2. INHALATION POISONING
• Inhalation is a major route for both acute and
chronic poisonings especially in occupational
toxicities.
• Inhalation is a route of poisoning with hazardous
poisons
• Absorption through inhalation is very rapid
• Large surface area
• High vascularity
8. SIMPLE ASPHYXIANTS
• Displace Oxygen thereby causing suffocation
• Alveolar displacement O2
• Non-irritating
• No direct mitochondrial toxicity
• CO2
• Nitrogen
• Helium
• Methane
9. CHEMICAL ASPHYXIANTS
• Interfere with the cellular transit of
oxygen
• They react in the human body to
interrupt either the delivery or
utilization of oxygen
• CO
• Cyanide
11. • Carbon dioxide is a colorless, odorless, non-
flammable gas at room temperature and is
required for plant and animal life.
• Carbon dioxide is produced naturally in the
body and during the burning of fossil fuels.
• Carbon dioxide can exist as a liquid or solid
depending on the temperature and pressure.
Its solid form is called dry ice.
• CO2is present in the atmosphere at 0.035%
12. SYMPTOMS OF CO2 TOXICITY
CO% Symptoms
2-3 Shortness of breath – Deep breathing
5 Breathing becomes heavy, sweating, pulse quickens
7.5 Headaches, dizziness, restlessness, breathlessness,
increased heart rate and blood pressure, visual distortion
10 Impaired hearing, nausea, vomiting, loss of
consciousness
15 May be lethal
25 Coma, convulsions, death
16. • Carbon monoxide is a colorless odorless non irritating gas.
Its density (0.968 relative to air), allows it to disperse
homogeneously within a room as it is released.
Sources
1. Endogenous:
• Normally the body produces small amount of CO during catabolism
of protoporphyrin ring of Hb.
• COHb normally dose not exceed 5%.
2. Exogenous:
• Incomplete combustion of carbonaceous materials.
• The major source is motor vehicle exhaust.
• At home, oil and gas heaters, kerosene heaters, charcoal grills all
emit CO.
• Tobacco cigarette smoking.
• Fires.
17. Factors Affecting CO Toxicity:
• Physical factors: CO is tasteless, odorless, colorless and
non-irritating so not noticed.
• Duration of exposure.
• Concentration of the gas in the inspired air.
• Muscular activity of the person.
• Decreased PO2 as in high altitude.
• Individuals with cardiovascular or pulmonary diseases
tolerate CO intoxication poorly.
• Lowered Hb% as in anemia.
• Neonates and fetus are more liable to CO toxicity because
fetal Hb has increased affinity to CO. In addition, fetal
elimination of CO is much slower than that of the mother.
18. Pathophysiology
1- CO has affinity to Hb (200-250 times) greater
than O2.
2- CO causes leftward shift of the oxyHb
dissociation curve: decrease release of O2
from Hb to tissues.
3- Myoglobin impairment:affinity to CO is 40
times greater than that to O2.
In the heart, carboxymyoglobin causes direct
myocardial depression and arrhythmias.
4- Mitochondrial impairment: CO interferes
with cellular respiration at the mitochondrial
level
19. Clinical Manifestations
(A) CNS: is most sensitive to CO poisoning
1- Acutely: headache, dizziness and ataxia
and slow thinking.
2- Longer exposure: syncope, seizures and
coma may occur.
3- Patients may present with symptoms of
an acute cerebrovascular accident (CVA).
20. 4- Recurrent symptoms syndrome: Occur in 10-20% of
patients with moderate CO toxicity:
Patient may have lucid interval of 1-40 days
followed by recurrence of symptoms as headache
dizziness, irritability, confusion, disorientation,
and memory problems. Patients usually recover
over 1-2 months.
Delayed neuropsychiatric sequelae: a severe form of
secondary deterioration characterized by appearance of
signs of neurologic or psychiatric impairment occur in up
to 95% of patients having loss of consciousness in the acute
phase of exposure.
