Common Poisonings

and Overdoses

Dr Ram Narayan
MD, FNB
Pesticides
 Specifically
organophosphates and
carbamates.

 They work by inhibiting

acetylcholinesterase.
So…

 Present with cholinergic

symptoms
Some of them used Medically
Neostigmine
Pyridostigmine
Edrophonium
Tacrine
Donepezil
Two Groups of Cholinergic Insecticides-
Carbamates-Aldicarb and Methomyl
Organophosphates-
Chlorpyriphos,Dursban, Diazinin,
Malathion and Parathion.
Organophosphorus (insecticides and
pesticides) Poisoning

 Cause irreversible inhibition of the enzyme

cholinesterase.
 Acetylcholine accumulates in various tissues.
 Excessive parasympathetic activity occurs.
 These agents are absorbed by all routes including
skin and mucosa.
Cholinergic Symptoms
 Clinical syndromes
 Symptoms of acute intoxication manifest quickly
usually within Minutes to few hours

 Evidence of cholinergic excess

 SLUDGE-BBB-> Salivation, Lacrimation, Urination,

Defecation, rapid Gastric Emptying

 Bradycardia, Bronchorrhea, Bronchospasm

 Respiratory insufficiency can result from muscle

weakness, decreased central drive, increased
secretions, and bronchospasm
Nicotinic Symptoms
 Think the days of the week !
 M ydriasis
 T achypnea
 W eakness
 T achycardia
 F asiculations
 W eekend: “Wee” ones : Pediatric patients tend to
present with a predominance of nicotinic symptoms!!!
 Intermediate syndrome
Fresh worsening after initial recovery.

Occurs 24-96 hours after exposure

Bulbar, respiratory, and proximal muscle

weakness are prominent features

Generally resolves in 1-3 weeks

Often need invasive ventilation and

hemodynamics monitoring and stabilization.
 OrganoPhosphorous-Induced Delayed
Peripheral Neuropathy (OPIDN)

Usually occurs several weeks after

exposure

Primarily motor involvement

May resolve spontaneously, but can

result in permanent neurologic
dysfunction
Management
Supportive Care
Decontamination
Atropine IV for Respiratory Manifestations
Pralidoxime for Neuromuscular
Manifestations.
 Management
 If the insecticide was in contact with skin or eyes, Wash
thoroughly. Bag/discard clothing.

 Deliver 100 percent oxygen via facemask; early intubation often

required; avoid succinylcholine

 Decontamination if ingestion within 1 hour give single dose

activated charcoal, adult 50 g (1 g/kg in children) unless airway
not protected or other contraindication.

 Atropine 2 to 5 mg IV/IM/IO bolus (0.05 mg/kg IV in children)

Escalate (double) dose every 3-5 minutes until bronchial
secretions and wheezing stop.

 TACHYCARDIA AND MYDRIASIS ARE NOT CONTRAINDICATIONS TO ATROPINE USE

 Hundreds of milligrams may be needed over several days in

severe poisonings
 Management Continued…

Inhaled ipratropium 0.5 mg may be helpful for

bronchospasm; may repeat
Pralidoxime (2-PAM) 1-2 g (20-40 mg/kg in children)
IV over 30 minutes; may repeat after 30 minutes or give
continuous infusion if severe poisoning.
Continuous infusion at 8 mg/kg/hour in adults (10-20
mg/kg/hour in children)
If no IV access, give pralidoxime 600 mg IM (15 mg/kg
in children <40 kg). Rapidly repeat as needed to total of
1800 mg or 45 mg/kg in children.
Pralidoxime is given with atropine
Benzodiazepine therapy
Diazepam 10 mg IV (0.1 to 0.2 mg/kg in children), repeat
as necessary if seizures occur. Do not give phenytoin.
In overdose situations, liver enzymes become
saturated, glutathione is depleted, NAPQI
(N-acetyl-p-benzoquinoneimine)
accumulates, and hepatic necrosis occurs
Pharmacokinetics
 Absorption

 Rapidly absorbed from the GI tract

 Peak 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 differences

No change in patients with renal
disease
With liver dysfunction, may increase
to 17 hours
 Toxicity
 Factors involved in predicting
hepatotoxicity
 total quantity ingested
 time from ingestion to treatment
 age of the patient
 alcohol
 enzyme 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)

 Symptoms 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 charcoal
 Should not be witheld
 dose 50-100 Grams

 Cathartic
 utilized to speed transit time
 Hemodialysis
 Limited benefit
 Damage occurs quickly

