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B. Wayne Blount, MD, MPH
Epidemiology
US Poison Centers receive 1.5 million calls a year regarding pediatric ingestions.
79% of these calls involve children younger than age six.
56% of pediatric exposures are from products around the house including medicines, cleaning agents, pesticides, plants and cosmetics.
Acute Poisoning in the Emergency Department
Common - 3-5% of ED attendances2000 Deaths per year
Often multiple drugsDON’T FORGET ALCOHOL !!
Epidemiology: “the numbers”Nearly 90% of exposures occur at homeDuring pre-adolescence: slight male
predominanceThis reverses in ages 13-19 with females
accounting for 55 %Children, especially under age 6, are
more likely to have unintentional poisonings
About half of all poisonings among teens are classified as suicide
Epidemiology: “the numbers”
Approximately 1/3 of ingestions of toxic medications occur with meds intended for someone else
DefinitionsArtery: The Study of Paintings
ObjectivesGeneral Principles in the Management of
ANY PoisoningSpecific management options with certain
substancesSalicylates Ethylene GlycolAcetominophen PesticidesIron LeadTricyclics Hydrocarbons
General Management -HistoryApplies to ANY episode of PoisoningWHATHOW MUCH (Ideally mg/Kg)WHENWHAT ELSE (Including Alcohol)WHYUse Paramedics, friends, relatives, anyone!!
General Management -1A (Airway)B (Breathing)C (Circulation)D (Disability-AVPU/ Glasgow Coma Scale)DEFG ( Don’t Ever Forget the Glucose)G (Get a set of basic observations)
General Management -2Use all your senses, search for the cluesLOOK
Track MarksPupil Size
HearType Breathing (Kussmaul, Hyperventilation)
FEELTemperature, Sweating
SMELLAlcoholFruityI would NOT taste
Specific Management Options-1
DECREASING DRUG ABSORPTION
Decontaminate
Gastric Lavage ( Unpopular - need to protect the airway, may push drug through pylorus into small bowel.)
Absorbants ( Activated Charcoal , usually within 1 hour of ingestion, longer repeated doses in drugs that delay gastric emptying e.g. Aspirin)
Specific Management Options -2
INCREASING DRUG ELIMINATIONAlkaline Diuresis (Aspirin)
Hemodialysis (Aspirin)
Specific Management Options - 3
ANTAGONISING THE EFFECTS OF THE POISON
Desferrioxamine (IRON)Naloxone (OPIATES)N Acetylcysteine (Acetominophen)Digibind (Digoxin)Flumazenil (Benzodiazepines)
DefinitionsBariumWhat doctors do when patients die
DiagnosisPhysical Exam:
Vital signs and general appearanceThorough PEClose attention to neuro exam
Pupils Reflexes and posture Mental status
Bowel soundsMucous membranes and skin moisture/appearanceCharacteristic odorsNosebleeds, needle tracks, blistering
Physical Exam FindingsSympathomimetic (meth, amphetamines, cocaine,
opiate withdrawal, PCP) Hyperthermia, tachycardia, hypertension, mydriasis,
warm/moist skin, agitatedCholinergic (organophosphates, betel nut, VX,
Soman, Sarin) SLUDGE (Salivation, Lacrimation, Urinary incontinence,
Diarrhea/Diaphoresis, GI upset/hyperactive bowel, Emesis)Anticholinergic (antihistamines, atropine,
phenothiazines, TCA) Hyperthermia, tachycardia, HTN, hot/red/dry skin,
mydriasis, unreactive pupils, unrinary retention, absent bowel sounds
Opioids (codeine, dextromethorphan, heroin) Miosis, respiratory depresssion, mental status depression
Diagnostic ConsiderationsBefore proceeding, consider other aspects of the
differential diagnosis ( CVA, trauma, meningitis, post-ictal state, behavioral or psych disorders).
