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					Toxicology: Childhood
      Poisonings




 CPT Lori Angerson-Bednash, DO
         05 March 2011
               Objectives
 List toxic substances or medications that
  are commonly ingested or inhaled by
  children

 Describe the general management
  principles and specific antidotes for
  ingestions and toxin exposures

 List community resources available for
  consultation in the management of a
  child with poisoning or toxin exposure
   Poison Control Center: 1-800-222-1222
America's poison centers are open 24
hours a day, seven days a week
           Introduction


 Since 1960, 95% decline in number of
 pediatric poisoning deaths
  Child-resistant packaging
  Heightened parental awareness
  Sophisticated interventions
             Introduction

 60% of poison control center calls are for
  children younger than 17 years
   Most accidental and minimally toxic
   Higher morbidity in adolescents
    (intentional exposures)
   Many pediatric patients will have
    unexplained signs and symptoms
                Statistics
             Age Distribution
 Almost 2.5 million human poisoning exposures

 Age 0-5    1.3 million (52%)

 Age 6-12   150,000    (6%)

 Age 13-19 170,000     (6.75%)

Though calls regarding children (age 0-5) account
  for more than 50 percent of all calls to poison
  centers, they account for less than 2 percent of
  the fatalities.
 Commonly Ingested Substances

 Infants and toddlers: seldom able to access
  substances out of reach
   Suspect parental or caregiver abuse

 Most ingestions occur in toddlers and kids < age 6
  with access to unsecured substances
  Commonly Ingested Substances

 Most ingestions cause mild or no symptoms, however
  ingesting even small amts may have consequences

 The most toxic substances in small kids include: iron,
  antidepressants, hypoglycemics, cardiovascular drugs,
  salicylates, anticonvulsants, and illicit drugs
Substances With Higher Toxicity
         in Children
Alcohols      Ethanol, Ethylene glycol (antifreeze),
              methanol
Caustic Agents Acids (toilet cleaners), alkalis (drain or
              oven cleaners), cleaning agents
Food flavoring Wintergreen Oil
Hydrocarbons Kerosene, oil, paint thineers, lighter fluid
Pesticides
Nail products
Antidepressants/antipsychiotics
Antimalarials
Cardiovascular Agents
Opiods
Statistics: Top Ten Childhood
           Poisonings
1. Cosmetics/Personal Care Products: 13%
2. Analgesics: 10%
3. Cleaning Substances (Household): 9%
4. Foreign Bodies/Toys/Miscellaneous: 7%
5. Topical Preparations: 7%
Statistics: Top Ten Childhood
           Poisonings
 6. Vitamins: 4%
 7. Antihistamines: 4%
 8. Cough & Cold Preparations: 3%
 9. Pesticides: 3%
10. Plants: 3%
Statistics: Top Ten Poisoning
Deaths in Children less than 5
 1. Analgesics: 13%
 2. Batteries: 13%
 3. Hydrocarbons: 10%
 4. Plants: 3%
 5. Cold and Cough: 7%
Statistics: Top Ten Poisoning
Deaths in Children less than 5
 6. Fumes/Vapors/Gases: 10%
 7. Pesticides: 10%
 8. Chemicals: 7%
 9. Household Cleaning Supplies: 7%
10. Antidepressants: 3%
    Statistics: Poison Control Calls-
                   2009
 >2.5 million human toxin exposures

 91% occurred in the home

 83% were unintentional

 Children less than 18 accounted for 65%

 Children < age 5 accounted for 53% exposures
   45% of these were in kids age 3 and younger

 1158 fatalities reported in 2009 from poisonings
   Included 25 kids < age 6
Initial Assessment: Overview
 ABCs always first

 Treat patient, not the poison

 Intravenous (IV) access and monitors

 Check blood sugar in any patient with altered
  mental status and lethargy
   “Coma Cocktail:” Assess and consider
    treatment with oxygen, IV dextrose or IM
    thiamine plus glucagon (if glucose < 80),
    and/or naloxone