Hyperbaric O2 therapy may prevent these sequelae.
21. (B) Cardiovascular System:
1- Palpitation and chest pain
2- Patchy myocardial infarction with ECG
changes of ischemia.
3- Tachycardia is common. Bradycardia
occurs in severe cases due to myocardial or
CNS hypoxia.
4- Atrial and ventricular arrhythmias.
5- Hypotension.
22. C. Other Systems:
SKIN
• Cherry red skin is rarely seen
• pallor or cyanosis are more frequent.
• Blisters resembling 2nd degree burn
may be seen in severe CO poisoning.
These bullae are thought to be due to
pressure necrosis and direct effects of
CO on the epidermis.
23. Eye: Blurring of vision, decreased dark adaptation
In severe cases frank blindness due to central
effect
Retina: Bright red retinal veins is an early sensitive
sign.
Respiratory:
Noncardiogenic pulmonary edema due to fluid shift
through alveolar-epithelial junction caused by direct
effect of CO on the capillaries.
Cardiogenic pulmonary edema due to myocardial
depression.
24. 4. Renal: Oliguric and non oliguric renal failure.
5. Blood: - Disseminated intravascular coagulation
(DIC).
6. Metabolic: - Lactic acidosis, hyperglycemia and
hypercalcaemia.
7. Muscles: Rhabdomyolysis.
8. GIT: Nausea, vomiting, abdominal pain
Diarrhea (may be misdiagnosed as gastroenteritis
or food poisoning specially in children or in a
group of patients.
25. Investigations
1. Carboxy hemoglobin (COHB) level; most helpful diagnostic test
• COHb level is 0-5% in normal individuals.
• Smokers may have COHb levels up to 10%.
• No difference between arterial and venous COHb.
• Measured by cooximeter which spectrophotometrically measures
the percentage of total hemoglobin saturated with CO.
2. Arterial blood gases:
PO2 may be normal
O2 saturation is accurate if directly measured and not calculated
from PO2.
Pulse oximeter shows falsely elevated O2 saturation.
Metabolic acidosis if present is usually due to lactic acidosis which
is a bad prognostic sign.
26. Management
1- Rapid removal from continued exposure.
2- Secure airway patency.
3- 100% O2 should be provided immediately . 100% O2 shortens CO t
1/2 and increases O2 delivered to tissue in physical solution.
4- Cardiac monitoring and IV access are necessary with rapid treatment of
any arrhythmias.
5- Blood samples for COHb level and other lab tests.
6- Rapid assessment of vital signs and treatment of any abnormality.
7- Hypotension improves with fluids but inotropics may be needed for
myocardial depression.
8- Do not aggressively treat acidosis with pH above 7.15 as this can increase
tissue hypoxia by left shift of oxyhemoglobin dissociation curve.
9- Serial neurologic examination including funduscopy.
10- CT scan and possibly MRI to be done as indicated
27. TREATMENT
1- Rapid removal from continued exposure.
2- Secure airway patency. Rapid assessment of vital signs and
treatment of any abnormality.
pulse oximetry is inadequate Oxygen saturation may appear
artificially high
3- 100% O2 should be provided immediately . 100% O2 shortens
CO t 1/2 and increases O2 delivered to tissue in physical
solution.
4-Blood samples for COHb level and other lab tests.
5- Do not aggressively treat acidosis with pH above 7.15 as this
can increase tissue hypoxia by left shift of oxyhemoglobin
dissociation curve.
6- Serial neurologic examination including funduscopy. CT scan
and possibly MRI to be done as indicated
28. HYPERBARIC OXYGEN
• Decrease COHb half
life
• Displaces CO from
tissues
• Improves oxygen
carrying capacity
• Limits lipid
peroxidation
• Improves dissolved
oxygen
29. HYPERBARIC OXYGEN: INDICATIONS
• Neurological damage
• Cardiovascular events
• Loss of Consciousness
• Persistent symptoms
• COHb > 25% ( some centers use >40%)
• COHb > 15% in pregnant woman
• Ideally within 6 hours of exposure
30. POSTMORTEM APPEARANCE
• Cherry red appearance, especially in the areas of
postmortem lividity. In dark people the color can be
made out in lips, nail beds, tongue, palms and soles.