 Hemoperfusion
 No benefit

 Peritoneal dialysis
 No benefit
Blood Sample
4 hour post ingestion APAP
level
 levels 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 CBC
 Creatinine, BUN, blood sugar, electrolytes
 Prothrombin times
 AST, ALT
 repeat q 24 hours
 elevations typically seen 24-36 hours post
ingestion
Rumack and Matthew Nomogram

500
Late
150
100 Not valid
50 after 24
hours
10

mcg/ml 4 8 12 16 20
Hours After Acetaminophen Ingestion
 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 substitute
 may supply inorganic sulfur, altering
metabolism

 Route of administration
 Orally
 IV not approved in the U.S.
 NAC dosing

 Oral 72 hour protocol

 Loading dose is 140 mg/kg

 Maintenance doses: 70 mg/kg

 Given every 4 hours x 17 doses
starting 4 hours after loading dose
 NAC supplied as 10 or 20% oral solution
 dilute 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
 IV Dosing of NAC

150mg/Kg IV in 200ml 5% Dextrose over

15minutes

Then 50Mg/Kg/Hour for next 4hours

Then 100Mg/Kg/Hour for Next 16 Hours.

Anaphylactoid reactions are well known in

some but not a contraindication to NAV.
 Prognosis
Poor Prognostic Indicators
at 24 to 48 hour post-ingestion include-

pH < 7.3 after adequate resuscitation

INR > 3

Serum Creatinine > 2.6

Hepatic Encephalopathy GrIII or GrIV

Hypoglycemia

Thrombocytopenia.
Acute poisoning does not predispose for cirrhosis.
 Acetominophen Summary
 APAP is present in many poly drug overdoses
 No symptoms may be present…screen
 150 mcg/ml at 4 hours is a “treat” level 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.
o If APAP levels cannot be obtained, assume a
toxic dose has been ingested, initiate NAC, and
continue until regimen complete.
 CO Poisoning

One of the most common fatal poisonings.

CO is a colorless, odorless gas.

Result of incomplete combustion of hydrocarbons.

Common sources of CO in poisonings include house fires

Improperly vented automobiles, gas heaters, furnaces,

hot water heaters, wood- or charcoal-burning stoves,
and kerosene heaters.

CO is produced when natural gas (methane or propane) burns.

 Mechanisms of CO Poisoning

Displacement of O2 from Hb

CO has 250times more affinity for Hb than does O2

Shifting of the O2-Hb dissociation curve to the left.

Inhibition of mitochondrial respiration

Possibly direct toxic effects on brain tissue

 Symptoms and Signs

Symptoms are nospecific & correlate to blood COHb.

Headache and nausea can begin when levels are 10 to 20%.

Levels > 20% commonly cause vague dizziness, generalized

weakness, difficulty concentrating, and impaired judgment.

Levels > 30% commonly cause dyspnea during exertion, chest

pain (in patients with coronary artery disease), and confusion.

Higher levels can cause syncope, seizures, and obtundation.

Hypotension, coma, respiratory failure, and death may occur,

usually when levels are > 60%.
In severe CO poisonings prominent

neuropsychiatric symptoms and signs

Eg. dementia, psychosis,parkinsonism,

chorea, amnestic syndromes

can develop days to weeks after

exposure and become permanent
 Diagnosis
Mostly straight forward with typical history of exposure.

Symptoms can be vague, nonspecific, and variable, the

diagnosis is easily missed for viral syndromes.

If people from the same dwelling, particularly a heated

dwelling, experience nonspecific flu-like symptoms &
Metabolic acidosis CO exposure should be considered.

If CO poisoning is suspected, the carboxyhemoglobin

level is measured with a CO-oximeter; venous samples
can be used because arteriovenous differences are
trivial.
ABGs and pulse oximetry, alone or combined, are
inadequate for diagnosis of CO poisoning
 Treatment
Patients should be removed from the source of CO and
stabilized as necessary.
100% O2 by nonbreathing mask.

Hyperbaric O2(in a chamber at 3 atm of 100% O2).

Hyperbaric O2 is advised for-
Life-threatening cardiopulmonary complications
Ongoing chest pain
Altered consciousness or LOC
A carboxyhemoglobin level > 25%
Hyperbaric O2 therapy should also be considered for
pregnant patients, possibly at lower serum CO levels
than in nonpregnant patients.
 Prevention
Sources of indoor combustion be correctly installed and
vented to the outdoors.

Exhaust pipes should be inspected periodically for leaks.

Cars should never be left running in an enclosed garage.

CO detectors should be installed because they provide

early warning that CO is free in a dwelling’s atmosphere.

