Pediatric Poisonings
Epidemiology
99% of ingestions by children under 6 are
unintentional.
Approximately 40% of ingestions reported
to the poison center by adolescents are
intentional.
Approximately 56% of adolescent
ingestions are by females.
Definiton
The poison means to injure or kill with a substance that in known or
discovered to be harmful .
The term poisoning cannotes clinical symptomatology, it also implies
that the toxic exposure is unintentional .
The term overdose implies intentional toxic exposure , either in the
form of a suicide attempt os as inadvertent harm secondary to
puposeful drug abuse .
The terms poisoning and drug overdose often are used
interchargeably , especially when prescription drugs are the agents ,
even though definiton a drug overdose does not produce poisoning
unless it causes clinical symtoms
The general approach to
poisoning
• 1.Stabilization
• 2. Laboratory assessment
• 3.Decontamination of the gastrointestinal
tract , skin , eyes
• 4.Administrate of an antidote
• 5.Elimination enhacement of the toxin
• 6.Observation and disposition
1.Stabilization
Resuscitation with establisment of the airway , adequate
support of ventilation .Particular attention should be
dirrected to abnormalities in the cervical spine and
temporomandibular joint
Continous cardiac and pulse oximetry monitoring
Maintenance of blood pressure and tissue perfusion
( may require the peovision of volume , correction of acid –base
disturbance , administration of pressor agents )
History
The following questions may be revealing
What other medicines are in the house?
What was the patient doung that day?
Have there been recent emotionally or traumatic events ?
Is the patient eating a special diet or taking a new health food ,
alternative medication or performance enhancer ?
Could the patient inadvertently have taken too much of prescribed
medication ?
If it can be identified , is the substance non toxic?
Physical examination
Body temperature – hypotermia( exposure to cold , hypoglicemia ,
barbiturates , ethanol ,overdose ) , hypertemia(LDS , cocaine ,
slicylates poisoning)
Bradycardia – overdose of digitalis ,beta blokers , calcium channel
blokers but also it may be seen iwith hypotermia and spinal cord
injury
Hypertension – intoxication with cocaine ,amphetamines ,
sympathomimetics
Lungs – inhalation of toxic gase s may produce wheezing
- tricyclic antidepressant overdose – pulmonary edema
- pneumothorax in patients who smoke cocaine ,
methamphetamina
Pupils – pinpoint pupils – overdose clonidine , opiates ,
organophosphate insecticids
Level of consciousness
2.Laboratory assessment
Complet blood count
Determination of serum electrolytes , glucose , BUN , creatinine and
calcium , urinalysis ,prothrombin time , hepatic enzymes
Pulse oxymetry , 12 lead electrocardiography
Arterial blood gases
The measurement of serum salicylate and acetaminofen levels is
generally added in the case of the patient with overdose of un
unknown substance , because these agents are often co- ingestants
or are contained in combination drugs
Performing a urine pregnancy test in teenager girls is wise
Urinary drug screening
Chest radiography – aspiration pneumonia , pulmonary edema ,
Ct scan – if underlying trauma is suspected
Lumbar punction – for ruling out meningitis in a patient with fever
and coma
3.Decontamination of the gastrointestinal
tract , skin , eyes
The range of dermal toxins is broad
Most of these substances are corrosive agents capable of producing
burns that may become full thickness( i.e third degree)
Other types of agents are irritants , sensitizers , allergens , vesicants
and exfoliants
The skin of infants is notable for beeing more permeable than that of
adults to substances of all classes
If the victim is immersed in atoxic fluid , the first step is his or her
extrication , the victim should be disrobe , wash with water
Emmergency medical personel should provide themselves every
level available of self- protection
3.Decontamination of the gastrointestinal
tract , skin , eyes
Initial management of all chemical ocular injuries requires
immediate decontamination by irrigation
Early application of a topical anesthetic is recomandated to facilitate
irrigation and anhance the patient comfort
The most commonly available solution include sterile water , normal
saline an lactated Ringer
The upper and the lower eyelids should be retracted ,inspected for
retained solid material and injury and irrigated
Immediate refferal to an ophthalmologist is necessary for all
significant burns
3.Decontamination of the gastrointestinal
tract , skin , eyes
Gastric lavage –involves blind placement of a large – bore gastric
tube into the stomach , in a patient who can either protect his or her
airway or in whom the airway has been protected by an
endotracheal tube , with the goal of removing toxicant remaining in
the stomach through a combination of instillation of water or
physiological saline , followed by suction or gravity induced drainage
The cycle of instillation/drainage is repeated until the effluent in clear
or until several liters of water /saline have been passed through the
tube. Left recumbent Trendelenburg’s position to reduce the risk of
aspiration
Indications – recent ingestion( less than 1 hr , unless the ingestion
involves agents that decrease gastric motility such as
anticholinergics)
Contraindications – low –viscosity petroleum products , corrosive and
inability to protect the aiway
Adverse effects – hypoxia , perforation of the gastrointestinal tract or
pharynx, aspiration pneumonitis , electrolyte abnormalities
3.Decontamination of the gastrointestinal
tract , skin , eyes
Activated charcoal – binds to diverse substances , rendering them
less available for systemic. absorbtion from the gastrointestinal tract
Single Dose – 1 g/kg in children max dose 50 g , 25-100 g in adults ,
administred orally( in water ) or via nasogastric tube .