• Skin blisters are seen sometimes in calves, buttocks,
wrists, and knees.
• Cherry pink color of blood and tissues
• Pulmonary edema
• In delayed deaths; necrosis and cavitation of basal
ganglia, especially globus pallidus.
32. • Cyanide is one of the most
rapidly acting lethal poisons
• A rare source of poisoning.
33. SOURCES
• Salts used in:
• Electroplating
• Mining extraction
• Photography
• Jewelry
• Nitroprusside (iatrogenic)
• Amygdalins: converted into cyanide in the
small intestine by bacteria.
• Fires
34. MECHANISM OF TOXICITY
• It has affinity for ferric iron & is capable
of binding to all enzymes and proteins
containing iron: Hb, myoglobin, catalase,
& cytochrome system
• Its most significant interaction is its
binding to ferric iron of the mitochondrial
cytochrome oxidase system
• The most sensitive organ systems to
cyanide toxicity are CNS and the
myocardium.
35. CLINICAL MANIFESTATIONS
1- Weakness, loss of energy, and pain
throughout the body.
2- CNS: headache, dizziness, weakness,
confusion
3- Cardiac: Chest pain may be due to
myocardial ischemia or pulmonary disease.
Tachyarrhythmias
Bradyarrhythmias have been reported.
36. 5- Respiratory: difficulty breathing.
6- GI: Nausea and vomiting may be due to
stimulation of the Vomiting center &
direct irritation on GIT
7- Skin & Fundoscopy: cherry red
appearance due to increased Hb
saturation in venous blood because of
inability to utilize O2.
37. TREATMENT
• Decontamination by removal of
the patient from the source,
removal of all clothes, and rapid
irrigation of the body with
copious amounts.
• Adequate intravenous access
40. TREATMENT: CYANIDE ANTIDOTE KIT
• Known or suspected
cyanide poisoning
• Metabolic acidosis
• End organ damage
41. NITRITES FOR CN
Hemoglobin
Methemoglobin
Amyl nitrite, sodium nitrite
Cyanomethemoglobin
Cytochrome-CN
Cytochrome Sodium
thiosulfate
Sodium
thiocyanate
Rhodanese
CN
Hemoglobin
Methemoglobin
Amyl nitrite, sodium nitrite
Cyanomethemoglobin
Cytochrome-CN
Cytochrome Sodium
thiosulfate
Sodium
thiocyanate
Rhodanese
CN
Caution if diagnosis is uncertain or if COHb is also suspected.
Can omit nitrites if uncertain exposure.
Caution
42. HYDROXOCOBALAMIN KIT (CYANOKIT)
• Hydroxocobalamin contains cobalt ion, which is able to
bind to cyanide with greater affinity than cytochrome
oxidase to form cyanocobalamin (nontoxic), which is
excreted in urine.
• Hydroxocobalamin:
• has few adverse effects
• tolerated by critically ill patients
• tolerated by patients with concomitant CO poisoning
• In France, it commonly is used in combination with
sodium thiosulfate. Low-dose hydroxocobalamin in
combination with sodium thiosulfate has been used
successfully to prevent cyanide toxicity due to prolonged
sodium nitroprusside infusions.
44. POSTMORTEM APPEARANCE
• External
• Odor of bitter almonds
• Brick red color of skin and mucous membranes
• Cyanosis of extremities
• Froth at mouth and nostrils
• Internal
• Hemorrhagic gastritis. Stomach wall may be
hardened
• Pulmonary and cerebral edema
• Disseminated petechiae in brain, meninges, pleura,
lungs, and pericardium