 Attempt to identify a specific toxidrome
  (ingestion syndrome)
 Initial Assessment: HISTORY

 Obtain detailed
  history of the type,
  amount and time of
  ingestion
 Use family or friends
  as historians
 May need to search
  the home
 Again, history,
  history, history!
   Initial Assessment:
  Physical Examination
 Directed physical examination

  Mental status changes
  Vital sign changes
  Pupillary size
  Skin signs
Initial Assessment: Pupillary Size
              MIOSIS




C   Cholinergics, Clonidine
O   Opiates, Organophosphates
P   Phenothiazines, Phenobarbital,
    Pilocarpine
S   Sedatives, Hyponotics
Initial Assessment: Pupillary Size
            MYDRIASIS

A    Antihistamines
A    Antidepressants
A    Anticholinergics,
     Atropine
S Sympathomimetics
(cocaine, caffeine,
ephedrine,
ampthetamines)
Initial Assessment: Skin Signs

Diaphoretic skin:
S-                  Sympathomimetics
O-                  Organophosphates
A-                  ASA (salicylates)
P-                  PCP (phencyclidine)
Red skin            Carbon monoxide (rare), boric
                    acid
Blue skin           Cyanosis, methemoglobinemia
Initial Assessment: Skin Signs
    DRY SKIN
    Anticholingeric Agents:
          Antistamnes
          TCAs
          Atropiine
          Scopolamine
          Belladona alkaloids
          Phenothiaines
Initial Assessment: Heart Rate
           Tachycardia
 Sympathomimetics
 Anticholinergerics
 Central Hallucinogens
 Drug Withdrawl States
 Nicotine
 Cholinergic Agents
 Thyroid Hormone
 Beta and Alpha-Adrenergic
 Toxic Alcohols
 Calcium Channel Blockers
 Heavy Metals
 Colchicine
 Nitrates
 Sodium Nitorprusside
  Initial Assessment: Heart Rate
            Bradycardia
Alpha-Adrenergic
Ergot Alkaloids
Sumatriptan
Clonidine (early)
Cholinergic
Steroids
Heavy Meta;s
MAOIs
Beta-Blockers
Cardiac Glycosides
Cyanide
Hyponotics
Antiarrhythmics
Drug Associated Odors
ODOR                       AGENT
Acetone (fruity) Ethanol, isopropyl,
                 chloroform,salicylates
Bitter Almonds   Cyanide
Garlic           Arsenic, organophosphat
Mothballs        Naphthalene, benzenes
Kerosene         Organophos, parathion
Freshly Mown Hay Phosgene
Rotten Eggs      Hydrogen sulfide
Wntergreen       Methyl Salicylate
          Initial Assessment:
   Directed diagnostics by history of
                ingestion
 Cardiotoxic meds (digoxin, calcium
 channel blockers, beta blockers,
 antiarrhythmics) or antidepressants
   Telemetry and/or 12-lead EKG, CXR

 Aspirants
   CXR

 Radio-opaque toxins
   CXR, Abdominal films
      Initial Assessment:
Directed diagnostics by history
          of ingestion
 Electrolytes (check anion gap and
  osmolar gap)

 Toxin screening rarely helpful

 Determining specific drug levels may
  be worthwhile
Laboratory Assessment
   Laboratory Assessment
 Initial tests- “rainbow labs” plus
  common substances ingested
  (tylenol)
 Probing subset guided by clinical
  suspicion
   Quantify theophylline, digoxin,
    anticonvulsants, TCAs
   Illicit drug screens

 Minimize blood draws in kids, if
  possible
          Treatment: Prevention or
          Minimization of Absorption
 Gastric decontamination (activated
   charcoal & gastric lavage)- no
   longer routinely recommended.
   Reserved for most severe cases with
   poison control center support

 Gastric lavage
   American Academy of Clinical
    Toxicology (AACT) recommends use
    for massive ingestions only
   For ER arrival within 1 hour of
    exposure