Indication –, fenitoin, glutetimid , acetaminofen , benzodiazepine
poisoning
Contraindications – ingestion of caustics , in case of risk for
gastrointestinal hemorrhage or perforation , in any patient in whom
the airway protection is not assured , in case of ileus or mechanical
bowel obstruction
Adverse reactions and complications – vomiting , duarrhea and
constipation , pulmonary aspiration , direct administration into the
lungs via misplaced nasogastric tube
3.Decontamination of the gastrointestinal
tract , skin , eyes
Multiple dose activated charcoal – used in the case of drugs that
undergo extensive enterohepatic or enteroenteric circulation
Indication
, theophyline
– carbamazepine , dapsone , phenobarbital , quinine
Contraindications – same as for single dose
- the presence of decreased peristalsis should
provoke caution
Cathartics – magnesium salts and nondigestible sorbitol . May
induce significant harm in children with renal disease .Manitol 20% dose 4-5 ml/kg , Sorbitol 70% 1-2 ml /kg .
Complications – nausea , vomiting , hypermagnesiemia and cardiac
dysrhythmias , dehydratation .
3.Decontamination of the gastrointestinal
tract , skin , eyes
Whole bowel irrigation –involves administration , by mouth or
nasogastric tube , of large amounts of an iso- osmotic polyethylene
glycol electrolite solution with the goal of removing unabsorbrd
toxicant from the gastrointestinal tract as rapidly as possible by
rectal expulsion .Dose 25 ml /kg/hr for 4 -6 hr .Total dose 500 ml
/hr under the age of 6 yrs , 1000ml /hr under the age of 10 yrs ,
1500-2000 ml /hr in adolescents
Indications – iron ,lithium , drug packets
Contraindications – mechanical or functional obstruction ,
gastrointestinal haemorrhage
3.Decontamination of the gastrointestinal
tract , skin , eyes
Whole bowel irrigation –involves administration , by mouth or
nasogastric tube , of large amounts of an iso- osmotic polyethylene
glycol electrolite solution with the goal of removing unabsorbrd
toxicant from the gastrointestinal tract as rapidly as possible by
rectal expulsion .Dose 25 ml /kg/hr for 4 -6 hr .Total dose 500 ml
/hr under the age of 6 yrs , 1000ml /hr under the age of 10 yrs ,
1500-2000 ml /hr in adolescents
Indications – iron ,lithium , drug packets
Contraindications – mechanical or functional obstruction ,
gastrointestinal haemorrhage
4.Administrate of an antidote
Only a small proportion of poisoned
patients are amenable to antidotal therapy
Only a few poisoning is antidotal therapy
urgent (e.g., CO, cyanide,
organophosphate and opioid intoxication)
Specific Intoxications and Their
Antidotes
Poison
Antidote
Indications
Acetaminophen
N-Acetylcysteine
(Mucomyst)
Serum level in “probable”
hepatotoxic range
Anticholenergics
Physostigmine
SVT with hemodynamic
compromise
Beta blockers
Bradycardia
Bradycardia
Benzodiazepines
Glucagon
Isopreterenol,
dopamine,
epinephrine
Flumazenil
Carbon monoxide
O2
Level > 5-10%
Cyanide
Amyl nitrite,
sodium nitrite,
sodium thiosulfate
Symptomatic intoxication
Digitalis
Specific Fab
antibodies
Symptomatic intoxication
Specific Intoxications and Their
Antidotes
Poison
Antidote
Indications
Ethylene glycol
Ethanol
Osmolar gap and metabolic ac
Serum level >20 mg/dl regardle
symptomatology
Iron salts
Desferoxamine
Symptomatic patients
Serum iron > 350 g/ml or > TI
Positive deferoxamine challeng
Isoniazid
Pyridoxine
(vit B6)
Methanol
Ethanol
Metabolic acidosis and elevate
osmolar gap regardless of sym
Methemoglobinemi
a producing agents
Methylene blue
Symptomatic poisoning
Methemoglobin level > 30-40 %
Narcotics
Naloxane
Symptomatic intoxication
Organophosphate
insecticides
Atropine
Pralidoxime
Cholenergic crisis
Fasciculation and weakness
Phenothiazines
Diphenhydramine
Symptomatic intoxication (ocul
crisis)
5.Elimination enhacement of the toxin
Forced diuresis by administering 2-3 times the maintenance
fluid to achieve U.O = 2-5 cc/kg/hr
(contraindicated in
pulmonary or cerebral edema and renal failure)
Urinary alkalinization to eleiminate weak acids(salicylates,
barbiturates and methotrexate), can be achieved by adding
NaHCO3 to the IV fluids, the goal is urine pH of 7-8
Serum alkalinization in triciclic antidepresant toxicity
Hemodialysis in low molecular weight substances with low
volume of distribution and low binding to plasma proteins
(barbiturate , methanol, ettilenglicol , heavy metals , lithium)
Hemoperfusion, protein binding is not a limitation
Special Pediatric Issues
ALL THINGS
TEND TO END
UP IN THE
MOUTHS OF
YOUNG
CHILDREN!!
