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Mike > Section 5: Chemicals > Flashcards

Section 5: Chemicals Flashcards

1
Q

5.1 Given an inhalation exposure, identify which substance is responsible.

A
  1. Utilize general knowledge of expected symptoms to determine responsible substance from a presented scenario.
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2
Q

5.2 Given an exposure with a cluster of patients, identify which chemical weapon of mass destruction is responsible.

A
  1. Nerve agents
    a. Ex: Tabun, Sarin, Soman, VX
    b. S/S: organophosphorus agents with muscarinic and nicotinic stimulation (SLUDGE)
  2. Vesicant (blistering) agents
    a. Ex: Nitrogen and Sulfur mustard, Lewisite (contains arsenic), Phosgene
    b. S/S: skin, ocular, pulmonary damage
  3. Choking agents
    a. Ex: Chlorine, lacrimator agents, Phosgene
    b. S/S: mucous membrane and respiratory irritation
  4. Blood agents
    a. Ex: Cyanide
    b. S/S: neuro and CV collapse
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3
Q

5.3 Identify the toxicity and symptoms of chemical exposures.

A
  1. Acids
    a. Immediate coagulation-type necrosis
    b. Creates eschar and self-limits further damage
  2. Gun Blue (Selenious acid)
    a. Upper GI corrosive injury, emesis, diarrhea, hypersalivation, garlic odor on breath, rapid deterioration of mental status progressing to coma, hypotension, resp depression, death
    b. 15ml of 2% selenious acid has been fatal
  3. Alkali
    a. Liquefactive necrosis with continued penetration into deeper tissues
    b. Extensive tissue damage
  4. Nitrites and Nitrates
    a. Smooth muscle relaxation (decreased preload and afterload with vasodilation)
    b. Cause hypotension and methemoglobinemia (cyanosis) (nitrates)
    c. Nitrites have potentiation of effects when used with phosphodiesterase inhibitors (sildenafil/Viagra)
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4
Q

5.4 Gases

A

5.4 Identify the toxicity and symptoms from exposure to gases.

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5
Q
  1. Ammonia
A

a. Gas and aqueous forms found in fertilizers, refrigerants, cleaning solutions, explosives
i. Household cleaners concentration 5% to 10%
ii. Commercial cleaners concentration 25% to 30%

b. Alkaline. Corrosive on contact with moist tissues
c. Exposure may be dermal, ophthalmic, respiratory, or GI

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6
Q

i. Ammonia (Dermal)

A
  1. S/S: Mild to severe burns
  2. Treatment
    a. Remove from source
    b. Irrigate
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7
Q

ii. Ammonia (Ophthalmic)

A
  1. S/S: Pain, redness, lacrimation, burns, vision loss
  2. Treatment
    a. Irrigate (up to several liters of saline) until pH 7.4
    b. Fluorescein exam
    c. Ophthalmology consult if corneal involvement
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8
Q

iii. Ammonia (Respiratory)

A
  1. S/S: Burning of nose/throat and cough
    a. Obstruction (stridor, hoarseness, wheezing, croupy sounds)
    b. Lower respiratory tract injury (wheezing or pulmonary edema)
  2. Treatment
    a. Remove from source
    b. Supplemental O2
    c. Early intubation if needed
    d. Bronchodilators for wheezing
    e. PEEP and avoid excess fluids to treat pulmonary edema
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9
Q

iv. Ammonia (GI)

A
  1. S/S: Oral/pharyngeal pain, dysphagia, difficulty maintaining secretions,
    chest/abdominal pain, possible esophageal or gastric perforation
  2. Treatment
    a. Water or milk to dilute
    b. No charcoal, induced emesis, or neutralization with acid
    c. Gastric Suction with NG (small tube)
    d. Chest and abdominal radiograph
    e. If solution >= 10% or dysphagia, drooling or pain, consider upper endoscopy
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10
Q
  1. Chloramine
A

a. Ammonia combined with chlorine or hypochlorite solutions produce chloramine gas
b. Irritant.
c. Exposure is generally respiratory

d. S/S: Similar to chlorine gas exposure
i. Chloramine fumes cause pneumonitis
ii. Less water soluble than chlorine. Symptoms may be more delayed

e. Treatment
i. Remove from source
ii. High flow O2

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11
Q
  1. Chlorine
A

a. Found in chemical manufacturing, bleaching, swimming pools, and disinfectants

i. Hypochlorite is aqueous solution of chlorine with water
b. Acidic. Irritant
i. Heavier than air

ii. Irritating odor; yellow-green gas
c. Exposure route dermal, respiratory, GI
d. S/S: Oxidative and corrosive when contacting moist tissues