 Ipecac
   Rarely used in the ED
     Activated Charcoal
 Can decrease the absorption of a wide
  variety of toxins in the stomach and
  intestine
 Most effective for:
   Tegretol, dapsone, phenobarb, quinine,
    theophylline, salicylates, dilantin, or
    depakene.
 NOT effective for:
   Pesticides, hydrocarbons, acids, alkalis,
    alcohols, iron, and lithium
        Activated Charcoal
 AACT recommends use only w/in 1 hr of
  drug ingestion
 Charcoal to drug ratio 10:1
  recommended
 Recommended dose
   If younger than 6 years : 1 to 2 g/kg
   If older than 6 years:   50 to 100 g
 First dose given w/ cathartic (i.e. sorbitol)
  to improve taste and transit through
  intestinal tract
                  Cathartics
 Studies of the effectiveness of cathartics are
  inconclusive
   Sorbitol
   Polyethylene glycol (safer)

 High-dose cathartics may be effective of ridding
  lower GI tract of toxins

 Complications related to systemic absorption
   Electrolyte disturbances and severe dehydration
   Neuromuscular impairment and coma

 May use once
       Whole Bowel Irrigation
 Golytely (PEG-ELS)
   Combination of electrolytes and
    nonabsorbable polyethylene glycol (PEG) for
    4 to 6 hours or until the rectal effluent
    becomes clear
     0.5 L/h for small children
     2 L/h for adolescents
   Useful to treat ingestions of heavy metals (iron,
    lithium) and sustained- release preparations
   Few clinical trials about effectiveness of this
    procedure in kids
Enhancement of Excretion
 Hemodialysis
   May be appropriate for lithium, salicylate,
    theophylline, methanol, atenolol,
    phenobarb, or valproic acid toxicity
   Consult toxicology and nephrology

 Urine alkalinization w/ sodium bicarb
   May be used for poisonings w/ salicylates,
    TCAs, phenobarb, herbicides, or
    methotrexate
          Syrup of Ipecac

 No clinical evidence that it improves patient
  outcomes, even given within minutes of toxin
  ingestion

 In 1992, the AACT recommended use of ipecac
  be abandoned b/c lack of evidence of
  usefulness

 The Amer Acad of Pediatrics agrees

 May use if no chance of getting to the ED within
  30-90 minutes.
     Specific antidotes

 Consult w/ Poison Control Center (1-800-222-
  1222)

 Usually given after patient is stable

 Preferably given within a few hours of ingestion

 May require multiple doses b/c of short durations
  of action
   Emergency Medications for
     Childhood Poisonings
 Indication         Medication Infants     Children


Hypoglycemia/AMS Dextrose 5 ml/kg@10 %
  4ml/kg@25%

Opioid overdose     Naloxone 0.1mg/kg under 5
                         0.1 to 0.8mg/kg over 5


 Intravenous thiamine (10 mg for infants and 10 to
  25 mg for children) should be given before
  dextrose is administered to prevent Wernicke
  encephalopathy.
                     Antedotes
Acetaminophen N-acetylcsteine 140mg/kg: 70mg/kg q4 for 17

Organophasphate Atropine 0.02mg/kg until titrated effect

CCB Ca Gluconate 100-200mg/kg and CaCl 20-30mg/kg

Cyanide Sodium Nitrate 3% 0.15-0.33mg/kg per hour

Iron Deferoxamine 5-15mg/kg per hour

Lead/Arsenic Dimercaprol 2.5 to 4mg/kg
Supportive Care & Disposition

  Monitoring

  Hospitalization

  Psych consult (adolescents w/ OD)

  SW/ CPS/ CID consults for suspected abuse

  Family education for children’s safety to prevent
   future unintentional poisonings
CASES
          Case 1: 18-year-old girl


 Brought to the ED by her boyfriend after
  ingesting "as much Tylenol as I could"