Which is Candy?
Sweet Tarts vs. Ecstacy
Physiologic Differences
Blood 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 Differences
Increased 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.
Acquired methemoglobinemia
- is caused by an external source, usually a drug or medication.
Methemoglobin is an aberrant form of hemoglobin arising from oxidation of iron in
the normal heme molecule from the ferrous form (Fe2+) to the ferric (Fe3+) form.
The presence of ferric heme molecules causes a structural change in the hemoglobin
molecule, resulting in reduced oxygen-carrying capacity and impaired unloading of
oxygen at the tissue.
This left shift in the oxygen saturation curve results in functional anemia.
Typically, red blood cells maintain a steady-state methemoglobin level of less than 1%
via 2 main enzymatic pathways.
Elevation in methemoglobin levels can be caused by congenital enzyme deficiencies
or exposure to exogenous oxidizing agents that disrupt the equilibrium established by
these pathways.
Causes – Nitrates fountain water in the first year of life , Sulfamides , EMLA
cream(lidocaine and prolocain),Nitric oxid ,Metoclopramid , Anilin diapers
With a methemoglobin level of 3-15% skin can turn to a pale gray or blue
(cyanosis). With levels above 25% the following symptoms may be present:
Cyanosis unaffected by oxygen administration
Blood that is dark or chocolate in color that will not change to red in the presence of
oxygen
Headache
Weakness
Confusion
Chest pain
When methemoglobin levels are above 70% death may result if not treated
immediately.
Blood from the heel sticks is chocolate-brown and does not become pink when
exposed to room air.
Management
1. Laboratory data – methemoglobin > 2% in new borne ,>1,5% in premature new
borne
Chemistry – serum electrolytes , liver enzyme , BUN , complete blood count ( CBC)
Management
2. Vital signs – cardiac and respiratory stabilisation, seizures treatment , O2
3.Decontamination – wash skin , gastric lavage( in case of ingestion)
4.For acquired methemoglobinemia the typical treatment is with methylene blue.
This is administered with an IV over a five-minute period and results are typically
seen within 20 minutes. Methylene blue reduces methemoglobin back to
hemoglobin. Dose 1 mg/kg , (concentration 1%) , max dose 7 mg/kg
If symptoms persist after 1 hour, repeat doses are given with caution, as
accumulation of the drug can result in increased production of methemoglobin .
5 .Ascorbic acid 30 mg/kg iv
6.If symptoms persist despite the above-outlined therapy, hemodialysis might be
required( metHb> 60% , hemolysis , sulfmethehemoglobinemia
Benzodiazepine Toxicity
Depending on the drug preparation and the presence of co -ingestants , the
time from ingestion to appearance of the drug in the systemic circulation is 10-20
min .
After absorbtion , benzodiazepines are higly protein bound , ranging from 70%99%.
Protein binding is greatest with highly – soluble drugs(diazepam 99% bound)
and least with more water soluble agents( alprazolam 70% bound) .
Only unbound drug is available to cross the blood- brain barrier and interact with
CNS receptors .
Benzodiazepines are metabolized predominantly in the liver by oxidation
and/or conjugation.
Elimination of benzodiazepine metabolites usually occurs via renal clearance
Respiratory failure – frequent -Triazolam ,Flunitrazepam ,
Physical Examination
Paradoxical agitation
Slurred speech
Altered mental status, impairment of cognition
Confusion
Drowsiness
Coma (Classic-isolated benzodiazepine overdose presents as coma with normal vital signs).