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12
Q

Chlorine (Dermal)

A
  1. Irritation, burns
  2. Treatment
    a. Remove from source
    b. Remove clothes and decontaminate
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13
Q

Chlorine (Respiratory)

A
  1. Irritation, wheezing, cough, rhinorrhea, respiratory distress, syncope, pulmonary edema
  2. Treatment
    a. Remove from source
    b. Humidified O2
    c. Bronchodilators for wheezing
    d. Low threshold for intubation
    e. Possible use of nebulized sodium bicarb
    No thermal injury appears to occur
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14
Q

Chlorine (GI)

A
  1. Burns, dysphagia, drooling, hematemesis, perforation
  2. Treatment
    a. Dilute with water
    b. Do NOT induce emesis
    c. Consider NG tube for gastric aspiration
    d. Possible need for endoscopy
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15
Q

Chlorine Evaluation:

A

i. Watch for hypochloremia & acidosis
ii. ABG for hypoxia
iii. CXR for pneumonitis and pulmonary edema

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16
Q
  1. Freon and other propellants
A

a. Mild CNS depressants/asphyxiants.
i. Well absorbed by inhalation or ingestion.
ii. Usually rapidly excreted in the breath within 15-60 min

b. Exposure route usually dermal or respiratory

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17
Q

c. Freon S/S

A

i. Mild irritant
ii. Direct freezing of the skin
iii. Hepatotoxic with large exposure
iv. May potentiate cardiac arrhythmias by sensitizing the myocardium

  1. Avoid epinephrine
  2. Tachyarrythmias may be treated with propranolol or esmolol
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18
Q
  1. Fume fevers (metal, polymer)
A

a. Source is often inhaled zinc oxide; can have symptoms from welding, melting, and flame
cutting of galvanized metal

b. S/S
i. Fever
ii. Malaise
iii. Myalgia
iv. Headache
v. *Should not have hypoxia or pulmonary infiltrates
1. If present, suspect chemical pneumonitis from another source

c. Treatment
i. S/S should self-resolve
ii. No decontamination is required. By time of s/s onset, exposure is past

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19
Q
  1. Hydrogen sulfide
A

a. Byproduct of decaying organic material. Pools of sewage or sludge, liquid manure. Industrial processes often found in petroleum refineries, tanneries, mines, pulp-making factories, sulfur hot springs, carbon disulfide production, commercial fishing holds, hot asphalt fumes.

b. Knock-down gas
i. “pit gas” – heavier than air
ii. Known for rotten egg smell
iii. cellular asphyxia (similar to cyanide)

c. Exposure route generally respiratory

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20
Q

d. Hydrogen Sulfide S/S

A

i. Chemical irritant at low doses
1. Upper airway, eye, skin, irritation
2. Chemical pneumonitis, non-cardiogenic pulmonary edema

ii. Acute systemic effects
1. n/v, headache, dizziness, confusion, sz, coma,

iii. Massive exposure
1. Immediate cardiovascular collapse, respiratory arrest and death

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21
Q

e. Hydrogen Sulfide Treatment

A

i. Remove from source

ii. Possible use of nitrites (sodium nitrite and amyl nitrite)
1. To promote methemoglobin (binds a component of the poisonous gas)
2. May cause hypotension and impaired O2 delivery

iii. Possible use of hydroxycobalamin
1. Not proven

iv. Possible use of hyperbaric oxygen

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22
Q
  1. Phosgene
A

a. Found in manufacture of dyes, resins, plastics, and pesticides; used as a war gas

b. Irritant
i. Heavier than air
ii. Smell of freshly mown hay
iii. Poorly water soluble
Enters lower airways
Does not cause immediate irritation

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23
Q

c. Phosgene S/S

A

i. Initial mild cough and minimal mucous membrane irritation
ii. Delayed dyspnea and hypoxemia (30 min-8 hrs)
iii. Resultant noncardiogenic pulmonary edema (up to 24 hrs)

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24
Q

d. Phosgene Treatment

A

i. Remove from source
ii. Remove clothes and decon
iii. Maintain airway
iv. Low threshold for intubation. Use large ETT (frequent suction)
v. monitor asymptomatic patient for 24 hrs after exposure
vi. No antidote