 Denies other medication use

 The ingestion occurred 3 hrs before arrival
         Case 1 Progression
 During examination she is anxious, diaphoretic, and
  complaining of nausea

 Physical examination results are unremarkable
  except for a mildly tender abdomen

 She is given 50 g of activated charcoal

 Her 4-hour acetaminophen level is 215   mg/mL
                Case Discussion:
                Acetaminophen
 The most widely used pediatric analgesic on the
  market

 Normal cytochrome P-450 conversion yields small
  amounts of free oxidants that are hepatotoxic

 Toxic dose:
   >140 mg/kg in children
   > 7 g in adults
    Case 1 Discussion: Tylenol OD
               Stages
 Stage 1: Early (4-12 hours), malaise, nausea, vomiting

 Stage 2: Quiescent /asymptomatic (24-72 hours),
  liver enzymes become elevated

 Stage 3: Liver failure (48-96 hours), elevated PT;
  death possible

 Stage 4: Hepatic abnormalities resolve (7-8 days)
    Case 1
  Discussion:
  tylenol OD
 Kinetics dictate
  a level at 4
  hours after
  ingestion
 Apply level to
  the
  management
  nomogram
     Case 1 Discussion:
 N-acetylcysteine (Mucomyst)
           Therapy
 Proved to be 100% effective when administered
  within 8 to 16 hours of exposure

 Load with 140 mg/kg orally
   Full regimen, 17 doses of 70 mg/kg every 4 hours

 IV NAC is efficacious
    Case 2: 2-year-old boy




 The boy wandered into the garage and drank from a
  bottle filled with antifreeze

 He seemed to swallow a few gulps and then cried,
  dropped the bottle

 The father then noticed the event, called the poison
  control center and was told to take the child to the
  ED for care
          Case2 Progression

 Pediatric assessment shows abnormalities in
  appearance only
   The child seems “drunk” with a decreased level of
     consciousness
                                                    o
 Vital signs: HR 120; RR 20; BP 80/Palpable; T 37.4 C;
  weight 12 kg



What class of toxin did the child ingest?
 Case 2 Discussion: Alcohols

 Ethanol - often causes hypoglycemia, ketosis

 Methanol - can cause blindness, profound osmolar
  gap, and metabolic acidosis

 Ethylene glycol - renal failure (calcium oxalate
  crystals), osmolar gap, and metabolic acidosis
           Case 2 Progression

 Patient has metabolic acidosis and an osmolar gap
  consistent with ingestion of ethylene glycol

 Treatment with alcohol begun
   Competes for alcohol dehydrogenase to prevent
     buildup of toxic metabolites

 Patient admitted to the pediatric intensive care unit
  (ICU)
      Case 3: 10-year-old girl




 Arrives with her parents who state that her behavior
  has been bizarre

 She is presently recovering from an active case of
  chicken pox and reports no fever, stiff neck, nausea,
  vomiting, or new rash

 She is extremely combative, hyperreflexic, with
  intermittent posturing when negatively stimulated
        Case 3 Progression
 Her pupils are dilated and reactive and
  demonstrate adequate venous pulsations
  with no papilledema

 Vital signs: HR 140; RR 20; BP 110/70; T
  40oC; weight 35 kg



Is there a toxidrome present, and what
   could be the possible substance?
                 Case 3 Discussion:
                  Anticholinergics
SYMPTOMS/SIGNS:

 Hot as a Hare (fever) Warm,
   dry, flushed skin

 Dry as a Bone

 Blind as a Bat (lack of
   accommodation)

 Red as a Beet                  TOXINS/DRUGS:
 Mad as a Hatter                 Antihistamines
   (disorientation, confusion,
   hallucinations, seizures,
   coma)                          Antipsychotics

 Addiitonal signs: dilated       Antispasmodics
   pupils, ileus, urinary
   retention, mild                Muscle relaxants
   hypertension, hypotension,
   dysrhythmias
                                  Tricyclics
         Case 3 Progression
 Patient received 50 g of activated
  charcoal and supportive care for a
  possible diphenhydramine poisoning

