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1. CARBON MONOXIDE POISONING
2. Carbon Monoxide (CO) An odorless, colorless, tasteless gas
Results from incomplete combustion of carbon- containing 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
3. Sources of Carbon Monoxide any combustible item Homes
Cigarette smoke House fires Automobile exhaust fumes Worksites
Including fumes from propane-powered equipment like forklifts
Commercial structures Smoke from charcoal-fired cook stoves &
ovens
5. 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
6. 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
7. 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
8. CO Levels Fresh air 0.06 - 0.5 ppm Urban air 1 300 ppm Smoke
filled room 2 16 ppm Cooking on gas stove 100 ppm Actively smoking
400 500 ppm cigarette Automobile exhaust 100,000 ppm
9. Expected Carboxyhemoglobin Levels Non-smokers 5% Smokers up
to 10% 5 6% for a 1 pack per day smoker 7 - 9% for a 2-3 pack per
day smoker Up to 20% reported for cigar smokers Urban commuter
5%
10. 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
11. Exposure Limits For CO OSHA 50 ppm as an 8-hour-weighted
average NIOSHA 35 ppm as an 8-hour-weighted average Set lower than
OSHA based on cardiac effects of CO
12. Symptoms of CO Poisoning Related to Levels and Exposure
Time 50 ppm no adverse effects with 8 hours of exposure (OSHA
limit) 200 ppm mild headache after 2-3 hours 400 ppm serious
headache and nausea after 1-2 hours (life-threatening >3 hours)
800 ppm headache, nausea, dizziness after 45 minutes; collapse and
unconsciousness after 2 hours; death within 2-3 hours 1000 ppm loss
of consciousness after 1 hour
13. Levels & Exposure Time Contd Source: NFPA Fire
Protection Handbook, 20th Edition 1600 ppm headache, nausea,
dizziness after 20 minutes; death within 1 hour 3200 ppm headache,
nausea, dizziness after 5-10 minutes; collapse and unconsciousness
after 30 minutes; death within 1 hour 6400 ppm headache, dizziness
after 1-2 minutes; unconsciousness and danger of death after 10 -15
minutes 12,800 ppm immediate physiological effects; unconsciousness
and danger of death after 1-3 minutes
14. Carbon Monoxide Absorption Dependent upon: Minute
ventilation Amount of air exchanged in the lungs within one minute
Duration of exposure The longer the exposure, the more the
absorption Concentration of CO in the environment The higher the
concentration, the greater the toxicity Concentration of O2 in the
environment The lower the O2 concentration to begin with, the
faster the symptoms will develop higher altitudes closed
spaces
15. CO Levels with Related Signs and Symptoms >5% - mild
headache 6-10% - mild headache, SOB with exertion 11-20% - moderate
headache, SOB 21-30% - worsening headache, nausea, dizziness,
fatigue 31-40% - severe headache, vomiting, vertigo, altered
judgment 41-50% - confusion, syncope, tachycardia 51 60% -
seizures, shock, apnea, coma
16. Signs and Symptoms CO Poisoning Carboxyhemoglobin levels of
60% Fatal Death Cherry red skin is not listed as a sign An
unreliable finding
20. Increased Risks Health and activity levels can increase the
risk of signs and symptoms at lower concentrations of CO Infants
Women who are pregnant Fetus at greatest risk because fetal
hemoglobin has a greater affinity for oxygen and CO compared to
adult hemoglobin Elderly Physical conditions that limit the bodys
ability to use oxygen Emphysema, asthma Heart disease Physical
conditions with decreased O2 carrying capacity Anemia
iron-deficiency & sickle cell
21. CDC Diagnostic Criteria Suspected CO exposure Potentially
exposed person but no credible threat exists Probable CO exposure
Clinically compatible case where credible threat exists Confirmed
CO exposure Clinically compatible case where biological tests have
confirmed exposure
22. Patient Assessment Continuously monitor SpO2 and SpCO
levels Remember that SpO2 may be falsely normal If EMS has used a
CO-oximeter, findings to be reported to the ED staff Generally,
results >3% indicate suspicion for CO exposure in non-smoker
Cardiac monitor 12 lead EKG obtained and transmitted to ED