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25
Q
  1. Simple asphyxiants
A

a. Inert gases or vapors that displace oxygen from air when present in high concentrations.
i. In low concentrations they have no effects.
b. Ex. Nitrogen, argon, helium, methane, propane, CO2

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26
Q

5.5 Identify the toxicity and symptoms from carbon monoxide exposure.

A
  1. Chemical asphyxiant (other chemical asphyxiants: hydrogen sulfide and cyanide)
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27
Q
  1. Exposure sources (CO)
A

a. Gas appliances
b. Charcoal grills
c. Combustion engine exhaust
d. Smoke from any fire
e. Cigarettes

  1. CO has 240x greater affinity for hemoglobin than oxygen
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28
Q
  1. For CO uptake to body dependent on?
A

a. Concentration of inspired CO
b. Pt’s minute ventilation
c. Duration of exposure

  1. Binds to hemoglobin. Can also bind to myoglobin
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29
Q
  1. CO S/S
A

a. n/v, headache, fatigue, dizziness, confusion, ataxia, syncope, sz, coma
b. dyspnea, chest pain, dysrhythmias, hypotension
c. death

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30
Q
  1. CO Treatment
A

a. 100% oxygen (NRB or Vent)
b. Check co-ox panel
c. Consider hyperbaric for hx of:
- i. Loss of consciousness, coma or seizures
- ii. Pregnancy
1. CO has higher affinity to fetal hemoglobin
- iii. CO level >40%

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31
Q

5.6 Identify the toxicity and symptoms of exposure to heavy metals.

A

Ex. Arsenic, lead, mercury,

cadmium, thallium, chromium, etc

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32
Q
  1. Arsenic
A

a. Most commonly ingested in contaminated food or water.
i. Inorganic is the more problematic form
ii. Frequently used as a wood preservative in industrial applications
iii. Some compounds are radio-opaque and may be seen on xray
iv. Arsine is a colorless, nonirritating, garlic-odored gas from industrial settings

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33
Q

b. Clinical presentation (Arsenic)

A

i. Phase one (fairly rapid within hours)
ii. Phase two (after 1-7 d)
iii. Phase three (after 1-4 wks)
iv. Acute poisoning s/s after 1-6 wks

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34
Q

i. Arsenic - Phase one (fairly rapid within hours)

A
  1. Profound cholera-like gastroenteritis (n/v/d/abd pain)

a. Tachycardia, hypotension, hemodynamic collapse, metabolic acidosis, rhabdo, renal failure

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35
Q

ii. Arsenic - Phase two (after 1-7 d)

A
  1. GI s/s and hypotension resolve
  2. Cardiovascular compromise
    a. Congestive cardiomyopathy, cardiogenic and non-cardiogenic
    pulmonary edema, prolonged QTc
  3. Encephalopathy
    a. Delirium, agitation, coma
  4. Elevated transaminases and proteinuria
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36
Q

iii. Arsenic - Phase three (after 1-4 wks)

A
  1. Begins with sensorimotor peripheral neuropathy
    a. Abnormal sensations in stocking-glove pattern
    b. Ascending sensory and motor deficits
    c. Pancytopenia
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37
Q

iv. Arsenic - Acute poisoning s/s after 1-6 wks

A
  1. Diffuse maculopapular rash
  2. Desquamation of palms and soles
  3. Periorbital edema
  4. Herpetic-like lesions
  5. Mees’ lines (white transverse striae on nails 4-6 wks post ingestion)
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38
Q

c. Arsenic Labs

A

i. Rapid blood levels are not useful

ii. May use 24-hr urine test

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39
Q

d. Arsenic Treatment

A

i. Avoid quinidine, procainamide and other type 1a antiarrhythmic agents due to
QT prolonging effect

ii. Avoid phenothiazines for antiemetics or antipsychotics d/t QT prolongation and
lowering of seizure threshold

iii. Chelate if seriously symptomatic
- 1. Unithiol (IV) or Dimercaprol/BAL (IM) (no BAL if peanut allergy)
- 2. Oral unithiol or oral succimer (DMSA)

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40
Q
  1. Lead
A

a. Exposure is most commonly due to ingestion. Lead is radiopaque.

i. Children are more sensitive than adults. Common symptoms in chronic
exposure include constipation and abdominal pain.