Labs to evaluate glucose, acid-base status and electrolytes, BUN/Cr, carboxyhemoglobin, hepatic enzyme levels, urinalysis (UA preg), serum osmolality, serum acetaminophen levels
EKGSave samples of blood, urine, gastric contentsGeneral qualitative tox screens of little value
(except when abuse is suspected), but are rapid and could offer clue to antidote; may have role in the difficult dx or critically ill; Quantitive measurements in certain toxic exposures
Diagnostic ConsiderationsOcular/dermal:
pH testing may reveal acid or alkali Hypoxemic while asymptomatic may suggest
methemoglobinemiaCardiac
EKG shows arrhythmia (TCA) Blood color on filter paper that remains brown after air
exposure suggests methemoglobinemia (possibly from benzocaine-containing products, aniline dyes, nitrites)
Signs of hypocalcemia in ethylene glycol, hydrofluric acid
Urine fluorescence in ethylene glycolFerric Cl creates purple reaction with salicylates and
phenothiazines in urineSmall opacities on x-ray may show halogenated
toxins, heavy metals, lithium, densely packed products, phenothiazines, enteric-coated meds
Diagnostic ConsiderationsMUDPILES CAT for high anion gap acidosis
Methanol or metforminUremiaDKAParaldehyde or phenforminIron, INH, IbuprofenLactic acidosisEthylene glycolSalicylatesCyanideAlcohol or acids (valproate)Toluene or Theophylline
Diagnostic ConsiderationsToxins requiring quantitative levels at a set
point:AcetaminophenCarbon monoxideEthanol, ethylene glycolHeavy metals (24 hour urine)IronMethanolMethemoglobin
Toxins requiring quantitative serial levelsAspirin/salicylates, tegretol, digoxin, phenobarbital,
phenytoin, VPA, theophylline
DefinitionsDilateLive longer than your kids
Common Toxidrome FindingsPhysical Findings Adrenergic
Anti-
cholinergic
Anti-
cholinesteraseOPIOID
Sedative-
hypnotic
RR Increased No change No change Decreased Decreased
HR Increased Increased Decreased Normal/
decreased
Normal/
decreased
Temp Increased Increased No change Normal/
decreased
Normal/
decreased
BP Increased NoChange/increased
No change Normal/
decreased
Normal/
decreased
Common Toxidrome FindingsPhysical Findings Adrenergic
Anti-
cholinergic
Anti-
cholinesterase
OPIOIDSedative-
hypnotic
Mental status
Alert/
agitated
Depressed/
Confused/
hallucinate
Depressed/
Confused/
Depressed Depressed
pupils Dilated Dilated Constrict Constrict Normal
Mucus membrane
Wet Dry Wet Normal Normal
skin Diaphoretic Dry Diaphoretic Normal Normal
Salicylates
PharmacologyIrreversibly inhibits the enzyme
cyclooxygenase. This inhibits prostaglandin synthesis.
Since prostaglandins are not synthesized, their downstream byproducts are never released such as: IL-6, TNF, and alpha and beta interferons.
Believed to directly inhibit neutrophils to decrease the inflammatory response.
PathophysiologySalicylates stimulate the brainstem to cause
hyperventilation (respiratory alkalosis).
Multifactorial renal impairment leads to accumulation of sulfuric and phosphoric acids.
Interfere with the Krebs Cycle limiting substrates for ATP generation.
Pathophysiology ContinuedUncouples oxidative phosphorylation
which leads to increased pyruvic and lactic acid level and generates heat.
Causes salicylate induced fatty acid metabolism which produces ketone bodies. This ketoacidosis contributes a significant portion to the overall metabolic acidosis.
Salicylate Poisoning
Ingestion of 150 mg/kg of salicylates causes intoxication.
Level of 50-80 mg/dL causes moderate symptoms.
Severe symptoms are associated with blood levels > 80 mg/dL.
Clinical ManifestationsEarly symptoms are usually non-specific such as nausea
and vomiting.
Tinnitus with or without hearing loss can also be an early sign.
Hyperventilation is often a warning sign of a significant ingestion. (respiratory alkalosis)
CNS signs can vary from vertigo to hallucinations to stupor. Coma is rare except in massive overdoses.
In large overdoses, almost every organ system becomes involved.
TreatmentAddress the A,B, C’s.Detailed history and exam.Laboratory evaluation and consider a blood
gas if your history suggests an ingestion.Activated charcoal should be given.
Evidence for multidose charcoal is equivocal.
The use of sodium bicarbonate.Measure serial salicylate levels and
chemistries.
Sodium Bicarbonate TherapyThe goal is to titrate the urinary pH to 8.
BUTExcretion of hydrogen will make it “nigh on
to” impossible to titrate your therapy to a urinary pH of 8.
Potassium must be monitored closely because if the potassium drops, the kidney will retain the potassium and excrete hydrogen.
Urine is alkalinized by administering 1-2 mEq/kg of sodium bicarbonate at
half hourly intervals for 4 hours in alkaline urine, salicylates do not
diffuse back into the tubular cells from the lumen.
Potassium salts should be given (3-5 mEq/kg/day) to replace the potassium losses
Indications for HemodialysisRenal failure.Congestive heart failure (relative).Acute lung injury.Persistent CNS disturbance.Severe acid-base or electrolyte imbalance,
despite appropriate treatment.Hepatic compromise with coagulopathy.Salicylate concentration (acute) >100
mg/dL.
