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.

Conference 09/14/22

Research “Life Cycle”

• complete required training courses
• develop a research project
• do a lit search
• Start plan/write protocol and IRB. 
• IRB submission. 
  • Must be approved by the IRB, takes time so plan accordingly. 
• Types of research
  • Human research
  • QI
  • Program eval
  • case report. 
• Collect data
• Data analysis (you don’t have to crunch numbers)
  • schedule something with Jacob, He’s awesome!
• Write the paper. Read papers. Learn the format and write it. 
• Publish: LONG process. 

Room 9 Follow up: Josh French

• 45 yo F presents via EMS after being found unresponsive. reports she fell earlier in the evening. “Oh btw she’s having a GI bleed” per EMS. 
• Unresponsive, ill appearing, GCS 3, severely hypotensive and requiring BVM for respiration. 
• Dark blood per rectum. 
• pH unreadable, hgb. unreadable, lactic acid greater than 20
• Triaged to CT with nonspecific findings of the abd/pelvis. 
• Upper vs Lower GI Bleed: Broad differential 
• Protip: BUN can be elevated from upper GI bleed due to absorption of blood through the upper GI tract. 
• Resuscitate, support pressures. get blood ASAP. 
• Needs a GI consultation for treatment of bleed through EGD/Colonoscopy. 
• MTP at U of L 
  • volume replaced exceeds patients estimated blood volume in a 24 hour period. 
  • 4 units RBC in 1 hour. 
  • 10 units of RBC, 10 units FFP/plasma, 2 units of platelets. 
• pmts who require significant blood products need calcium! Citrate as a preservative will bind the body’s calcium. 
• Resuscitate until normotensive. 

One Pill can Kill: Kaci Eastep, PEM. 

Incidence

• 70,000/year pediatric ingestions. 
• Peak incidence 1-3. 
• Most mild or clinically negligible. 

CCBs

• pediatric patients rely primarily on heart rate for cardiac output. 
• ingestion causes bradycardia, hypotension 
• Decon if able with charcoal. 
• ABC’s: atropine, pressers, fluids if needed. 
• Calcium, high dose insulin, glucagon, lipid infusion. 

Camphor (icy-hot, bengay, vics vapors)

• causes rapid GI distress in 10-20 minus. 
• delirium, restlessness, seizures
• coma, CNS depressant. 

Clonidine + Opioids

• clonidine has opioid receptor agonism and may look largely like opioid intoxication. used for ADHD treatment. 
• naloxone, higher doses required for clonidine. Up to 10mg. Start high dose. 
• Lomotil- diphenoxylate (opioid) + atropine
• Able to provide intranasal narcan for free upon discharge. 

TCAs

• leading cause of pediatric toxicities until 1993. 
• multiple areas of receptor interactions primarily norepinephrine and serotonin. 
• CNS depression, seizure, arrhythmia, anticholinergic toxicity. 
• treat with Bicarb. 1-2mEq/Kg. Alkalinize urine to expedite urinary secretion. 

Salicylates: peptobismol, oil of wintergreen, Aspirin

• minumum 150mg/kg for toxic dose.
• nausea, vomiting, diaphoresis, tinnitus(ototoxicity), pulm edema, hyperthermia, coma, death
• Mixed AG acidosis with resp alkalosis. 
• Alkalinize urine (bicarb). for severe ingestions hemodialysis. 

Sulfonylurea

• stimulate insulin release. 
• leads to profound hypoglycemia
• Treat with octreotide 1-2 microgram/kg/dose and dextrose as needed. 

Toxic Alcohols: ethylene glycol, windshield wiper fluid, rubbing alcohol. 

• Methanol: visual disturbances, AG acidosis, treat with 
• Ethylene Glycol: renal dysfunction, calcium oxalate crystals.  AG acidosis
• Isopropanol: no AG acidosis, increased osmolar gap. 
• toxic alcohols are broken down by alcohol dehydrogenase, which is targeted by fomepizole (used for methanol and EG) 
• Can technically use ethanol
• Hemodialysis for severe ingestions. 

Beta Blocker toxicity.

• One of the most commonly prescribed drugs.
• Onset of toxicity depends on type of beta blocker (instant vs extended release)
• Hypoglycemia is helpful in differentiating from calcium channel blocker overdose.
• Decon if possible with charcoal or whole bowel irrigation
• Stabilize with atropine for bradycardia, pressors for hypotension. Will require HIGH dose for pressors.
• Glucagon is gold standard: increases cardiac inotropy without beta agonism.
  • 5-10mg initial dose
  • Needs to be given early.
• Calcium to increase vascular tone
• High Dose insulin
  • 1u/kg/hr with D50 or dextrose containing fluids.
  • Takes 30-60 minutes to take effect so start early
• Intralipid
  • Theoretically works as “lipid sink” to absorb active drug
  • Only feasible with lipophilic drugs
• Dialysis,ECMO
• Dispo
  • Admit ALL sotalol ingestions due to long onset of action.