Respiratory depression
Hypotonia
Diagnosis
Qualitative urine screening for the presence of benzodiazepnes or their metabolites provide
rapid useful information in evaluation of patients with un unknouwn cause of CNS depression.
A negative screening result does not rule out the presence of a benzodiazepine.
Qualitative screening of urine or blood may be performed but rarely influences treatment.
Quantitative plasma measurements are not available in most hospitals and provide no
significant therapeutic direction to the trating pshysician.
Plasma concentration of benzodiazepines correlate very poorly with the severityof toxic
effects( CNS depression) or mortality.
Treatment
Single-dose activated charcoal is not routinely recommended as the risks far
outweigh the benefit( fast absorbtion).
Activated charcoal - single dose 1 g/kg
Hypotension - use Dopamine
Coma and respiratory depression - Flumazenil 0,1 mg /kg in 30 sec , if the patient
is still in coma after 30 sec a second dose will be use.
In long-term benzodiazepine users, Flumazenil may precipitate withdrawal and
seizures; in patients taking benzodiazepines for a medical condition, flumanazenil
may result in exacerbation of the condition.
Respiratory support may be necessary
Barbiturate toxicity
Long action > 48 hr ( fenobarbital , mefobarbital)
Medium action (amobarbital)
Short action 3-4 hr(ciclobarbital,secobarbital)
VeryShort < 30 min (thiopental)
Physical Examination
Barbiturates mainly act in the CNS, though they may indirectly affect other organ
systems. Direct effects include sedation and hypnosis at lower dosages
1. The CNS depressant effect mimics that of ethanol(ataxia ,slurred speech
lethargy ,coma)
2. Coma - decreased pupillary light reflex ,decreased deep tendon reflexes ,
myosis in severe cases.
3. Respiratory exam -acute respiratory distress syndrome ,apnea,hypoxia
4. Cardiovascular exam –hypotension,tachycardia,bradycardia,diaphoresis,shock
5. Renal dysfunction due to acute tubular necrosis( muscle necrosis and
calcification may be associated with acute renal failure)
Physical Examination
6. Coma blisters are lesions that occur in the setting of a variety of neurological
diseases. Although most commonly associated with barbiturate overdose, they can be
seen in the setting of coma due to other etiologies. Blisters develop 48–72 h after the
onset of unconsciousness.They typically appear as blanchable erythematous pathches
at pressure points of the skin .
A biopsy of the lesion shows epidermal or subepidermal blisters with characteristic
necrosis of the sweat glands .Over the next 2-3 days these patches become blisters or
erosions , but they usually heal spontaneously over 1-2 weeks
Management
Attention to the airway and hypoxia
Vital signs( risk of cardiovascular compromise and hypotermia)
Ruling out hypoglicemia ( missing diagnosis can have grave
consequences)
Activated charcoal – 1 g/kg , for patients who have a compromised
airway , endotracheal intubation is advised prior to giving charcoal
Laboratory evaluation – basic electolites and glucose . Serum
barbiturate levels can be useful in gauging the clinical course of
therapy , screenin assays employing semiquantitative
immunoassays of serum and urine are readly avilable . BUN ,
hepatic enzymes may have increased values .
ECG ,EEG
Management
Urine alkalinization is of theoretical value in the treatment of
phenobarbital overdose but not overdose of other barbiturates
According of the theory of ion trapping , phenobarbital , as a weak
acid , will be poorly reabsorbed by the renal tubules if it can be
ionized in the milieu of an alkaline urine (NaHCO3 1-2 mEq/kg until
urinay Ph 7,5- 8 )
Such alkalinization is rarely achieved in clinical practce without the
unwanted effects of metabolic alkalosis or hypernatremia .
Multiple dose activated charcoal has been shown to be more
effective in decreasing phenobarbital half life in adults and neonates
.
Extracorporeal removal by hemodialysis or hemoperfusion is also
effective in removing the barbiturates , although they are reserved
for the most severe cases
Pesticides
Specifically
organophosphates and
carbamates.
They work by inhibiting
acetylcholinesterase.
Present with
cholinergic symptoms
Cholinergic Symptoms
Cholinesterase - 2 forms
1 . RBC form - true cholinesterase
2. plasma form - pseudocholinesterase.
Cholinesterases →hydrolyze the neurotransmitter
acetylcholine into inactive fragments.
Organophosphates form an initially reversible bond with the
enzyme cholinesterase.