DefinitionsImpotentDistinguished, Well Known
Ethylene Glycol and Methanol
fomepizole
Mg, B6
folate
thiamine
The Osmolar Gap
TreatmentFomepizole or ethanol – both inhibit
alcohol dehydrogenase. Cofactors
PyridoximeFolateMagnesiumThiamine
Fomepizole DosingLoading dose
15 mg / Kg
Next 4 doses10 mg / Kg
Subsequent doses15 mg / Kg
Dosing schedule is every 12 hours except during dialysis. Then it is every 4 hours during dialysis as it gets dialyzed off.
DefinitionsNitratesCheaper than day rates
PesticidesSpecifically
organophosphates and carbamates.
They work by inhibiting acetylcholinesterase. So…
Present with cholinergic symptoms
Organophosphorus (insecticides and pesticides) Poisoning
Organic phosphate insecticides cause irreversible inhibition of the enzyme cholinesterase. As result acetylcholine accumulates in various tissues. Excessive parasympathetic activity occurs. These agents are absorbed by all routes including skin and mucosa.
Cholinergic Symptoms
Symptoms manifest quickly usually
within a few hours Include weakness, blurred vision,
headache, giddiness, nausea, and pain in chest.
Sweat profusely. papilledema may occur.
Reflexes absent and sphincter control lost.
Nicotinic SymptomsThink the days of the week !M ydriasisT achypneaW eaknessT achycardiaF asiculationsW eekend: “Wee” ones : Pediatric patients
tend to present with a predominance of nicotinic symptoms!!!
Weakness from Pesticides
TreatmentIf the insecticide was in contact with
skin or eyes, Wash thoroughly .
Atropine 0.02 mg / Kg IV. Repeat as needed and titrate to respiratory secretions. It will likely take massive doses!!
Pralidoxime (2-Pam) 20-40 mg / Kg bolus followed by 10-20 mg / Kg /hour infusion.
Remember to send RBC and Plasma Cholinesterase levels upon arrival and daily.
DefinitionsRectumDamn near killed him
In overdose situations, liver enzymes become saturated, glutathione is depleted, NAPQI(N-acetyl-p-benzoquinoneimine) accumulates, and hepatic necrosis occurs
PharmacokineticsAbsorption
Rapidly absorbed from the GI tractPeak concentration usually occurs between 60 and 120 minutes
Peak plasma levels almost always occur within 4 hours
Half life
Average 2 hours– range 0.9 to 3.25 hours
No age related differencesNo change in patients with renal diseaseWith liver dysfunction, may increase to 17
hours
ToxicityFactors involved in predicting hepatotoxicity
total quantity ingestedtime from ingestion to treatmentage of the patientalcoholenzyme inducing medications
serum concentration in relation to Rumack nomogram
Toxic dose
In adults, threshold for liver damage is 150 to 250 mg/kg
Children under 10 appear to be more resistant
Potential liver damage
Adults: > 150 mg/kg in acute dose
Adults: > 7.5 Grams in 24 hours (chronic)
Children (<10 yrs): > 200 mg/kg
4 Stages of Acetaminophen Poisoning
Phase I (30 minutes to 4 hours)
Within a few hours after ingestion, patients experience anorexia, nausea, pallor, vomiting, and diaphoresis. Malaise may be present.
Patient may appear normal
Phase II (24 to 48 hours)
SX Less severe. May seem like recovery. Right upper quadrant pain may be present due to hepatic damage.
Liver enzymes become abnormal. Prothrombin time may be prolonged. Renal function may begin to deteriorate.
Phase III (3 to 5 days)
Characterized by symptoms of hepatic necrosis. Coagulation defects, jaundice, and renal failure have been noted. Hepatic encephalopathy has been noted. Centrilobular necrosis. Nausea and vomiting . Death due to hepatic failure.
Phase IV (4 days to 2 weeks)
Complete resolution or death
Activated charcoalShould not be withelddose 50-100 Grams
Catharticutilized to speed transit time
HemodialysisLimited benefitDamage occurs quickly
HemoperfusionNo benefit
Peritoneal dialysisNo benefit
Blood Sample
4 hour post ingestion APAP levellevels drawn earlier may be erroneous
levels may be accurate out to 18 hours
Plot level on Rumack-Matthews nomogram
150 mg/dl at 4 hours is possibly toxic
Do not use therapeutic “normal” values to determine potential toxicity!
Baseline CBCCreatinine, BUN, blood sugar, electrolytesProthrombin timesAST, ALT
repeat q 24 hourselevations typically seen 24-36 hours
post ingestion
mcg/ml 4 8 12 16 20 24Hours After Acetaminophen Ingestion
150
5
10
50
500
Rumack and Matthew Nomogram
100
Late
Not valid after 24 hours
If APAP level plots above the possible risk line administer N-acetylcysteine (NAC).
