General Approach to the Poisoned Patient PT2

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General Approach to the Poisoned Patient PT2

• Presented by Dr. Levy
• Prepared by
• Dr. Trey Woods D.O. PGY1
• Emergency Medicine Residency
• St. JosepH Health Center
• Warren Ohio

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Salicylates

• Inhibits cyclooxygenase therefore
• Inhibits platelet thromboxane synthesis
• Decreased platelet aggregation
• Inhibits prostaglandin/prostacyclin synthesis
• Decreased inflammation, renal blood flow, gastric
  mucous production, others effects
• UNCOUPLES OXIDATION/PHOSPHORYLATION
• RESPIRATORY CENTER STIMULANT
• ALTERATION OF CARBOHYDRATE METABOLISM
• ACID BASE DISTURBANCES

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Salicylates

• GENERAL PICTURE HYPERTHERMIC, HYPERPNEIC,
  ALTERED MENTAL STATUS
• CNS AGITATION, CONFUSION, SEIZURES, COMA
• CV EFFECTS -CHF , ARRHYTHMIAS
• PULMONARY -NON CARDIOGENIC PULMONARY EDEMA (ARDS
  PICTURE)

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ASA Pharm

• Rapidly absorbed from GI tract
• 2/3 in first hour
• Peak plasma level in 3-4 hours
• Large doses decrease GI motility
• Pylorospasm
• Prolonged absorption
• Bound to serum albumin
• Once saturated, small doses will greatly increase
  free drug levels

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ASA Clearance

• SA is conjugated in liver with Glycine and
  Glucuronic Acid
• Small amount is hydroxylated
• All forms cleared by kidneys
• Acute Toxicity Liver conjugative system is
  overwhelmed
• Elimination of free SA dependant on kidneys
• Half life from 15-30 hours
• Urine pH above 8.0 maintains SA molecules in
  ionized form
• Inhibits reabsorption across the renal tubule
• Increases renal clearance

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ASA Tox

• Due to oral intake or absorption through skin
  (usually pediatric)
• Acute or Chronic
• Acute toxicity usually in children, young adults
• Chronic toxicity usually in elderly
• Pediatric Chronic- due to over aggressive
  dosing
• Very dangerous

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ASA PathoPHYS

• Acid/Base Disturbances
• Fluid/Electrolyte Disturbances
• Hallmark of ASA toxicity Mixed respiratory
  alkalosis with metabolic acidosis
• Children lt2 years metabolic acidosis
  predominates
• Older children/adults respiratory alkalosis
  predominates

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• RESPIRATORY Alkalosis (usually 1st)
• SA in brain stimulates medullary respiratory
  center causing hyperpnea
• Increased alveolar ventilation, Increased depth
  of breaths
• Results in panting dog breathing pattern
• Decreases PaCO2 causes alkalosis
• METABOLIC ACIDOSIS (usually later)
• SA in cells inhibits Krebs cycle enzymes
• Increases lactic, pyruvic acid levels
• SA uncouples oxidative phosphorylation
• Results in Wide Anion Gap Metabolic Acidosis,
  Increased metabolic rate, Increased body temp

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ASA PathoPHYS

• Acute Toxic Exposure
• 200-300 mg/kg (500 mg/kg or higher doses are
  potentially fatal)
• Chronic Toxic Exposure
• Toxicity may occur at much lower doses
• Pediatric chronic exposure to excessive doses can
  be very dangerous
• Initial Symptoms Tinnitus/Impaired Hearing,
  Nausea and vomiting begin in 3-8 hours,
  Hyperthermia, Panting dog respiratory pattern,
  Dehydration and Impaired consciousness-children
  are more predisposed this

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ASA Patho-PHYS

• More serious, but less common symptoms
• Dyspnea due to pulmonary edema--High morbidity if
  not recognized
• Oliguric Renal Failure
• Hemorrhage-rare even with antiplatelet properties
• Acid/Base Disturbances
• Fluid/Electrolyte Disturbances
• Hallmark of ASA toxicity Mixed respiratory
  alkalosis with metabolic acidosis
• Children lt2 years metabolic acidosis
  predominates
• Older children/adults respiratory alkalosis
  predominates

