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.