If NAC is indicated, full regimen should be followed. Do not stop NAC early if nomogram indicates toxic possibility
N-acetylcysteine (NAC)Mechanism of action
glutathione substitutemay supply inorganic sulfur, altering
metabolism
Route of administrationOrally
IV not approved in the U.S.
NAC dosing
Oral 72 hour protocolLoading dose is 140 mg/kg
Maintenance doses: 70 mg/kgGiven every 4 hours x 17 doses starting 4 hours after loading dose
NAC supplied as 10 or 20% oral solutiondilute to 5% final concentration with
juice or soft drink
May be administered via NG tube
If emesis occurs within 1 hour of administration, repeat the dose
DefinitionsTabletA small table
Acetominophen SummaryIn overdose, APAP may overwhelm the liver stores of glutathione. A rise in liver enzymes may occur. Timely administration of NAC may protect the patient from hepatic damage. Therapy should be initiated as soon as possible, but NAC is beneficial at any time. If APAP levels cannot be obtained, assume a toxic dose has been ingested, initiate NAC, and continue until regimen complete.
Points to rememberAPAP is present in many poly drug overdoses No symptoms may be present…screen150 mcg/ml at 4 hours is a “treat” levelNAC loading dose is 140 mg/kgNAC maintenance doses are 70 mg/kgOnce NAC is started, DO NOT DCMetoclopramide 0.1-1.0 mg/kg is very
effective in controlling nausea/vomiting associated with APAP toxicity
SummaryEpidemiologyApproach to the poisoned pateintSpecific toxidromesOther than the General approach, will
probably have to look up treatmentsCall the Poison Hot Line
DefinitionsBenignWhat you be after you be 8
IronThe most common
cause of death in toddlers.
Classically taught as having five clinical stages.
Remember prenatal vitamins, supplements, and “natural products”.
IronToxic doses occur at 10-20mg/Kg of
elemental iron.
Prenatal vitamins typically contain about 65 mg of elemental iron.
Childrens vitamins contain about 10-18 mg of elemental iron.
The Five StagesStage 1
Nausea, vomitting, abdominal pain and diarrhea.Stage 2
This is the latent phase often between 6-24 hours as the patient resolves GI symptoms.
Stage 3Shock stage involving multiple organs including
coagulopathy, poor cardiac output, hypovolemia, lethargy and seizures.
Stage 4Continuing of hepatic failure and ongoing oxidative
damage by the iron in the reticuloendothelial system.Stage 5
Gastric outlet obstruction secondary to scarring and strictures.
ManagementDetailed history and physical including a rectal
exam for frank blood.Aggressive fluid resuscitation and intravenous
access.Whole bowel irrigation and KUB to look for pills.Laboratory analysis for CBC, chemistry, and iron
levels (peak around 4 hours).Will often require repeat levels with a repeat
chemistry.TIBC has no utility in the acute overdose setting.
Management
ManagementIf the patient is in shock, remember to at least
type and screen (if not cross match) for blood.Give deferoxamine before iron level is back if
the patient is in shock.Deferoxamine was derived from streptomyces
pilosus.Hypotension and allergic reactions are seen.ARDS is a known complication and usually
limit its use to 24 hours or less.
Review ArticlesMichael JB, Sztanjnkrycer MD. Deadly pediatric
poisons: nine common agents that kill at low doses. Emergency Medicine Clinics of North America 2004; (22): 1019-1050.
Bar-Oz B, Levichek Z, Koren G. Medications that can be fatal for a toddler with one tablet or teaspoonful. Pediatric Drugs 2004; 6(2): 123-126.