The organophosphate-cholinesterase bond can
spontaneously degrade, reactivating the enzyme, or can
undergo a process called aging( the first 72 hours
,Oxime treatment can be used)
The process of aging results in irreversible enzyme
inactivation
Inactivation of the enzyme
→acetylcholine will accumulate at the
synapse, leading to overstimulation and
disruption of nerve impulses.
▼
Nicotinic stimulation at the motor
endplate(Skeletal-muscle depolarization
and fasciculations )
Muscarinic effects occur at the
postganglionic parasympathetic
synapses, causing smooth-muscle
contractions in various organs
Muscarinic Symptoms
Sweating
Miosis
Lacrimation and salivation
Bronchorrhea
Bradycardia
Emesis, diarrhea, Abdominal cramping
and intestinal hypermotility
Urinary incontinence
Nicotinic Symptoms
Remember the days of the week !
Mydriasis
Tachypnea
Weakness
Tachycardia
Fasiculations
Pediatric patients tend to present with a
predominance of nicotinic symptoms!!!
Central nervous system
Anxiety
Seizures
Central respiratory paralysis
Altered level of consciousness and/or
hypotonia
Weakness from Pesticides
Intermediate Syndrome- IMS
-proximal muscle weakness , weak neck flexors
,respiratory failure
-onset 24- 72 h after acute cholinergic crisis , can last
several days or weeks
Delayed polyneuropathy
-symmetric demyelinisation process
- patient notice the onset of weakness and paresthesias
about 3-6 month after initial ilness
- no known treatment , resolution over 6 month to 1 year
Laboratory test
CBC count to rule out infectious causes.
Chemistry tests may be useful in ruling out
electrolyte disturbances, renal and liver
test
RBC cholinesterase tests may reveal
decreased activity, which confirms the
diagnosis.
Chest x ray , ECG
Treatment
Decontamination involves removing all of the patient's
clothing and washing him or her with water and soap.
Ensure airway support and ventilation
Circulatory support with intravenous (IV) access, fluids,
and cardiac and pulse oximetry monitoring
Gastric decontamination with activated charcoal should
be performed in cases of ingestion.
Treatment
Atropine 0.02 mg / Kg IV. Repeat as needed
and titrate to respiratory secretions. It will
likely take massive doses!!(every 3-5 min)
Toxogonin (for Romania) – 4-8 mg/kg iv in 30
min , will adm again after 4-6 h
Pralidoxime (2-Pam) 20-40 mg / Kg bolus
followed by 10-20 mg / Kg /hour infusion.
Fresh frozen plasma 10 ml/kg
Remember to send RBC and Plasma
Cholinesterase levels upon arrival and daily.
Corrosive injury
Clinical Presentation
1.Hyperacute phase - ( first minutes – 1 h ) - retrosternal pain , dysphagia
, hematemesis , salivation , dysphagia ,agitation, septic shock.
Oropharyngeal examination ( specialist physician) – hiperemia , edema ,
burns , false membranes
2.Acute phase – next 3 weeks , clinical signs of postcaustic esophagitis
and complications (hematemesis , melenic stool , caustic laringitis
secondary to glotic edema, respiratory distress , coughing , bronhospasm
, asphyxia, esophageal or gastric perforation , abdominal pain ).
The test of choice for proper stageing of esophageal burn severity is
upper gastrointestinal endoscopy .
3. Subacute phase – 3- 6 weeks .General state will improve , patient
without fever , without dysphagia .
Systemic infections and aclorhidria can develop .Esophageal strictures (
corrosive alkalis) and piloric stenosis( corrosive acids) shall constitute in
this phase .
4.Chronic phase – after 6 weeks , dysphagia for solid food and
hipersalivation , dehydration , malnutrition. Treatment for esophageal
strictures -repetead bougienage can be started in this phase +/gastrostomy .
Hospital management
-Intensive Care Unit
-Otolaringologic exam
-General status , shock signs( arterial hypotension)
-Chemistry – Complete blood count (CBC), electrolyte levels, BUN levels,
creatinine level, and ABG levels may all be helpful as baseline values and as
indications of systemic toxicity.
- Chest radiograph - pneumomediastinum , mediastinitis, pleural effusions,
pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign
body).
The absence of findings does not preclude perforation or other significant injury.
- Endoscopy – in the first 24 h but not in the first 4 h after ingestion
Carbon Monoxide (CO)
An odorless, colorless, tasteless gas
Results from incomplete combustion of carboncontaining fuels
Gasoline, wood, coal, natural gas,
propane, oil, and methane
Affects 40 – 50,000 Americans annually who need to
seek care
Kills an additional 6,000 persons annually in the USA
CO is the #1 cause of poisoning in industrialized
countries
What Effect Does Carbon Monoxide Have
on Hemoglobin?