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ASA TX

• SUPPORTIVE
• 5 goals
• Decrease absorption of ASA
• Correct fluid/electrolyte/acid-base problems
• Maintain blood glucose levels
• Decrease tissue SA burden
• Increase elimination of ASA

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ASA TX

• Activated Charcoal Initial dose
• Pediatrics 1g/kg in children
• Adults 50-100 g for adults
• Repeat dosing of AC for very large overdose
• Enteric coated forms Whole bowel irrigation
• Goal of therapy is urine output of 2-3 mL/kg/hr
• Risk of pulmonary/cerebral edema with
  over-hydration
• Initial rehydration Correct K with IVF

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ASA

• Optimum urine pH to enhance SA clearance is
  7.5-8.0
• NaHCO3 1-2 mEq/kg IV over two hours, titrate to
  goal pH.
• Important to ensure prior or concomitant
  potassium replacement
• Closely monitor ABG-maintain serum pH between
  7.45-7.55
• Indications for hemodialysis AMS/Coma, Renal or
  hepatic failure, Pulmonary Edema/ARDS, Severe
  acid/base imbalance, Failure to respond to
  AC/Urine alkalinization

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Acetaminophen TX

• CRITICAL HISTORY
• WHEN?HOW MUCH? ANYTHING ELSE?WHY?
• DOES NOT CAUSE ACUTE SXS
• ACTIVATED CHARCOAL 50G PO ONLY GIVE IF PT IS
  AWAKE AND ALERT AND PROTECTING AIRWAY

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ASA TX

• INITIATE TREATMENT WITH
• MUCOMYST SHOULD BE STARTED WITHIN 8 HRS
• COMPLICATIONS
• TOXIC DOSE gt140 mg/kg
• LIVER FAILURE CENTRAL LOBULAR NECROSIS
• RENAL FAILURE
• HEPATIC ENCEPHALOPATHY
• COAGULOPATHY

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Acetaminophen

• Patients surviving initial liver injury/failure
  complications begin to recover
• LFTs normalize in 5-7 days or more
• Liver function eventually returns to normal
• Liver completely regenerates over months
• N-acetyl cysteine (NAC)
• Free sulfhydryl group similar to GSH
• If treatment begun within 8 hrs, nearly 100
  prevention of hepatotoxicity
• Efficacy continues even after 8 hrs post-ingestion

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N-acetyl cysteine (NAC)

• Oral or IV form
• 140 mg/kg loading dose, 17 subsequent doses of 70
  mg/kg, every 4hrs after

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Dig

• Preparations
• 1. Pharmaceutical
• 2. Plants (oleander, foxglove, red squill)
• 3. Toad venom (Bufo)
• Toxic dose
• 1 mg in a child, 3 mg in adult
• Pathophysiology
• Inhibit sodium-potassium ATPase, Potentiate vagal
  tone, decrease sinus and AV node conduction,
  Increase automaticity in Purkinje fibers,
  Increased intracellular calcium

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DIG Presentation

• Acute
• GI symptoms
• Hyperkalemia
• Cardiac dysrhythmias
• Bradycardias, blocks Most common is PVCs
• PAT with block most commonly caused by digoxin
  toxicity
• Chronic
• Altered mental status, Bradycardia, blocks, Hypo
  or hyperkalemia

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DIG TX

• Diagnosis
• Bradycardia, hyperkalemia, elevated levels
• Levels not useful in first 6 hours unless low
• Treatment
• Treat hyperkalemia in standard fashion, except
  calcium which is contraindicated
• Atropine, pacing. Lidocaine, Avoid class Ia
  antiarrythmic agents (quinidine, procainamide),
• Digoxin antibody fragments
• Hyperkalemia (gt 6.0)
• Symptomatic dysrhythmias