TCA Overdose- Clinical features ANTICHOLINERGIC EFFECTS
Dry Mouth, Dry Eyes, Dilated Pupils, Urinary Retention, Blurred Vision, Dizziness, Palpitations, Pyrexia without sweating
CNS Effects- Confusion, Delerium, Coma, Convulsions, Myoclonus and Respiratory Depression
TCA Overdose Clinical FeaturesCardiac Toxicity (quinidine effects)
Heart Block, Asystole, Bradycardia, Tachycardia, Ventricular Dysrythmias
ECG Changes - broadening of QRS complex, Widened QT Interval
TCA Overdose- Management 1Mainstay of initial management is
Supportive. Try not to give other drugs ontop with a few specific exceptions
A- May need intubatingBC- Give IV fluids if low BPD -Control convulsions with Diazepam
TCA Overdose Management 2Activated Charcoal if more than 4 mg/Kg
within 1 hour.N.B WATCH OUT FOR THE AIRWAY
Correct Hypoxia with OxygenCorrect Acidosis with Na BicCorrect any arrythmias with Na Bic (i.e
start by controlling the acid base disturbance)
• Epidemiology• Clinical features• Investigation• Treatment
Epidemiology Accidental – 33 to 60% in India &
other developing countries
Reasons for high incidence1. Extensive use for cooking & lighting in
low socioeconomic status2. Stored in soft drink bottles, beer bottles
within reach of children
Clinical featuresAge – 1 to 3 years more than 70% symptomatic within
10 hours
SYMPTOMS
RS – breathlessness, coughCNS – convulsions, coma GPE – fever, restlessness, cyanosisGI – vomiting, diarrhea
Lab InvestigationsBlood – Leukocytosis
X – Ray changes
Changes appear within one hour - commonly right basal infiltrates - emphysema - pleural effusion - pneumatocoeles
Severity scorePARAMETERSPARAMETERS ABSENTABSENT PRESENTPRESENT OTHERSOTHERS
FEVER FEVER 00 11 00
SEVERE SEVERE MALNUTRITIONMALNUTRITION
00 11 00
RESP. DISTRESSRESP. DISTRESS 00 22 44
CNS SYMPTOMS CNS SYMPTOMS 00 22 44
• >4 – Significant• <7 – Likely to survive• >8 –– Risk of death is increased
ManagementAvoid emeticsAvoid gastric lavage – In case of massive
amount use a cuffed endotracheal tubeAfter lavage leave magnesium or sodium
sulphate in the stomachOxygen may be usefulAssisted VentilationAntibiotics - Penicillin G 50000/Kg/24 hrs IV
qid Kanamycin – 10-15mg/Kg/24 hrs - IM bdSteroids – Not helpful
Complications• Pneumothorax• Pneumatocoeles• Pleural effusion• Bronchopneumonia• Coma
Pralidoxime (PAM) is given in dose of
25-50 mg/kg IM or IV over 30 min infusion. The dose may be repeated in 1-2 hours, then at 6-12 hour intervals as needed. Monitor for hypertension. Never inject morphine, theophylline, aminophylline or chlorpromazine. Intravenous fluids should only be given with caution. No oral tranquilizers are administered. Artificial respiration may be necessary to sustain life.
Hydrocarbon PoisoningThese may be divided into aliphatic or
aromatic compounds. Aliphatic hydrocarbons include kerosene, turpentine, lubricating oils, tar and have greatest risk of aspiration and pulmonary symptoms. Aromatic compounds have mainly neurological and hepatic toxicity and include benzene compounds.
Type of toxicity with a hydrocarbon
depends on its volatility, viscosity or surface tension. The lower is viscosity, more is the risk of pulmonary aspiration. Mineral spirit, kerosene and furniture polish have both low volatility and viscosity and thus carry a higher risk of aspiration pneumonia.
Benzene derivates, toluene and xylene
are components of various solvents and degreasers. These are highly volatile but have low viscosity. Inhalation is the primary route of toxicity which manifests with CNS symptoms. Gasoline and naphtha are constituents of lighter fuel and lacquer diluent and primarily cause depression of the central nervous system (CNS).
Turpentine oil is highly volatile but has low
viscosity also. Toxicity results from inhalation and gastrointestinal absorption. They can also cause CNS toxicity.
Halogenated hydrocarbons are used as solvents and spot removers. Freon is used as a refrigerant.
Toxic exposure to hydrocarbons may result in cardia, gastrointestinal, neurological, pulmonary, renal, hepatic, metabolic and hematological manifestations.
Induced emesis or gastric lavage is
contraindicated for kerosene oil poisoning. It is done only when large quantities of turpentine have been ingested or the hydrocarbons product contains benzene, toluene, halogenated hydrocarbons, heavy metals, pesticides or aniline dyes. Other specific modalities including steroids and antibiotics are not efficacious.
Carbon Monoxide PoisoningClinical manifestations include
headache, cyanosis, convulsions, and coma.
Patients are administered 100 percent oxygen and
if carboxyhemoglobin levels are above 40 percent, hyperbaric oxygen therapy is considered.
Lead PoisoningExposure to lead occurs from old lead
based deteriorated house paint (in old houses) and dust and soil contaminated with lead such as from leaded gasoline, lead electrode plates from old automobile batteries, adultered food, folk remedies, broken lead typesets scattered around old printing establishments. Food may be adulterated with colored metallic salts or the black collyrium used as surma may contain a proportion of black oxide of lead.