Hemoglobin molecules each contain
four oxygen binding sites
Carbon monoxide binds to hemoglobin
This binding reduces the ability of blood
to carry oxygen to organs
Hemoglobin occupied by CO is called
carboxyhemoglobin
Body systems most affected are the
cardiovascular and central nervous
systems
Effects of Carbon Monoxide
Oxygen cannot be transported because the CO binds
more readily to hemoglobin (Hgb) displacing oxygen
and forming carboxyhemoglobin
Premature release of O2 prior to reaching distal tissue
leads to hypoxia at the cellular level
Inflammatory response is initiated due to poor and
inadequate tissue perfusion
Myocardial depression from CO exposure
Dysrhythmias, myocardial ischemia, MI
Vasodilation – from increased release of nitric oxide;
worsening tissue perfusion and leading to syncope
Half-life of Carbon Monoxide
Half-life – time required for half the
quantity of a drug or other substance to be
metabolized or eliminated
CO half-life on 21% room air O2 – 4 - 6
hours
CO half-life on 100% O2 – 80 minutes
CO half-life with hyperbaric O2 – 22
minutes
CO Poisoning
Symptoms are often vague, subtle, and non-specific;
can easily be confused with other medical
conditions;
Flu – nausea, headaches
Food poisoning - nausea
Cardiac and respiratory conditions –
shortness of breath, nausea, dizziness,
lightheadedness
CO enters the body via the respiratory system
Poisoning by small amounts over longer periods of
time or larger amounts over shorter time periods
Assessment for CO Exposure
EMS may be summoned to monitor the air quality for the
presence of carbon monoxide
 Airborne CO meters are used and documentation
made whether there is a patient transport or not
A more immediate concern is the level of CO in the
patient’s blood
 RAD 57 monitors are a non-invasive tool that allows
results in less than 30 seconds
 Rapid diagnosis leads to rapid and appropriate
treatment
Assessment for CO Exposure
EMS may be summoned to monitor the air quality for the
presence of carbon monoxide
 Airborne CO meters are used and documentation
made whether there is a patient transport or not
A more immediate concern is the level of CO in the
patient’s blood
 RAD 57 monitors are a non-invasive tool that allows
results in less than 30 seconds
 Rapid diagnosis leads to rapid and appropriate
treatment
RAD 57 Device
Used like a pulse ox
Non-invasive tool
Readings within
seconds
Helps to quickly hone
in a diagnosis
Used in ED and in the
field
Guidelines
SpCO level readings
SpCO levels <5%
Normal in non-smokers; no treatment
SpCO levels >5%
5-10% normal in smokers
In non-smokers, treat with 100% O2
EMS should be transported for further
evaluation
Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of <15 – 20%
Mild severity
Headache – mild to moderate
Shortness of breath
Nausea and vomiting
Dizziness
Blurred vision
Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of 41 - 59%
Severe
Dysrhythmias, palpitations
Hypotension
Cardiac ischemia
Confusion
Respiratory arrest
Pulmonary edema
Seizures
Coma
Cardiac arrest
Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of >60%
Fatal
Death
Cherry red skin is not listed as a sign
An unreliable finding
Remember that SpO2 may be falsely
normal
Pulse Oximetry
Device to analyze infrared signals
Measures the percentage of oxygenated
hemoglobin (saturated Hgb)
Can mistake carboxyhemoglobin for
oxyhemoglobin and give a false normal
level of oxyhemoglobin
Never rely just on the pulse oximetry
reading; always correlate with clinical
assessment
Pulse CO-oximeter Device
Hand-held device
Attaches to a finger tip similar to pulse ox device
Most commonly measured gases in commercial
devices include
Carbon monoxide (SpCO)
Oxygen (SpO2)
Methemoglobin (SpMet)
Other combustible gases
Without the device, need to draw a venous sample of
blood to test for CO levels
Treatment CO Poisoning
Increasing the concentration of inhaled oxygen can
help minimize the binding of CO to hemoglobin
Some CO may be displaced from hemoglobin when the
patient increases their inhaled oxygen concentrations
Treatment begins with high index of suspicion and
removal to a safer environment
Immediately begin 100% O2 delivery , hyperbaric
chamber
Treatment CO Poisoning
Guidelines from different sources may vary when to
initiate treatment based on SpCO levels
Treatment levels vary significantly
 If you do not have a CO-oximeter to use, maintain a heightened
level of suspicion and base treatment on symptoms
Monitor for complications
 Seizures(diazepam)