Calcium Channel Blocker Toxicity

• Very commonly prescribed drug
• Significant toxicity in overdose, especially in pediatric population. An extra dose of prescribed CCB can cause significant toxicity.
• Extended vs immediate release. Up to 16 hours in some formulations.
• Symptoms of toxicity range from dizziness to hemodynamic collapse. Non-DHPs present primarily with bradycardia.
• Can cause severe High anion gap metabolic acidosis.
• Hyperglycemia rather than hypo

• Treat hypotension and bradycardia aggressively with atropine/pressors or pacing if needed
• Decon if able
• Be cautious with fluids as decreased CO can lead to volume overload.
• IV calcium indicated, clinical response variable.
• High dose insulin therapy
  • 1-10u/kg/hr with dextrose containing fluid.
• Lipid emulsion
  • CCBs are lipophilic
• ECMO,LVAD

• Disposition

• Extended release toxicity should all be admitted for observation. 

Hypothermia and Cold Injuries

• Any core body temperature measurement less than 95º F or 35º C
• 4 methods of heat loss
  • Thermal radiation (lose most heat here!)
  • Convection
  • Conduction
  • Evaporation

• Non-freezing cold injuries
  • Trench Foot: prolonged foot immersion in cold water.
    • Dry and warm feet. Do not massage feet 
    • Do not submerge in warm water.
  • Chilblains: cold exposure injury without freezing of tissue. Paresthesias, erythematous tissues. 12+ hours after exposure.
    • Require treatment! Nifedipine 20mg TID, Pentoxifylline, Topical Steroids
• Frost Bite
  • 4 stages with advancing levels of tissue damage. IV being down to muscle.
  • Treat with warm circulating water. Local and superficial may be discharged. Treat supportively.
  • Do not rub extremities, allow to refreeze, or use dry heat for treatment.

• Hypothermia
  • Mild 92-95, moderate 82-90, severe 77-82.
  • CNS, Coagulopathy, Circulatory, Respiratory
    • CNS depression, amnesia, ataxia
    • Decreased clotting factors, decreased platelet functions.
    • Myocardial irritability
    • Oxygen demand decreased.
  • EKG Changes
    • J point elevation throughout (Osborne wave)
    • QT prolongation
    • Shortened PR interval.
  • Commonly decompensates into V. Fib arrest.
• Treatment
  • Mild: passive external warming. Blankets, warm rooms
  • Moderate: Active external. Bair Hugger, blankets
  • Severe: Active internal warming.
    • Warm fluids,
    • Bladder lavage
    • Chest lavage
    • Intubate, warmed O2.
  • When to cease resuscitation or NOT to initiate.
    • DNR if, obvious lethal injury,
    • Hyperkalemia greater than 12
    • Avalanche with ice/snow in airway >35 minutes.
    • AFTER rewarming, once pt is 89ºF and in asystole, may cease efforts.
  • CPR Pearls
    • ACLS code drugs DON’T WORK at low temps.
      • Multiple recommendations. Most recent recommends..
      • 1 defibrillation, 1 epi. Warm 5 degrees C and reattempt. Initiate full ACLS protocol at 30º C.
    • AVOID SUCCINYLCHOLINE. The temporary rise in K may lead to inappropriate cessation of efforts.
  • Running the code
    • ABCs
    • Warmed, humidified air.
    • Core body temp with rectal or bladder probe.
    • Femoral central line. AVOID IJ as irritating myocardium can lead to more arrhythmia.
    • 2 pigtail chest tubes bilaterally for warm thoracic lavage.

Bites and Stings

• Venomous snakes
  • 9000 snake envenomations a year in the US.
  • 2000 treated as such
  • 5-6 deaths annually.
  • 2 deadly snake families. Pit vipers, coral snakes.
• US pit vipers
  • 99% of all venomous bites in the US
  • Triangular head, elliptical pupil.
• Single row of anal plates more indicative of venomous snake.
• Slight chance of anaphylaxis associated with envenomation. Consider EPI if pressor requirement.