 Physostigmine not given in this case
   Indicated only for patients in coma or
    with delirium or unstable vital signs

 Patient recovered completely in 24 hours
        Case 4: 3-year-old girl

 Brought in by parents after they found her with a
  container of dishwasher detergent in her hands

 Patient is asymptomatic

 Physical examination results, including for the mouth,
  are completely normal

What class of toxin did she ingest, and what are your
 further management priorities?
Case 4 Discussion: Caustics

 Drain cleaners, glucose reagent tablets, oven
  cleaners and dishwasher detergents

 Do NOT lavage or give activated charcoal

 Presence of symptoms of ingestion or oral burns
  mandates endoscopy

 This patient was discharged home with follow-up
  instructions
  Case 5: 2-year-old boy




 Brought in by paramedics after grandmother
  stated he was “not acting right”

 Grandmother thinks he might have ingested
  some of her medications (digoxin, furosemide,
  and an antihypertensive agent)
         Case 5 Progression
 Pediatric assessment reveals abnormality
  in appearance
   Examination shows a lethargic toddler
    with no other physical findings; pupils 1
    to 2 mm

 Vital signs: HR 70; RR 20; BP 80/palpable; T
  37oC; weight 13 kg

What is the likely substance ingested by this
 toddler?
  Case 5 Discussion: Clonidine

 Central-acting antihypertensive; also used to treat
  narcotic withdrawal and sometimes
  postmenopausal symptoms

 Comes as very small tablets and skin patches

 Pediatric ingestion causes:
   Low blood pressure (after transient hypertension), miosis,
     and coma

 Naloxone may reverse the respiratory depression
         Case 5 Progression

 ECG normal; serum digoxin level zero

 No response to naloxone

 Patient admitted; good outcome with supportive
  care
   Case 6: 5-year-old boy




 Drank from a soda bottle containing
  gasoline

 Patient cried immediately, gagged and
  coughed, and then vomited

 The poison control center was contacted
  and the patient referred to the ED for
         Case 6 Discussion:
          Hydrocarbons
 Available as degreasers, solvents, fuels,
  and pesticides

 4 major groups: aliphatic, alicyclic,
  aromatic, halogenated

 Toxic effects may be pulmonary,
  cardiovascular, or systemic
       Case 6 Discussion:
  Hydrocarbons-Management
            Issues
 Admit all symptomatic patients, and obtain
  ABGs, chest radiograph, and ECG

 Absence of symptoms within 4 to 6 hours
  speaks strongly against the possibility of
  chemical pneumonia

 Do NOT administer ipecac, and do NOT use
  prophylactic corticosteroids or antibiotics
      Case 6 Progression
 Patient remained asymptomatic for 4
 hours

 Discharged home with instructions for
 parents to return immediately to the
 ED if cough, shortness of breath, or
 fever develops
    Case 7: 5-year-old boy



 Brought in by paramedics from school,
  where nausea, vomiting, and bloody
  diarrhea developed

 Patient states he ate some of his mother’s
  prenatal vitamins before breakfast and now
  feels sick

 The bottle, which contained 30 tablets of
  ferrous sulfate, is now empty
Case 7 Discussion: Iron ingestion

  The toxic component is based on elemental iron load

  Most children's preparations contain less iron than
   adult preparations
    Children’s: 3-25 mg/pill
    Adult: 37-65 mg/pill (5-10 of these can kill a child)

  One of the most FATAL poisonings in kids < age 6
     Case 7 Discussion: Iron

 Symptoms can be seen at ingested doses of 15 to 30
  mg/kg

 Ingestions of 40 mg/kg are potentially serious

 Ingestions greater than 60 mg/kg may result in critical
  condition
    Case 7 Discussion: Iron
           Ingestion
     Clinical Presentation
 GII Stage (30min- 6hours)
   Abdominal pain, nausea, VOMITTING, and
    diarrhea; may progress to shock
 Latent Stage (relative stability or quiescent
  phase occurring 6-24 hours)
   Apparent clinical improvement
 Shock stage
   May be followed by abrupt onset of coma,
    shock, seizures, coagulopathy, and death
     Case 7 Discussion: Iron-
      Clinical Presentation
Hepatotoxicity stage (12-96 hours)
   Occurs within 48 hours; bad prognosis.