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Beta-Blocker OD

• MYOCARDIAL DEPRESSION
• BRADYCARDIA--SINUS or AV BLOCK
• VENTRICUAR TACHYCARDIA
• TORSADES DE POINTES (SOTALOL)
• CNS
• COMA, SEIZURES (PROPRANOLOL) HYPOGLYCEMIA
  (PEDS)

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Beta-Blocker OD

• GENERAL MANAGEMENT
• AIRWAY MANAGEMENT
• DECONTAMINATION Activated Charcoal LAVAGE IF
  INTUBATED
• Seizures and CNS Depression
• GLUCOSE, CORRECT HYPOXIA BENZODIAZEPINES
• HEMODIALYSIS (ATENOLOL, NADOLOL)

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Beta-Blocker OD

• ATROPINE?
• GLUCAGON 3.5-5 mg IV then gtt at 1-5mg/hr
• Norepinephrine
• AMRINONE
• PACING
• USUALLY REFRACTORY
• TX OF CV COMPLICATIONS
• WIDE COMPLEX DYSRHYTHMIA SODIUM BICARB
• TORSADES DE POINTES MAGNESIUM OVERDRIVE PACING

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CCBs OD

• MECHANISM
• INHIBITS CA ENTRY INTO SMOOTH MUSCLE
• IMPAIRED EXCITATION/CONTRACTION COUPLING
• INHIBITS INSULIN RELEASE
• CELLULAR HYPOGLYCEMIA

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CCBs OD

• 3 CLASSES
• DIHYDROPYRIDINE (PERIPH RESIST)
• BENZOTHAZEPINE (AV NODE,CONTRACTILITY)
• PHENYLALKYLAMINE (ALL)
• MYOCARDIAL DEPRESSION
• BRADYCARDIA WITH AV BLOCK/ASYSTOLE
  HYPOTENSION
• CNS
• COMA SEIZURES METABOLIC HYPERGLYCEMIC,
  ACIDOSIS

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CCBs OD

• TREATMENT
• ABCS
• MYOCARDIAL DEPRESSION
• FLUIDS
• CALCIUM CHLORIDE 10 CC OF 10 SOLUTION
• NOREPINEPHRINE GLUCAGON (VARIABLE RESULTS)
• BRADYCARDIA/BLOCKS
• ATROPINE PACING

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Anti-Cholinergic

• ANTICHOLINERGIC SYNDROME
• DRUG CAUSES
• ANTIHISTAMINES - diphenhydramine
• ANTIPARKINSON DRUGS
• ANTIPSYCHOTICS
• ANTISPASMODICS
• CYCLIC ANTIDEPRESSANTS
• MUSCLE RELAXANTS
• OTC MEDS
• PLANTS/MUSHROOMS - Jimson Weed

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Anti-Cholinergic

• DDX
• SYMPATHOMIMETIC SYNDROME
• SEPSIS
• WITHDRAWAL SYNDROME (DTS)
• TX
• IV FLUIDS, COOLING MEASURES, TREAT SEIZURES, ACLS
  FOR ARRHYTHMIAS
• GASTRIC EMPTYING/AC
• /- PHYSOSTIGMINE

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Heavy Metal

• IRON
• Preparations--Amount of elemental iron depends on
  the preparation Ferrous sulfate 20, Ferrous
  fumarate 33, Ferrous gluconate 12, Ferrous
  chloride 28
• Toxic dose 40 - 60 mg/kg elemental iron
• Pathophysiology
• Corrosive effect--Can cause hemorrhagic necrosis
  and perforation or Severe hypovolemia from GI
  fluid loss
• Cellular toxicity--Vascular damage, Cellular
  dysfunction leading to lactic acidosis and
  necrosis

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Iron Cont.