23. 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
24. 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
25. Treatment CO Poisoning Guidelines from different sources
may vary when to initiate treatment based on SpCO levels Report
levels to the ED MD Remember >5% in non-smokers is abnormal
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
Cardiac dysrhythmias Cardiac ischemia
26. CO Poisoning and CPAP CPAP could assist in fully
oxygenating hemoglobin If considered, EMS to contact Medical
Control for permission to use CPAP The ECRN would need to relay
report to the ED MD to obtain an order for CPAP
27. 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
28. 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 10% Nitrites can also cause hypotension
42. Signs and Symptoms Methemoglobinemia 1-3% SpMet normal,
asymptomatic 3-15% SpMet slight grayish-blue skin 15 20% -
asymptomatic but cyanotic 25 50% - headache, dyspnea, confusion,
weakness, chest pain 50 -70% - altered mental status, delirium
Methemoglobinemia is also a complication when Benzocaine (to
decrease the gag reflex) is used even under normal 2 second spray
time frame
43. Cyanokit This kit uses hydroxocobalamin A form of Vitamin
B12 (cyanocobalamin) Binds with the cyanide ion Eliminated through
the kidneys Preferred kit if concomitant CO and cyanide poisoning
suspected Significant signs and symptoms with low CO levels
Decreased cardiac output, decreased heart rate Hypotension, shock,
and falling ETCO2 levels Signs & symptoms of CO and cyanide
poisoning indistinguishable
44. Arsenic Poisoning
45. Arsenic in the World Arsenic is ubiquitous in the
environment. It ranks 20th in abundance in the earth's crust, 14th
in seawater, and 12th in the human body. 20th 14th 12th
46. Possible Arsenic poisoning Today, arsenic poisoning occurs
through industrial exposure, from contaminated wine or moonshine,
or because of malicious intent. The possibility of heavy metal
contamination of herbal preparations and so-called nutritional
supplements must also be considered.
47. Poisonous Compounds of Arsenic Arsenic oxide or Arsenic
Trioxide It is the most common form of arsenic used. It is also
known as White Arsenic. No taste or smell and is sparingly soluble
in water. It is heavier than water by three and half times but
freely floats on water.
48. Uses Of Arsenic Fruit sprays Sheep-dips Weed-killers Rat
poisons Fly papers Calico printing Taxidermy Preserving timber and
skin against white ants
49. Mode Of Action Arsenic interferes with cellular respiration
by combining with the sulphydryl groups of mitochondrial enzymes.
It particularly targets vascular endothelium leading to increased
permeability, tissue edema and hemorrhage, especially in the
intestinal canal.
50. Mode Of Action Locally it causes irritation of the mucous
membranes and remotely depression of the nervous system. Arsenic
also interferes with glycolysis.
51. Circumstances Of Poisoning It is cheap Easily obtained
Colourless No smell No taste Small quantity is required to cause
death. Can be easily administered with food or drink. Onset of
symptoms is gradual Symptoms simulate those of Cholera. Arsenic is
the most popular Homicidal poison
52. Circumstances Of Poisoning Disadvantages Of Arsenic: It
delays putrefaction Can be detected in completely decomposed
bodies. Can be found in bones, hairs and nails for several years.
Can be detected in charred bones or ashes.
53. Signs And Symptoms 1. The Fulminant type 2. The
Gastroenteric Type
54. The Fulminant type Massive doses of arsenic when rapidly
absorbed cause death in one to three hours from shock and
peripheral vascular failure. All the capillaries are markedly
dilated, especially in the splanchnic area with a marked fall of
blood pressure.
55. The Gastroenteric Type This is the common form of acute
poisoning and resembles bacterial food poisoning. Symptoms usually
appear half to one hour after ingestion, but may be delayed many
hours especially when arsenic is taken with food. Burning and
colicky pain in the esophagus, stomach and bowel occur. Intense
thirst and severe vomiting which may be projectile are the common
symptoms.