If CO is suspected in a dwelling, windows should be

opened, and the dwelling should be evacuated and
evaluated for the source of CO.
 Take Home Message
CO poisoning (eg, caused by house fires, improperly vented
automobiles, gas heaters, furnaces, hot water heaters, wood- or
charcoal-burning stoves, or kerosene heaters) is one of the most
common fatal poisonings.

Consider toxicity is patients with nonspecific symptoms (eg, flu-

like symptoms in winter) or unexplained metabolic acidosis.

Measure CO level with a CO-oximeter.

Do not rule out toxicity based on a normal CO level because

levels can decrease rapidly, particularly after treatment with
supplemental O2.

Treat with 100% O2.

For severe poisoning, consult an expert or poison control center

to discuss treatment with hyperbaric O2.
Salicylates
Pharmacology
 Irreversibly 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.
Pathophysiology
 Salicylates 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 Continued
 Uncouples 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 Manifestations
 Early 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.

Treatment
 Address 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 Therapy
 The goal is to titrate the urinary pH to 8.

BUT
 Excretion 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 Hemodialysis
 Renal 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.
Ethylene Glycol and Methanol
fomepizole

folate

thiamine

Mg, B6
The Osmolar Gap
Treatment
 Fomepizole or ethanol – both inhibit alcohol
dehydrogenase.
 Cofactors
 Pyridoxime
 Folate
 Magnesium
 Thiamine
Fomepizole Dosing
 Loading dose
 15 mg / Kg
 Next 4 doses
 10 mg / Kg
 Subsequent doses
 15 mg / Kg
 Dosing schedule is every 12
hours except during
dialysis. Then it is every 4
hours during dialysis as it
gets dialyzed off.
Iron
 The most common cause
of death in toddlers.
 Classically taught as
having five clinical stages.
 Remember prenatal
vitamins, supplements,
and “natural products”.
Iron
 Toxic 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 Stages
 Stage 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 3
 Shock stage involving multiple organs including coagulopathy, poor
cardiac output, hypovolemia, lethargy and seizures.
 Stage 4
 Continuing of hepatic failure and ongoing oxidative damage by the
iron in the reticuloendothelial system.
 Stage 5
 Gastric outlet obstruction secondary to scarring and strictures.
Management
 Detailed 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
Management
 If 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.
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 Features
 Cardiac Toxicity (quinidine effects)
 Heart Block, Asystole, Bradycardia,
Tachycardia, Ventricular Dysrythmias
 ECG Changes - broadening of QRS
complex, Widened QT Interval
TCA Overdose- Management 1
 Mainstay of initial management is Supportive. Try
not to give other drugs ontop with a few specific
exceptions
 A- May need intubating
B
 C- Give IV fluids if low BP
 D -Control convulsions with Diazepam
TCA Overdose Management 2
 Activated Charcoal if more than 4 mg/Kg within 1
hour.
 N.B WATCH OUT FOR THE AIRWAY
 Correct Hypoxia with Oxygen
 Correct Acidosis with Na Bic
 Correct 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 incidence
1. Extensive use for cooking & lighting in low
socioeconomic status
2. Stored in soft drink bottles, beer bottles within
reach of children
Clinical features
 Age – 1 to 3 years
more than 70% symptomatic within
10 hours

SYMPTOMS

RS – breathlessness, cough
CNS – convulsions, coma
GPE – fever, restlessness, cyanosis
GI – vomiting, diarrhea
Lab
 Blood – Investigations
Leukocytosis

X – Ray changes
Changes appear within one hour
- commonly right basal infiltrates
- emphysema
- pleural effusion
- pneumatocoeles
Severity score
PARAMETERS ABSENT PRESENT OTHERS