• Clinical presentation
• Stage I 1 - 4 hours
• Vomiting and diarrhea, which can be bloody,
  secondary to corrosive effects--Fluid loss can
  result in shock, renal failure, death
• Stage II Latent period over next 12 hours
• Stage III 12 - 24 hours Coma, shock, seizures,
  coagulopathy, hepatic failure, death
• Stage IV Scarring from corrosive effect can
  lead to pyloric stricture, obstruction

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More Iron

• Diagnosis Consider in any child with acute
  onset of GI symptoms, Not on routine toxicology
  screen, Visualization of radiopacities on
  abdominal x-ray (chewable vitamins and iron are
  not seen on x-ray)
• Serum iron levels Check level in 2 - 4 hours if
  chewable, Level in 4 - 6 hours for other
  preparations
• TIBC is useless
• If iron level not available, a WBC gt 15,000 and
  glucose gt 150 suggest a serum iron level gt 300
  µg/dL
• Symptomatology varies if level 350 - 500 µg/dL,
  most patients have symptoms if level 500 µg/dL
• Serial levels to determine peak or if suspect
  bezoar

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More Iron TX

• Treat shock with IV fluids, If hemorrhagic
  gastritis is present, may require blood
  replacement
• Gastrointestinal decontamination
• Gastric lavage useful, If abdominal x-ray shows
  tablets after lavage, perform whole bowel
  irrigation, Activated charcoal does not bind
  iron, If bezoar forms, may require endoscopic
  removal or gastrotomy
• Deferoxamine Indicated in patients with severe
  GI symptoms, shock, acidosis, or serum iron level
  gt 500 µg/dL Intravenous route is preferred and
  dose is 10 - 15 mg/kg/hr with a maximum daily
  recommended dose of 6 - 8 gms
• May see urine color change (vin rose) due to
  excretion of deferoxamine - iron complexd. Most
  significant side effect of deferoxamine therapy
  is hypotension, which is rare if the rate of
  administration is lt 15 mg/kg/hr

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Lead

• Sources
• Obtained from smelting and refining natural ores,
  and Lead storage batteries
• Used in production of pipes, brass, bronze,
  steel, ammunition, solder, as an Additive, Use in
  house paint stopped since 1970's, but still used
  in commercial paints, Exposure may occur from
  renovation of building painted before the 1970's,
  Children at risk from ingestion of contaminated
  dust, soil, or paint chips, Absorption also
  occurs after inhalation

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More Lead

• Pathophysiology
• Binds to sulfhydryl groups resulting in
  inhibition of enzymatic processes, Interacts with
  cations (calcium, zinc, iron), Can see
  alterations in cellular and mitochondrial
  membranes, neurotransmitter synthesis and
  function, heme synthesis, and nucleotide
  metabolism
• Target organs are CNS, kidney, reproductive and
  hematopoietic

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Lead Presentation

• Acute ingestion (Uncommon)
• Abdominal pain, anemia (hemolytic), toxic
  hepatitis 2.
• Subacute or chronic is more common
• Constitutional symptoms Fatigue, malaise,
  irritability, anorexia, weight loss, arthralgias,
  myalgias, hypertension
• GI Nausea, constipation or diarrhea, crampy
  abdominal pain
• CNS Impaired concentration, headache, but Can
  see encephalopathy with irritability, ataxia,
  delirium, coma, seizures (which is a
  life-threatening emergency)
• Chronic low-level exposures in children can
  result in decreased intelligence and
  neurobehavioral abnormalities, growth retardation

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Lead Pres cont.

• Peripheral motor neuropathy Affects upper
  extremities primarily Can cause severe extensor
  weakness (wrist drop)
• Hematologic Normochromic or microcytic anemia
  ii. Can see basophilic stippling, hemolysis
• Renal Reversible acute tubular dysfunction,
  chronic interstitial fibrosis, hyperuricemia
• Reproductive Decreased sperm number and
  function, Increased risk of miscarriage,
  decreased gestational age, low birth weight, and
  impaired neurologic development