Lead Poisoning Chronic lead intoxication occurs
usually in children who eat non-edible substances (pica) and manifests as pain in abdomen and resistant anemia. Lead is deposited in the bones. Acute infections may mobilize lead from storage areas in bones and cause acute lead poisoning leading to acute lead encephalopathy.
In these cases the child may be left
with neurological sequelae. Lead inhibits sulfhydryl enzymes and formation of heme. Heme precursors such as porphyrins accumulate in the blood and are excreted in the urine. Screening for lead intoxication is done by measuring zinc protoporphyrin or blood lead levels.
TreatmentIn symptomatic children, therapy is
usually started with dimercapol (BAL) (75 mg/m2 every 4 hourly IM). BAL may be stopped after 48 hours, while calcium disodium edetate is used for another 3 days but at a lower dosage of 50 mg/kg or 1000 mg/M2 per 24 hours by continuous IV infusion.
Maximum daily dose should not
exceed 500 mg/kg. Stop BAL when blood lead level falls below 60 microgram/dL. Give a second course of edetate alone if blood lead rebounds to 45-69 microgram/dL. A second course of edetate in combination with BAL is recommended for rebound lead level of >70 microgram/dL. Wait for 5-7 days in between the two courses.
Special Pediatric IssuesALL THINGS TEND TO END UP IN THE MOUTHS OF YOUNG CHILDREN!!
Which is Candy?
Sweet Tarts vs. Ecstacy
Physiologic DifferencesBlood brain barrier still more permeable to toxicologic
substances until around 4 months. No studies demonstrating increased permeability, rather this is
an estimate based on toxicity noted with smaller doses than expected.
Higher metabolic demands.
Decreased ability to glucuronidate in the infant period. Second trimester pregnancies that were terminated showed only 10% activity of the P-450 system. No better studies to date, but most believe between ages 2-4
years that glucuronidation is equivalent to adults.
Decreased glycogen stores.
Physiologic DifferencesIncreased body surface area can lead to
thermoregulatory issues.
Children reside lower to the ground. This puts them at higher risk for ingesting compounds heavier than air. Often adults will NOT have the same exposure.
Inability to avoid hazards – they do not read warning labels or “Do Not Enter” signs.
The Expanded “One Pill Kill”
The Deadly Pediatric PoisonsCalcium Channel
BlockersCyclic
AntidepressantsLomotilOpiates / Opioids
Salicylates (methyl)Toxic AlcoholsSulfonylureasCamphorClonidine and
imidazolinesAntimalarials
Calcium Channel BlockersThree major classes
PhenylalkylamineBenzothiazepineDihydropyridine
Block L-type channelsCause hypotension,
bradycardia, and arrythmias.
Immediate and sustained release.
Usually not the childs medication.
Calcium Channel BlockersManage A, B, C’sCheck Labs and
EKGFluidsCalciumGlucagonPressorsHigh Dose InsulinAtorpine and Pacing
Calcium Channel BlockersMay be able to wean
pressors with insulin.Insulin dosage is 1
unit / kg bolus and 0.5 units / kg / hour drip.
Monitor sugar Q20 minutes for the first few hours.
Most will NOT become hypoglycemic.
Cyclic AntidepressantsThey were the leading cause of poisoning
fatality until 1993.They interfere with reuptake of biogenic
amines and serotonin at the nerve terminal.Manifest toxicity by anticholinergic effects,
alpha-1 inhibition, sodium channel blockade, and can inhibit GABA.
Cause CNS and cardiovascular toxicity with arrythmias leading to mortality.
EKG Findings
EKG Findings
Cyclic Antidepressant ManagmentManage A, B, C’s aggressivelyOptimize electrolytesFollow serial EKG’s and use Bicarb if:
QRS >100 or 110 msecaVr > 3 mm
If bicarbonate and magnesium are not effective, lidocaine is the antidysrhythmic of choice.
Norepinephrine is the pressor of choice for refractory hypotension.
Is it the Sodium or the Bicarb?The answer is
BOTH!
Sodium overcomes the partial blockade from cyclic antidepressants.
Alkalinization does change binding properties.
How does the bicarb work?Initially thought to increase protein binding
thus limiting free drug in the bloodRat study using alpha-1 acid glycoprotein
(AAG) only decreased arrhythmias at massive doses. AAG is a proven TCA binder.
Current theories is that the ionic form of the TCA binds to the sodium channel causing blockade and the bicarbonate changes the TCA from the ionic form to the neutral form causing less blockade.
LomotilAntidiarrheal agent containing both
diphenoxylate and atropine.
Both agents are absorbed by the GI tract and absorption may be delayed in overdose due to inhibitory effects on smooth muscle motility.