56. Signs And Symptoms Acute severe arsenic poisoning Vital
signs - Tachycardia and hypotension, even shock CNS - Altered
mental status, delirium, coma, and seizures (acute encephalopathy)
Frequently, patients exposed to arsenic have a garlic smell to
their breath and tissue fluids.
57. Signs And Symptoms Arsine gas exposure manifests with an
acute hemolytic anemia and striking chills. Hemoglobinuria causes
the urine to appear black, and the patient becomes rapidly obtunded
and shocky. Shaking chills are often described in these patients.
Frequently, patients exposed to arsenic have a garlic smell to
their breath and tissue fluids.
58. Signs And Symptoms Acute exposures generally manifest with
the cholera-like gastrointestinal symptoms of vomiting (often times
bloody) and severe diarrhea (which may be rice-watery in character
and often bloody); these patients will experience acute distress,
dehydration (often), and hypovolemic shock.
59. Chronic toxicity is more insidious and may manifest as a
classical dermatitis (hyperkeratosis with a classical "dew drops on
a dusty road" appearance) Telugu Doctors.co.in
60. whitish lines (Mees lines) that look much like traumatic
injuries are found on the fingernails. Contact dermatitis may also
be induced in occupational arsenic poisoning. Arsenic dust coming
into contact with the skin produces four main types of reactions:
1. Toxic 2. Eczematous 3. Combined toxic and eczematous and 4.
Reactions characterized by follicular lesions. Telugu
Doctors.co.in
61. Laboratory Studies Complete Blood Count Microcytic
Hypochromic Anemia Obtain a CBC with indices and a reticulocyte.
Acute hemolytic anemia is the rule with arsine exposure. Type and
screen or crossmatch blood for the transfusion in patients exposed
to arsine gas.
62. Laboratory Studies 1. Serum Magnesium 2. Serum Potassium 3.
Serum Sodium 4. Serum Calcium 5. Serum Chloride Serum Electrolytes
Do Serum electrolytes in patients with Diarrhea and Vomiting Telugu
Doctors.co.in
63. Laboratory Studies Blood arsenic concentrations should not
exceed 50 mcg/L. The reported half-life of arsenic in blood
immediately following ingestion is in hours, while whole- body
clearance may be in days or months and is apparently dose- related.
Serum Electrolytes Plasma Arsenic Analyser Serum Arsenic Analysis
Telugu Doctors.co.in
64. Laboratory Studies Urine spot test for arsenic 24-hour
urine collection for total arsenic excretion Methylarsonic acid
(MMA) and dimethylarsenic acid (DMA) metabolites of arsenic in the
body Urine analysis Telugu Doctors.co.in
65. Laboratory Studies Reports of prolongation of the QT and
ventricular fibrillation after acute arsenic intoxication make
careful attention to cardiac status imperative. ECG Changes Telugu
Doctors.co.in
66. Laboratory Studies Nerve conduction studies may confirm
Peripheral neuropathy An abdominal radiograph may reveal the
presence of radio- opaque densities Other Tests Telugu
Doctors.co.in
67. Treatment and management Airway Breathing Circulation
Pre-Hospital care Emergency Department Hemodynamic stabilization to
counteract GI loses Orogastric lavage for acute arsenic poisoning
Whole bowel irrigation with polyethylene glycol may be effective to
prevent GI tract absorption of arsenic. Telugu Doctors.co.in
68. Treatment and management Dimercaprol (BAL in Oil):
First-line agent for treating arsenic poisoning. May be
administered to patients with renal failure. Succimer (DSMA): used
only in childhood lead poisoning. Dimerval (DMPS): accepted DOC for
treating most heavy metal poisonings. Chelation Agents Telugu
Doctors.co.in
69. Treatment and management Hemodialysis is especially useful
in a patient with arsenic poisoning with renal failure or with
impending renal failure. Hemodialysis Telugu Doctors.co.in