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Lead DX

• Consider in any patient with multisystem
  dysfunction including abdominal pain, headache,
  anemia or in any child with neurobehavioral
  abnormalities or developmental delays
• Levels Whole blood lead level is the most
  useful indicator of exposure,
• Levels of 10 - 25 µg/dL have been associated with
  neurobehavioral abnormalities in children--Adults
  tolerate much higher levels than children
• Levels of 25 - 60 µg/dL may be associated with
  headache, irritability, and neuropsychiatric
  effects. Can see anemia
• Levels of 60 - 80 µg/dL may be associated with GI
  effects and renal effects
• Levels gt 80 µg/dL are associated with overt
  intoxication g
• Levels gt 100 µg/dL are usually seen in patients
  with encephalopathy and neuropathy

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Lead DX

• Free erythrocyte protoporphyrin (FEP) or zinc
  protoporphyrin (ZPP)
• Levels gt 35 µg/dL are seen with lead-induced
  inhibition of heme synthesis, Elevations lag
  behind exposure by weeks, High blood lead and
  normal FEP or ZPP indicate recent exposure
• X-ray-- May be useful after ingestion of lead
  paint, glazes, chips, or lead weights

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Lead TX

• Encephalopathy
• BAL followed by Calcium EDTA and BAL
• Symptomatic intoxication without
  encephalopathy--Oral DMSA or Calcium EDTA
• Asymptomatic children with elevated levels (gt 45
  µg/dL)--Oral DMSA
• Asymptomatic adults --Oral DMSA if levels gt 80 -
  100 µg/dL
• Decontamination
• Lavage for acute ingestion
• If abdominal x-ray is positive after lavage,
  whole bowel irrigation (WBI)
• Remove patient from exposure!

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Arsenic

• Is a metalloid with an affinity for -SH Groups
• Inorganic sources pesticides, rat poison,
  smelting industries, and seaweed.
• Organic sources seafood, antiparasite/antimicrob
  ial agents, and pressure treatment of wood.
• Highly lethal but odorless arsine gas (ASH3) is
  used in semiconductor industry
• Lewisite(dichloro-2-chlorovinylarsine) is Mustard
  Gas
• Pathophys inhits pyruvate dehydrogenase,
  interferes with cellular uptake of glu, and
  uncouples ox-phos

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Arsenic

• Presentation Acute (within hours) Severe GI
  symptoms--n,v,d, or bleeding. Hypotension and
  tachy 2nd to vol depletion and direct myocardial
  suppression.
• Other possible Renal(ATN), CNS(agitation, coma,
  sz), encephalopathy, pulm edema, rhabdo.
• Chronic stocking glove peripheral neuropathy,
  morbilliform skin rash, malaise, myalgia,
  abdominal pain, memory loss, and personality
  changes. Mees lines (horizontal white deposits
  in the finger/toe nails) found (4-6 wks post
  ingestion)
• Dx and DDx ECG prolong QT, or tachydysrhytmia,
  and radiograph may show radiopaque in alimentary.
  Confirm by 24-hr Urine arsenic lvl. Consider
  sepsis, addisons ds, hypo/hyper thyroid,
  porphyria, encephalopathy, peripheral neuropathy
  and other metal poison.

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Arsenic

• Tx
• ACLS( avoid antiarrhytmia agents that prolong QT
  (ie class Ia, Ic, and III agents), hypotension
  (fluid resus)
• Whole bowel irrigation with PEG
• Chelation with BAL 3-5 mg/kg IM every 4hrs if
  severe.
• Succimer (BAL)350mg/m2 PO tid for 5 days, then
  bid for 14 days for pts stable and tolerate oral
  intake.

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Case 1

• A 19 y/o raver dropped off in your ED by his
  raving buddies after punching the bouncer and
  trying to jump out of his friends car into the
  middle of the Interstate 80.
• He is cursing and screaming
• BP 200/110, P 120, T 100.7, R 22,
• O2 97 RA

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Case 1

• The raver continues to curse and yell
• He is diaphoretic, pupils dilated, piloerection
  is noted
• What toxidrome is presented here?