GI scarring (2-8 weeks)
   GI damage may scar, resulting in pyloric
    stricture or other intestinal obstruction

  What is the value of a serum iron
   level?
   Case 7 Discussion: Iron-
 Management by Serum Level
 In symptomatic patients, treat with
  deferoxamine

 In asymptomatic patients, obtain
  abdominal radiograph and a 4-hour iron
  level
   If level less than 400 mg/dL and patient remains
    asymptomatic, may discharge
   If level more than 400 mg/dL, treat with deferoxamine
     Case 7 Discussion: Iron-
         Management

 Ipecac or lavage if recently ingested

 Abdominal radiograph

 Whole bowel irrigation is effective and safe

 Avoid instilling intragastric antidotes

 Gastrostomy
      Case 7 Discussion: Iron-
          Management

 Early signs of toxicity necessitate deferoxamine
   15 mg/kg per hour (maximum, 6 g/d)

 “Vin rose” urinary color change is unreliable
        Case 7 Progression
 Patient complaining of abdominal pain

 Abdominal radiograph shows some pills in stomach

 Fluid hydration, whole bowel irrigation, and
  deferoxamine begun

 Patient admitted to pediatric ICU
      Case 8: 6-year-old boy

 Brought to the ED by ambulance because of
  respiratory distress; his parents state that he awoke
  that morning and went outside to play, returning in
  distress

 Pediatric assessment reveals:
   Appearance – lethargic
   Work of Breathing - retractions
   Circulation - diaphoresis
         Case 8 Progression
 Respiratory distress with wheezing and rales in all
  fields; copious secretions

 Nonfocal neurologic examination results with
  lethargy; pupils are 1 mm and reactive
                                                        o
 Vital signs: HR, 50; RR, 70; BP, 90/palpable; T, 37.8 C;
  weight, 25 kg
What class of toxic exposure does this patient
 demonstrate?
         Case 8 Discussion:
     Organophosphates - Clinical
           Presentation
 Diarrhea

 Urination

 Miosis

 Bradycardia

• Bronchosecretions
• Emesis
• Lacrimation
    Case 8 Discussion:
Organophosphates Treament

 Atropine (vagal blockage)
  Large doses (0.5-10 mg IV) may be
   necessary

 Pralidoxime (cholinesterase regenerator)
  20 to 50mg/kg per dose (IM or IV)
  Not indicated in carbamate exposures
       Case 8 Progression

 Patient intubated after RSI (rocuronium and
 midazolam)

 Patient received 5 mg of atropine during 40
 minutes and 1 g of pralidoxime in the ED

 Patient admitted to pediatric ICU
    Case 9: 3-year-old girl




 Fever, progressive sleepiness, and
  respiratory distress; onset 2 hours after
  ingesting something from a kitchen
  cabinet

 Pediatric Assessment Triangle reveals:
  Appearance - lethargic; Work of
  Breathing - tachypnea; and normal
  Circulation
       Case 9 Progression

 Patient responds to mother's voice;
  neurologic examination; no focal deficits

 Vital signs: HR, 140; RR, 60 (deep); BP,
  90/70; T, 40oC; weight, 12 kg



What toxic substance did this child ingest?
Case 9 Discussion: Salicylates

 Central stimulation of the respiratory
  center = respiratory alkalosis

 Uncouples oxidative phosphorylation and
  interrupts glucose metabolism

 Alters platelet function and bleeding time

 May act as vasoactive agents; cerebral
  edema
     Case 9
   Discussion:
Salicylates-Toxic
      Dose
 Therapeutic dose
  = 10 to 15 mg/kg
 Toxic dose is more
  than 150 mg/kg
 Nomogram useful
  ONLY in single-
  dose acute
  exposures
Case 9 Discussion: Salicylates-
   Clinical Manifestations