 Cardiac dysrhythmias
 Cardiac ischemia
Long Term Effects CO Exposure
Hypoxemia follows CO exposure
Effects of hypoxemia from CO exposure is
dependent on presence of underlying
diseases
Hypoxemia can cause the formation of
free radicals – dangerous chemicals
Long Term Cardiovascular
Effects
Myocardial injury from hypoxia and cellular damage
Pump failure
Cardiac ischemia
Later development cardiovascular
complications
Premature death especially if myocardial
damage at the time of initial exposure
Factors increasing myocardial injury risk
Male gender
History hypertension
GCS <14 when patient first found
Long Term Neurological Effects
Effects are primarily affective (mood) and cognitive
(thought)
 Increased depression and anxiety regardless if
exposure accidental or suicidal attempt
 Phenomenon called delayed neurological syndrome
(1 - 47% of cases)
More likely if there was a loss of consciousness
Behavioral and neurological deterioration
Memory loss, confusion, ataxia, seizures, urinary
& fecal incontinence, emotional lability,
disorientation, hallucinations, mutism, cortical
blindness, psychosis, gait disturbances,
Parkinsonism
Mushroom poisoning
Poisonous mushrooms contain compounds
that are toxic to humans and animals
Mode of action well known yet generally
there are few antidotes available
7 major toxin groups are recognized as
poisonous and an 8th toxin group of mainly
gastrointestinal irritants
Toxins organized into 4 major categories
based on physiological action
Mushroom poisoning
- 2 major categories on the basis of the time from
ingestion to the development of symptoms
1. Early symptom category –
Symptoms generally appear within the first 30 min – 3 hours of mushroom ingestion
. Favorable prognosis
2 . Late symptom category – Signs and symptoms begin to appear between 6 and
24 hours after ingestion and may include hepatotoxic, nephrotoxic syndromes
1.Early symptom category - clinical exam
Muscarinic syndrome - increased salivation, perspiration, lacrimation ,abdominal
pain, severe nausea, diarrhea, blurred vision, and labored breathing within 15-30
minutes of mushroom ingestion.
Death is rare but may result from cardiac or respiratory failure in severe cases.
Coprine poisoning - 0.5-2 hours after ingesting ethanol include headache, nausea,
vomiting, flushing, chest pain, and diaphoresis (as is typical of the disulfiram
syndrome) and may last for 2-3 hours.
Coprine-containing mushrooms generates a metabolite that inhibits acetaldehyde
dehydrogenase.
Ibotenic acid and muscimol poisoning ( Amanita pantherina) – 30 min after ingestion
delirium , halucination and coma
Mushroom poisoning
- 2 major categories on the basis of the time from
ingestion to the development of symptoms
A . Early symptom category –
Symptoms generally appear within the first 30 min – 3 hours of mushroom ingestion
. Favorable prognosis
B. Late symptom category – Signs and symptoms begin to appear between 6 and
24 hours after ingestion and may include hepatotoxic, nephrotoxic syndromes
A .Early symptom category - clinical exam
Muscarinic syndrome - increased salivation, perspiration, lacrimation ,abdominal
pain, severe nausea, diarrhea, blurred vision, and labored breathing within 15-30
minutes of mushroom ingestion.
Death is rare but may result from cardiac or respiratory failure in severe cases.
Coprine poisoning - 0.5-2 hours after ingesting ethanol include headache, nausea,
vomiting, flushing, chest pain, and diaphoresis (as is typical of the disulfiram
syndrome) and may last for 2-3 hours.
Coprine-containing mushrooms generates a metabolite that inhibits acetaldehyde
dehydrogenase.
Ibotenic acid and muscimol poisoning ( Amanita pantherina) – 30 min after ingestion
delirium , halucination and coma
B . Late symptom category
Severe intoxications , requiring Intensive care therapy .
Amanita phalloides poisoning
- Amatoxins are extremely potent hepatotoxins, are actively absorbed from the
gastriontestinal tract .
Once absorbed through the gut , amatoxins are transported into hepatocytes by
non specific transport system .Circulating amatoxin is not metabolized but
excreted by the biliary system and the kidney.
Enterohepatic recirculation and biliary excretion of amatoxins are significants .
They are not denatured by boiling ,and hence cooking deadly Amanita mushroom
does not render them nontoxic .
Clinical presentation – 3 stages
Stage 1 - 6- 24 h , after ingestion ,
- nausea , vomiting , cholera- like diarrhea , metabolic acidosis , anuria ,
hematuria.