FEVER 0 1 0
SEVERE 0 1 0
MALNUTRITION
RESP. DISTRESS 0 2 4
CNS SYMPTOMS 0 2 4

• >4 – Significant
• <7 – Likely to survive
• >8 –– Risk of death is increased
 Management
 Avoid emetics
 Avoid gastric lavage – In case of massive amount use a
cuffed endotracheal tube
 After lavage leave magnesium or sodium sulphate in the
stomach
 Oxygen may be useful
 Assisted Ventilation
 Antibiotics - Penicillin G 50000/Kg/24 hrs IV qid
 Kanamycin – 10-15mg/Kg/24 hrs - IM bd
 Steroids – 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.
Calcium Channel Blockers
 Three major classes
 Phenylalkylamine
 Benzothiazepine
 Dihydropyridine
 Block L-type channels
 Cause hypotension,
bradycardia, and
arrythmias.
 Immediate and sustained
release.
 Usually not the childs
medication.
Calcium Channel Blockers
 Manage A, B, C’s
 Check Labs and EKG
 Fluids
 Calcium
 Glucagon
 Pressors
 High Dose Insulin
 Atorpine and Pacing
Calcium Channel Blockers
 May 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 Antidepressants
 They 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 Managment
 Manage A, B, C’s aggressively
 Optimize electrolytes
 Follow serial EKG’s and use Bicarb if:
 QRS >100 or 110 msec
 aVr > 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 blood
 Rat 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.
Iron
 The most common cause
of death in toddlers.
 Classically taught as
having five clinical stages.
 Remember prenatal
vitamins, supplements,
and “natural products”.
Iron
 Toxic 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 Stages
 Stage 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 3
 Shock stage involving multiple organs including coagulopathy, poor
cardiac output, hypovolemia, lethargy and seizures.
 Stage 4
 Continuing of hepatic failure and ongoing oxidative damage by the
iron in the reticuloendothelial system.
 Stage 5
 Gastric outlet obstruction secondary to scarring and strictures.
Management
 Detailed 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
Management
 If 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.
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 Features
 Cardiac Toxicity (quinidine effects)
 Heart Block, Asystole, Bradycardia,
Tachycardia, Ventricular Dysrythmias
 ECG Changes - broadening of QRS
complex, Widened QT Interval
TCA Overdose- Management 1
 Mainstay of initial management is Supportive. Try
not to give other drugs ontop with a few specific
exceptions
 A- May need intubating
B
 C- Give IV fluids if low BP
 D -Control convulsions with Diazepam
TCA Overdose Management 2
 Activated Charcoal if more than 4 mg/Kg within 1
hour.
 N.B WATCH OUT FOR THE AIRWAY
 Correct Hypoxia with Oxygen
 Correct Acidosis with Na Bic
 Correct 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 incidence
1. Extensive use for cooking & lighting in low
socioeconomic status
2. Stored in soft drink bottles, beer bottles within
reach of children
Clinical features
 Age – 1 to 3 years
more than 70% symptomatic within
10 hours

SYMPTOMS

RS – breathlessness, cough
CNS – convulsions, coma
GPE – fever, restlessness, cyanosis
GI – vomiting, diarrhea
Lab
 Blood – Investigations
Leukocytosis

X – Ray changes
Changes appear within one hour
- commonly right basal infiltrates
- emphysema
- pleural effusion
- pneumatocoeles
Severity score
PARAMETERS ABSENT PRESENT OTHERS

FEVER 0 1 0
SEVERE 0 1 0
MALNUTRITION
RESP. DISTRESS 0 2 4
CNS SYMPTOMS 0 2 4

• >4 – Significant
• <7 – Likely to survive
• >8 –– Risk of death is increased
 Management
 Avoid emetics
 Avoid gastric lavage – In case of massive amount use a
cuffed endotracheal tube
 After lavage leave magnesium or sodium sulphate in the
stomach
 Oxygen may be useful
 Assisted Ventilation
 Antibiotics - Penicillin G 50000/Kg/24 hrs IV qid
 Kanamycin – 10-15mg/Kg/24 hrs - IM bd
 Steroids – 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.
 Common Toxidrome Findings
Physical
Anti- Anti- Sedative-
Findings Adrenergic OPIOID
cholinergic cholinesterase hypnotic

RR Increased No change No change Decreased Decreased

HR Increased Increased Decreased Normal/ Normal/

decreased decreased

Temp Increased Increased No change Normal/ Normal/

decreased decreased

BP Increased NoChange No change Normal/ Normal/

/increased decreased decreased
 Common Toxidrome Findings
Physical Anti-
Anti- Sedative-
Findings Adrenergic cholinestera OPIOID
cholinergic hypnotic
se
Mental Alert/ Depressed/ Depressed/ Depressed Depressed
status agitated Confused/ Confused/
hallucinate
pupils Dilated Dilated Constrict Constrict Normal

Mucus Wet Dry Wet Normal Normal

membrane

skin Diaphoretic Dry Diaphoretic Normal Normal

Lomotil
 Antidiarrheal 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.
Lomotil
 Patients 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 / Opioids
 Typically 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 Dosing
 Usually 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 Action
 Sulfonylureas 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.
Sulfonylureas
 Since 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.
Octreotide
 The 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 Facts
 A 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.
Camphor
 Aromatic ketone
derived from plants.
 Acts as a topical
rubefacient.
 Usually ingested as a
liquid.
 Often in preparations
combined with other
medicines such as
salicylates.
Camphor
 Initial 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.
Camphor
 Ingestions 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.
Carbon Monoxide Poisoning
 Clinical 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 Poisoning
 Exposure 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.
Treatment
 In 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.