect osmol gap. 

Antidotes

  • Ethanol: cheap, requires continuous infusion/administration, not as effected as fomepizole, requires frequent levels. If needed PO in encouraged over IV administration. 
  • Fomepizole: preferred antidote, expensive, some GI irritation and transaminase elevation. 
  • Both inhibit alcohol dehydrogenase. 
  • Administer antidote if any signs or symptoms of ingestion is present. 
  • Administer if methanol or EG levels are >20mg/%

Hemodialysis

fomepizole is very effective and may decrease need for dialysis.

consider with severe end organ damage, coma, seizure, renal failure.

Adjunct therapies: folic acid for methanol, thiamine and pyridoxine for EG. Sodium Bicarb for pH <7.20 according to Goldfrank’s.

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