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Sympathomimetic

• Hypertension, tachycardia, diaphoresis, psychotic
  behavior
• Tmt
• 1.Benzos
• 2.Benzos
• 3.Nitroprusside, phentolamine(hypertensive
  emregency) or dexmedetomidine
• 4.Do NOT acidify urine

Crystal, Ice, Meth, Crank
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Case2

• And yet another 19 y/o raver brought in by his
  friends for similar behavior as the guy on your
  last shift.
• BP180/90, P95, T98.7, R20, O298RA
• He is as pissed off as the other guy, pupils
  dilated, his face is red, but he is not sweating
  like your previous guy
• Toxidrome?

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Anticholinergic

• Presents similar to sympathomimetic without the
  diaphoresis
• Turns out this particular patient got Benadryl
  instead of MDMA. When the first one did not work,
  he ate 20 more
• TMT supportive, cool, benzodiazepines, consider
  physo if not TCA or widened QRS/sodium channel
  effects

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Case 3

• 25 y/o landscaper brought by his coworker into
  the ER obtunded
• BP 90/40 P-40 R-8 T-98.7 O2-75NRB
• He is obtunded, has copious wet secretions and
  diarrhea, pupils pinpoint
• What toxidrome is presented here?

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Cholinergic

• DUMBELS-
• Diarrhea, Urination, Miosis, Bradycardia, Emesis,
  Lacrimation, Salivation
• TMT
• decontaminate pt. if organophophate
• Atropine
• 2-PAM until secretions dry

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CASE 4

• You are working the Saturday night shift when a
  18 y/o female is dropped out of a speeding
  cadillac. (AKA Homey Ambulance service)
• She is taking shallow breaths and is unconscious
• BP-90/40, P-50, R-5, T-97.8, O2-68NRB

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CASE 4

• Her pupils are pinpoint and her respiratory
  effort is minimal
• You notice marks on her arms
• Toxidrome?
• Opioids
• TMT
• Naloxone
• supportive

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An important note

• Opioids and sedative hypnotics can appear the
  same
• Pupils will usually be spared with
  sedative-hypnotics (s-h)
• Respirations mostly preserved with s-h
• Examples
• GHB, benzos, ethanol, barbiturates

(Georgia Home Boy, Liquid X, Scoop)
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Case 5

• This patient is a 35 y/o female with a history of
  depression and multiple psychiatric admissions
  for OD
• Her husband brings her to the ED saying he thinks
  she overdosed again
• BP-175/100, P-125, T-100.7, R-22, O2-98

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Case 5

• She is agitated and can not stop moving around
• In spite of IV fluids, she remains tachycardic
  and somewhat psychotic
• What drug has she overdosed on/toxidrome?

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SSRI/Serotonin syndrome

• Altered MS, agitation, fever, tremors, ataxia
• Be careful as serotonin syndrome can mimic
  thyrotoxicosis (a deadly disease if missed), NMS,
  MAOIs/tryptophan, and withdrawal symptoms
• Usually diagnosed per med history
• Can present weeks after stopping SSRI
• TMT
• benzos
• supportive
• cyproheptadine

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Antidotes

• Acetaminophen-NAC
• Arsenic-BAL
• Mercury-BAL
• Lead-Dimercaprol, EDTA
• Carbon monoxide-O2, hyperbaric in severe/pregnant
• Cyanide-amyl nitrite OR sodium nitrite, sodium
  thiosulfate
• Ethylene glycol/methanol-ethanol, fomepizole

• Iron-deferoximine
• Nitrites-methylene blueOrganophosphates-atropine,p
  ralidoxime (2-PAM)Opioids-naloxonePhenothiazines-d
  iphenhydramine,BenzotropineIsoniazid
  (INH)-pyridoxineDigoxin/Oleander-Digitalis Fab
  fragments

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In Summary

• ABCs including early antidotes
• GI decontamination early
• Get a good overdose history if possible
• Look at the patient and try to match clinical
  symptoms with a toxidrome
• Look for skin markings/do you smell anything
  unusual?
• Get poison center involved

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Questions?