 Vomiting, hyperpnea, tinnitus, and
 lethargy

 Severe intoxication: coma, seizures,
 hypoglycemia, hyperthermia, and
 pulmonary edema

 Death is due to cardiovascular collapse
 Case 9 Discussion: Salicylates-
  Enhancement of Elimination

 Urinary alkalinization with sodium
  bicarbonate to maintain urine pH > 7

 Hemodialysis is very effective for drug
  removal and to correct acid-base
  disturbances
       Case 9 Progression

 6-hour salicylate level was 70 mg/dL
 (moderate toxicity)

 Patient received IV sodium bicarbonate
 and was admitted to the pediatric ICU
  Case 10: 15-month-old boy




 He was last seen well 2 hours ago when his
 parents placed him into a car seat in the
 back of their 20-year-old car and began
 driving to grandmother’s house

 His parents noted feeling sick and when
 they checked the toddler, he “looked
 pale” and attempts to wake him failed
        Case 10 Progression

 On arrival in the ED, the child is afebrile with
  normal vital signs

 He responds symmetrically to pain only, and
  pupils are reactive and midrange; O2 sat.
  98%

 CBC, ECG, and chest radiograph results are
  normal

What could be the possible toxic exposure in
 this case?
         Case 10 Discussion:
         Carbon Monoxide
 Carbon monoxide–hemoglobin affinity
  250 times oxygen-hemoglobin bond;
  results in decreased saturation

 Nonirritating, tasteless, colorless, odorless
  gas

 Sources include smoke inhalation; auto
  exhaust; poorly ventilated charcoal,
  kerosene, or gas heaters; and cigarette
  smoke
       Case 10 Discussion:
       Carbon Monoxide
 Toxic effects are a consequence of
 cellular hypoxia

 Concentrations of 20% produce
 neurologic symptoms; if more than 60%,
 death

 Pulse oximetry may be falsely normal

 Peak level may have occurred in the field
 before oxygen therapy
     Case 10 Discussion:
  Carbon Monoxide-Therapy
 Administer oxygen in highest
 concentration, reducing half-life of CO-
 Hgb from 6 hours (room air) to 1 hour

 Hyperbaric therapy
  Indicated for patients with neurologic
   dysfunction, pregnant women, patients
   in unstable condition, and possibly for
   children with levels more than 25%
     Case 10 Progression
 Carboxyhemoglobin level, 27%

 Patient given 100% oxygen

 Transferred to hyperbaric chamber for
 therapy
               Conclusion
 The poison control center can be a valuable
  resource for families and physicians

 1-800-222-1222 POISON CONTROL CENTER

 Manage ABCs, supportive care, history-directed
  diagnostics and therapeutics

 Recognition of toxidromes can assist in directed
  management of patients with specific toxic
  ingestions or exposures
QUESTIONS?
                  References

   “Evaluation and Management of Common Childhood Poisonings,”
    American Family Physician, 1Mar09, pp 397-403.

   “Acetaminophen Poisoning: an Evidence-Based Consensus Guideline
    for Out-of-Hospital Management,” Clinical Toxicology, 2006 44-,1-18.

   “Iron Ingestion: an Evidence-Based Consensus Guideline for Out-of-
    Hospital Management,” Clinical Toxicology, 43:553–570, 2005.

   “2009 Annual Report of the American Association of Poison Control
    Centers’ National Poison Data System (NPDS): 27th Annual Report”.
    Clinical Toxicology (2010) 48, 979–1178.

   Up-to-Date online 2011

   American Academy of Clinical Toxicology website

   Poison Control Center website

				
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