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41
Q

b. Lead - Clinical presentation

A

i. Mild
1. BLL > 40 ug/dL
2. Fatigue, moodiness, hypertension, decreased interest in activities

ii. Moderate
1. BLL >80 ug/dL
2. Headache, memory loss, fatigue, irritability, insomnia, muscle
pain/weakness, abd pain, anorexia, weight loss, neuropathy, anemia

iii. Severe
1. BLL >100-150 ug/dL
2. Encephalopathy (coma, sz, delirium, increased ICP), foot/wrist drop, abd
pain, vomiting, anemia, nephropathy

42
Q

c. Lead - Labs

A

i. Capillary BLL used for screening. Venous BLL should be used for confirmation
- 1. 10 ug/dL is current action level for CDC in pediatric lead exposure

ii. CBC may show microcytic anemia and basophilic stippling on smear
- 1. Stippling indicates a toxic injury to bone marrow

43
Q

d. Lead - Treatment

A
  1. Chelation is indicated in children with level > 45 ug/dL; symptomatic
    adults; or adults with level >70 ug/dL

a. Chelation with Succimer (DMSA) – Oral if tolerated
b. Chelation with BAL (IM) & Calcium EDTA (IV) for more severe
toxicity
c. Consider whole bowel irrigation
d. Endoscopic removal or surgery considered if retained foreign
body
e. Recheck levels 1 day after chelation initiation and again 7-21 d
after chelation

44
Q
  1. Mercury
A

a. Exposure in three primary forms: elemental (metallic); inorganic; organic

45
Q

b. MOA - Mercury

A

i. Corrosive effect on GI tract

ii. Prevent catecholamine catabolism (cause sympathomimetic s/s)
- 1. Mimics pheochromocytoma (s/s intermittent flushing and HTN) and
Kawasaki’s (s/s strawberry tongue no conjunctival injections)

46
Q

Sources - Mercury

A

i. Sea animals with high potential for bioaccumulation

- 1. Shark, swordfish, mackerel, tuna, tilefish, crab

47
Q

Clinical presentation - Mercury

A

Inhalation
Inorganic Ingestion (caustic)
Organic Ingestion
Chronic Toxicity

48
Q

i. Inhalation - Mercury

A

i. Inhalation
1. Fever, chills, n/v/d, abd pain, decreased vision, metallic taste,
pulmonary edema or chemical pneumonitis may develop

49
Q

ii. Inorganic Mercury ingestion (caustic)

A
  1. Oropharyngeal pain, hematemesis, hematochezia, intestinal necrosis,
    renal failure, shock
50
Q

iii. Organic Mercury ingestion

A
  1. CNS manifestations (dysarthria, ataxia, constriction of visual field,
    hearing impairment, paresthesias). Slow onset but permanent effects
51
Q

iv. Chronic Mercury toxicity

A
  1. “pathological shyness”
  2. Acrodynia
    a. Chronic exposure to heavy metals. “Pink’s disease” manifests by painful pink discoloration of hands/feet with sweating, HTN, neuro changes, photophobia, and peeling rash
52
Q

Prevention - Mercury

A

i. Do NOT vacuum spilled mercury as it may aerosolize (more dangerous)

53
Q

Labs - Mercury

A

i. Whole blood levels for acute
ii. Urine levels for chronic
1. Hair levels for chronic organic mercury (urine not accurate)

54
Q

Treatment - Mercury

A

i. Elemental mercury (metallic)
1. DMSA/Succimer (PO)
2. Unithiol (DMPS) PO
3. Penicillamine (PO)
a. GI Side effects limit use
4. AVOID BAL (may cause redistribution of mercury to brain)

ii. Inorganic mercury salts
1. Unithiol (DMPS) IV
2. BAL (IM)
3. DMSA/Succimer (PO)

iii. Organic
1. DMSA/Succimer (PO)
2. NAC (organic)
3. AVOID BAL (may cause redistribution of mercury to brain)

  • YES Activated charcoal
  • No dialysis for mercury removal
55
Q
  1. Cadmium
A

a. Inhalation exposure is common during mining and smelting of zinc, copper and lead
* s/s similar to metal fume fever
1. fever, chills weakness, headache, n/v
2. may have pulmonary edema

b. Ingestion exposure: water, and food (esp shellfish, liver and kidney meats)
i. GI distress (corrosive effects). Pulmonary, facial and pharyngeal edema reported
ii. Renal failure and skeletal system effects