• Envenomation by pit vipers

• Venom varies among species.
  • Seriousness of envenomation varies based on several factors. Size, agitation of snake, age of victim, depth of wound etc.
  • Different venoms attack different systems (neurotoxin vs local destruction)
  • ¼ to 1/3 of bites are “dry bites”
  • Venom causes local tissue necrosis, severity of envenomation cannot be determined by initial symptoms.
• Minimal Envenomation
  • Swelling, ecchymosis, local pain
  • NO systemic signs.
• Moderate Envenomation
  • Swelling extends up extremity, severe pain
  • Mild systemic symptoms: nausea/vomiting, generalized weakness.
• Severe Envenomation
  • Significant soft tissue swelling
  • Severe pain
  • Resp. distress.
  • Vital sign instability, hypotension, shock
  • Coagulation abnormalities
  • RBC lysis
• Coral Snakes
  • Far less common envenomations
  • Neurotoxic component to venom.
  • Neurological symptoms, respiratory collapse.
  • NO ANTIVENOM produced. Limited supply.
  • Effect of bite may be delayed up to 12 hours. All require 24 hour surveillance in ICU.
  • Severe envenomation
    • Any systemic symptoms
    • Respiratory distress.
• Treatment
  • Look for wound. If no wound, very unlikely that envenomated by crotalid.
  • Get to hospital ASAP
  • Don’t chase a snake. Take pictures if possible.
  • Elevation of limb will diffuse cytotoxic venom and decrease local tissue damage.
  • DO NOT: torniquet, ice pack, suction, extrication kit.
  • Pressure wraps that obstruct lymphatic drainage may assist.
  • 2 antivenoms approved for US for pit viper envenomation.
    • Cro-Fab
    • ANAVIP
  • No pre-treatment necessary
  • Administer to all moderate to severe envenomations.
  • Send coral snake envenomations to Florida. Call tampa poison control center.
  • Antivenom Dosing (CroFab)
    • Initial dose:4-6 vials bolus and repeat that dose until symptoms are controlled.
    • 2 vials q6x3 for maintenance.
  • ANAVIP is cheaper, just as effective and does not require maintenance dosing.
  • We currently carry CroFab. Will switch to ANAVIP (allegedly)

• Copperhead envenomation
  • A small study has shown that administration of crofab only minimally decreases pain and disability in affected patient.

• Spider Bites
  • 3 dangerous spiders in US.
  • Brown recluse, brown recluse, hobo.
• Black Widow
  • Pain, anxiety, muscle cramps, paresthesia, may be some paralysis.
  • Can cause systemic symptoms.
  • Cool the area with ice or ice water.
  • Analgesia and anxiolysis
  • Antivenom: Merk; infrequently used (10% anaphylactic rate)
  • Give antivenom for uncontrollable pain, pregnancy with fetal distress, priapism
• Brown Recluse
  • Rare spider bite
  • Most bites in Midwest
  • Painless bites with 2-8 hours before symptom onset.
  • Systemic illness especially in pediatric cases.
  • No antivenom.

Toxicology small group

• Acetaminophen toxicity
  • Toxic dose: 150 mg/kg over 2 days. 10g in one dose or as calculated with Acetaminophen level and Rumack-Matthew Nomogram.
  • Rumack-Matthew Nomogram can be used to calculate toxicity. Can only be used in single oral exposure/acute toxicity.
  • Treatment, NAC indicated for known toxic dose
    • IV 150mg/kg over 1 hour>50mg/kg over 4 hours> 100mg/kg over 24 hours.
    • Admit all patients requiring treatment.
    • No data for pre 4 hour levels. Obtain 4 hour level. If highly suspicious for large ingestion then treat prior to 4 hour mark.
  • Tylenol PM
    • Co-ingestion with Benadryl
    • Bendryl theoretically slows gut absorption and gut motility.
    • Pts who were nontoxic initially may cross into toxic levels multiple hours later.
• TCA Toxicity
  • Multiple MOAs
    • Inhibits norepi and serotonin reuptake.
    • Anticholinergic
    • Sodium channel blockade
    • H1 properties
    • K channel blockade in myocytes
    • GABA blockade.
  • Narrow therapeutic index.
  • Toxic  dosing: 10 mg/kg moderate. 30mg/kg severe
  • Increased QRS, QT prolongation, tachycardia, agitation, AMS,
  • Can progress to torsades
  • Treat with 1-2meq/kg IV bolus of NaBicarb. Repeat until improvement or pH 7.5-7.55.
  • All other care is supportive.
  • Other treatments after bicarb
    • Lidocaine 1mg.kg
    • Hypertonic saline
    • Intralipid
    • ECMO
  • 6 hours minimum obs, admission if symptomatic.

• Salicylate toxicity
  • Salicylic acid can lead to profound acidosis.
  • Zero order kinetics in OD
  • Mild: <150 mg/kg.
    • Ototoxicity
    • GI irritation
    • AG metabolic acidosis.
  • Moderate 150-300 mg/kg
    • Resp alkalosis/hyperventilation
    • AMS
    • Fever
  • Treatment
    • ABCs
    • Fluids
    • Decon with charcoal
    • Bicarb for urine alkalization
    • Can be dialyzed if severe toxicity.
  • Disposition
    • DC: serial levels show decline, asymptomatic
    • Admit: any enteric coated ingestion with any symptomology and increasing levels.
    • Avoid intubation as long as possible. Intubating these people with profound acidosis will drop pH and cause arrest.