Stage 2 – 12-48 hr after ingestion – apparent recovery , levels of hepatic enzyme
rise during this stage
Stage 3 – 24-72 hr after ingestion , progresive hepatic and renal failure ,
coagulopathy, cardiomiopathy , encephalopathy , convulsions , coma , death
Clinical forms
a.Benign forms – without hepatic failure , complete cure in 10- 15 days .
The patients will have gastroenteric syndrome ( 2- 5 days) , jaundice ,
hepathomegaly ( 3- 5 days).
b.Severe forms – protrombinic activity 80-50% , cure in 3- 5 weeks .
The patient will have gastroenteritic syndrome 3- 7days , astenia(2-3 weks) , high
levels of hepatic enzymes( 1000-2000ui/l) , jaundice , hepatomegaly +/- digestive
haemorrhage
c.Severe forms - hepatic enzymes rise 24-36 hr after ingestion , protrombinic
activity< 50% , without encephalopathy ( cure in 4- 8 weeks) or death beetween
days 7 -12 .
The patient will have severe gastroenteritis , rising hepatic enzymes and toxic
hepatitis .
Toxic hepatitis
Definition - citolitic hepatitis with onset in the first 24-36 hr .
Severe evolution in days 4 and 5 , significant augmentation of hepatic enzymes in
days 3- 5 .
1.Severe hepatic failure – decreased values of factor V < 50 % , without
encephalopathy and jaundice
2.
Extremely hepatic failure - decreased values of factor V < 50 % , with
encephalopathy and jaundice .
Renal failure is caused by hypovolemia in the first days , amatoxins will induce
tubular necrosis from the day 5 .
Biological test - rise of hepatic enzymes after 36 hr .Protrombinic activity will be
decreased after 48 hr +/- Disseminated Intravascular Coagulation .
Protrombinic activity < 3% and liver enzyme > 9000ui/l involve a severe prognosis
.
Evolution – death in the days7-12 or cure in 2- 4 weeks .Liver cirrhosis is possible
.
Treatment of Amatoxin Poisoning
A . Admission in the first 6 hr
Supportive care - pump stomach, restore fluid
balance
Activated charcoal to absorb toxins in
stomach – every 4-6 hr
Rehydration
Other treatments
Other Treatments
Several drugs are thought to reduce
uptake of amatoxins into liver cells based



High dose penicillin G (incredibly high levels) one million units/kg ( max 20 mil ui)
Silibinin (water soluble extract of milk thistle) –
25mg/kg /day ,every 6 hr
Cimetidin and N Acetyl cystein
Treatment of Amatoxin Poisoning
B . Admission after 6 hr
Bad prognosis – hepatic and renal failure , dehydration
, encephalopathy
Treatment
1. Hydration
2.Activated charcoal to absorb toxins in stomach – every
4-6 hr
3.Antitoxinic treatment
4.Plasmapheresis - separate blood, remove plasma,
replace with fresh plasma,
5.Liver transplant
4.Increased intracranial pressure – Manitol 0,25-0,5g/kg
Psychoactive drugs
Legal highs are novel psychoactive substances wich are either synthetic
chemicals , plant or fungal material wich are intended to elicit a psyhoactive
response , being either stimulant , hallucinogenic , sedative or a
combination of the three phenomena .
Europe has seen an explosion in the number of new compounds (from
2008 ), that are appearing on the internet wich display high and close
structural similarity with existing and controlled drugs of abuse , but wich
are marketed as not for human consumption or even as plant food , bath
salts , pond clear.
Synthetic compounds are – cathinones , cannabinoides , amphetamines ,
piperazine ( cigarettes , pills , ) -Spice gold , Spice Diamond
Classification
1.Spice products - plants used asn a sunstitute for cannabis( for smokers)
2.Plant food - hallucinogenic or aphrodisiac plants (Scutellaria galericulata –
skullcap) , cannabinol
3.Bath salts – mephedrone , effects cocaine like( nasal bleeding , nasal burns ,
halucinations, circulation problems , seizures , death)
4.Hallucinogenic plants – mushroom (Amanita pantherina , Psilocybe) ,
piperazine derivates , cactus seeds
5.LSD - Ipomoes violacea and Agryreia nervosa seeds ,
6. Kratom ( Mitragina Speciosa) – effects cocaine like ,contain piperazine ,induce
addiction
Agryeia nervosa
Mitragina Speciosa
Clinical presentation
Increased sweating , hyperesthesia , anxiety , paranoia , depression ,
addiction
Cardiac involvement in plants alkaloid like
Risk of death secondary to cardiac or neurological disturbances
Treatment
There is no antidotal therapy
Vital sign monitoring