Diphenoxylate is an opoid that is metabolized to difenoxin which is 5 times more potent than the parent compound and has half life of 12-14 hours.
LomotilPatients manifest
signs and symptoms of opiate toxicity.
Respond well to naloxone and supportive care.
Current recommendations are for a minimum of 24 hour observation.
Opiates / OpioidsTypically present with respiratory
depression, altered mental status, and miosis.
Address the patient like any other “altered mental status”
Key point is to remember to consider an opiate ingestion.
Naloxone DosingUsually start with 0.01-0.1 mg / Kg.
Repeat as frequently as needed to reverse symptoms.
If a drip is required, calculate how much naloxone was used in the first hour and start the drip at 2/3 that dose.
Sulfonylureas
Mechanism of ActionSulfonylureas keep
the potassium efflux channel closed.
This keeps the cell depolarized which allows the voltage-gated calcium channel to remain open.
This stimulates insulin release.
SulfonylureasSince sulfonylureas stimulate insulin
release, this can result in prolonged hypoglycemia.
Continued doses of dextrose will continue to stimulate insulin release.
Octreotide works by antagonizing insulin release. Exact mechanism is still being debated.
OctreotideThe dose is 1-2 mcg / Kg bolus IV or SC.
Some papers suggest a continuous infusion while others suggest an every 8 hour dosing regimen.
If placed on an octreotide regimen, the octreotide must be off a minimum of 24 hours without another episode of hypoglycemia before discharge.
Key FactsA retrospective study showed 4 of 25 patients
developed delayed hypoglycemia including 1 at 16 hours post ingestion.
If a sulfonylurea is ingested, a minimum of 24 hours of observation is recommended.
CamphorAromatic ketone
derived from plants.Acts as a topical
rubefacient.Usually ingested as
a liquid.Often in
preparations combined with other medicines such as salicylates.
CamphorInitial symptoms are gastrointestinal distress
and generalized feelings of warmth.Symptoms usually progress quickly to
nervous system involvement from restlessness to seizures.
Delayed seizures have been reported up to 9 hours after ingestion.
CamphorIngestions of 1-2 grams have been fatal in
children.A 19 month old died after ingesting 5 ml
of 20% camphorated oil.Asymptomatic patients should be
observed 6-8 hours and discharged if not developing symptoms.
Remember about hydrocarbon aspiration if product is an oil with a history of coughing or vomitting.
Clonidine and ImidazolinesClonidine is an alpha-2 agonist that is used
for hypertension.Imidazolines, such as oxymetazoline (afrin)
are used as decongestants.Symptoms typically present like an opiate
overdose ?
Why?
? Like an Opiate Overdose ?They are NOT structurally related to opiates.The alpha-2 receptor targeted by clonidine
has significant functional overlap with the opiate receptor. Both may be located on the same neuron, both coupled by via G-protein to the same potassium channel.
May require larger doses of naloxone to reverse symptoms.
AntimalarialsThese include cloroquine,
hydroxychloroquine, quinine and their relatives.
They work by both sodium channel blockade as well as blockade of the potassium rectifier channel.
These lead to QRS widening as well as QT prolongation.
Torsades is a known complication of overdose.
SymptomsSmall therapeutic index.Presents with symptomatology known as
“cinchonism” which is tachycardia, nausea, vomitting, hearing loss, tinnitus, headache, vertigo, dystonia, and diarrhea.
Patients often known to have a flushed appearance.
TreatmentThese patients require aggressive
management of electrolytes.If the QRS widens, treatment with sodium
bicarbonate is indicated.Magnesium should be used for Torsades.If ventricular arrythmias occur despite
optimal management, lidocaine is the treatment of choice. (Avoid class 1a, 1c)
Selected Toxic Dosages
• Epidemiology• Clinical features• Investigation• Treatment
Epidemiology Accidental – 33 to 60% in India &
other developing countries
Reasons for high incidence1. Extensive use for cooking & lighting in
low socioeconomic status2. Stored in soft drink bottles, beer bottles
within reach of children
Clinical featuresAge – 1 to 3 years more than 70% symptomatic within
10 hours
SYMPTOMS
RS – breathlessness, coughCNS – convulsions, coma GPE – fever, restlessness, cyanosisGI – vomiting, diarrhea
Lab InvestigationsBlood – Leukocytosis
X – Ray changes
Changes appear within one hour - commonly right basal infiltrates - emphysema - pleural effusion - pneumatocoeles
Severity scorePARAMETERSPARAMETERS ABSENTABSENT PRESENTPRESENT OTHERSOTHERS
FEVER FEVER 00 11 00
SEVERE SEVERE MALNUTRITIONMALNUTRITION
00 11 00
RESP. DISTRESSRESP. DISTRESS 00 22 44
CNS SYMPTOMS CNS SYMPTOMS 00 22 44
• >4 – Significant• <7 – Likely to survive• >8 –– Risk of death is increased
ManagementAvoid emeticsAvoid gastric lavage – In case of massive
amount use a cuffed endotracheal tubeAfter lavage leave magnesium or sodium
sulphate in the stomachOxygen may be usefulAssisted VentilationAntibiotics - Penicillin G 50000/Kg/24 hrs IV
qid Kanamycin – 10-15mg/Kg/24 hrs - IM bdSteroids – Not helpful
Complications• Pneumothorax• Pneumatocoeles• Pleural effusion• Bronchopneumonia• Coma
Pralidoxime (PAM) is given in dose of
25-50 mg/kg IM or IV over 30 min infusion. The dose may be repeated in 1-2 hours, then at 6-12 hour intervals as needed. Monitor for hypertension. Never inject morphine, theophylline, aminophylline or chlorpromazine. Intravenous fluids should only be given with caution. No oral tranquilizers are administered. Artificial respiration may be necessary to sustain life.
Hydrocarbon PoisoningThese may be divided into aliphatic or
aromatic compounds. Aliphatic hydrocarbons include kerosene, turpentine, lubricating oils, tar and have greatest risk of aspiration and pulmonary symptoms. Aromatic compounds have mainly neurological and hepatic toxicity and include benzene compounds.
Type of toxicity with a hydrocarbon
depends on its volatility, viscosity or surface tension. The lower is viscosity, more is the risk of pulmonary aspiration. Mineral spirit, kerosene and furniture polish have both low volatility and viscosity and thus carry a higher risk of aspiration pneumonia.
Benzene derivates, toluene and xylene
are components of various solvents and degreasers. These are highly volatile but have low viscosity. Inhalation is the primary route of toxicity which manifests with CNS symptoms. Gasoline and naphtha are constituents of lighter fuel and lacquer diluent and primarily cause depression of the central nervous system (CNS).
Turpentine oil is highly volatile but has low
viscosity also. Toxicity results from inhalation and gastrointestinal absorption. They can also cause CNS toxicity.
Halogenated hydrocarbons are used as solvents and spot removers. Freon is used as a refrigerant.
Toxic exposure to hydrocarbons may result in cardia, gastrointestinal, neurological, pulmonary, renal, hepatic, metabolic and hematological manifestations.
Induced emesis or gastric lavage is
contraindicated for kerosene oil poisoning. It is done only when large quantities of turpentine have been ingested or the hydrocarbons product contains benzene, toluene, halogenated hydrocarbons, heavy metals, pesticides or aniline dyes. Other specific modalities including steroids and antibiotics are not efficacious.
Carbon Monoxide PoisoningClinical manifestations include
headache, cyanosis, convulsions, and coma.
Patients are administered 100 percent oxygen and
if carboxyhemoglobin levels are above 40 percent, hyperbaric oxygen therapy is considered.
Lead PoisoningExposure to lead occurs from old lead
based deteriorated house paint (in old houses) and dust and soil contaminated with lead such as from leaded gasoline, lead electrode plates from old automobile batteries, adultered food, folk remedies, broken lead typesets scattered around old printing establishments. Food may be adulterated with colored metallic salts or the black collyrium used as surma may contain a proportion of black oxide of lead.
Lead Poisoning Chronic lead intoxication occurs
usually in children who eat non-edible substances (pica) and manifests as pain in abdomen and resistant anemia. Lead is deposited in the bones. Acute infections may mobilize lead from storage areas in bones and cause acute lead poisoning leading to acute lead encephalopathy.
In these cases the child may be left
with neurological sequelae. Lead inhibits sulfhydryl enzymes and formation of heme. Heme precursors such as porphyrins accumulate in the blood and are excreted in the urine. Screening for lead intoxication is done by measuring zinc protoporphyrin or blood lead levels.
TreatmentIn symptomatic children, therapy is
usually started with dimercapol (BAL) (75 mg/m2 every 4 hourly IM). BAL may be stopped after 48 hours, while calcium disodium edetate is used for another 3 days but at a lower dosage of 50 mg/kg or 1000 mg/M2 per 24 hours by continuous IV infusion.
Maximum daily dose should not
exceed 500 mg/kg. Stop BAL when blood lead level falls below 60 microgram/dL. Give a second course of edetate alone if blood lead rebounds to 45-69 microgram/dL. A second course of edetate in combination with BAL is recommended for rebound lead level of >70 microgram/dL. Wait for 5-7 days in between the two courses.