56
Q

c. Labs - Cadmium

A

i. Blood levels (acute)

ii. Urine levels (chronic)

57
Q

d. Treatment - Cadmium

A

i. Symptomatic
ii. No chelation. No charcoal. No dialysis.
iii. Do not use BAL, penicillamine or EDTA d/t increased risk for renal damage

58
Q

Arsenic (chelator)

A

Initial Chelator
- Unithiol, BAL

Secondary Chelator
- Oral unithiol or oral succimer
(DMSA)

59
Q

Iron (chelator)

A

Chelator

- Deferoxamine

60
Q

Lead (chelator - encephalopathic)

A

Chelator

- BAL, Calcium EDTA

61
Q

Lead (chelator - not encephalopathic)

A

Chelator

- Oral succimer (DMSA), Unithiol

62
Q

Mercury elemental (chelator)

A

Chelator
- succimer (DMSA), unithiol,
penicillamine
AVOID BAL

63
Q

Mercury inorganic (chelator)

A

Chelator

- Unithiol, BAL, Succimer (DMSA)

64
Q

Mercury organic (chelator)

A

Primary Chelator

  • Succimer (DMSA)
  • Avoid BAL.*

Secondary Chelator
- Give NAC and AC

65
Q

Cesium (radioactive metal) - chelator

A

Chelator

- Prussian blue

66
Q

Americum (radioactive metal) - chelator

A

Chelator

- DTPA or EDTA

67
Q

Thalium (soft metal) - chelator

A

Primary Chelator
- Prussian blue

Secondary Chelator
- AC, BAL

68
Q

5.7 Given a dermal exposure to caustic chemicals,

A

identify the appropriate treatment.

69
Q
  1. Caustic (alkalis) and Corrosive (acids)
A

a. Injury worse with pH <3 or > 11

b. Injury depends on
i. Ph
ii. Concentration
iii. Amount consumed
iv. Duration of contact

70
Q

c. TAR level

Titratable acid or alkaline reserve (TAR)

A

Amt of tissue required to neutralize substance. The larger the number, the greater ability to damage.

71
Q

d. Treatment (Caustic and Corrosive)

A
  • Airway
  • Antiemetics
  • Fluids
  • Avoid heroic decon techniques (NO charcoal; dilution not always recommended,
    no NG unless massive hydrofluoric acid with systemic effects
  • Endoscopy 12-24 hrs. consult surgery if evidence of perforation
72
Q

i. Acids

A
  1. Common ex: automotive batteries, metal, toilet and tile cleaners, roach powders, antiseptics, swimming pool products, rust removers and some drain cleaners
  2. Immediate coagulation type necrosis that creates a protective eschar
73
Q

ii. Alkalis

A
  1. Common ex: drain cleaners, detergents, lye, ammonia, toilet bowel cleaner, hair relaxers, metal cleaner, bleach
  2. Liquefactive necrosis with continued penetration into deeper tissues
74
Q

iii. Button batteries

A
  1. Corrosive effects from metal salts, direct impaction, and possible discharge of electrical current at site of impaction
75
Q

iv. Other agents

A
  1. May act by alkylating, oxidizing, reducing or denaturing cellular proteins or by defatting surface tissues
76
Q

f. Toxicity

A

i. Increased by concentration, duration of exposure and volume ingested

77
Q

i. Inhalation

A
  1. Upper resp tract irritation or injury, pneumonitis, noncardiogenic pulmonary edema
78
Q

ii. Eye or skin

A
  1. Immediate pain, redness, blistering, burns and blindness
79
Q

iii. Ingestion

A
  1. Oral pain, dysphagia, drooling, throat/chest/abdominal pain, perforation, hematemesis, strictures
80
Q

iv. Systemic toxicity

A
  1. May occur after inhalation, dermal or ingestion exposure
81
Q

a. Formaldehyde

A

i. Metabolic acidosis and fomate poisoning

82
Q

b. Hydrofluoric acid (automotive rim cleaner)

A

i. Hypocalcemia and hyperkalemia

83
Q

c. Methylene chloride

aerosol and pesticide products and is used in the manufacture of photographic film

A

i. CNS depression, cardiac arrhythmias, converted to CO

84
Q

d. Oxalic acid (oxalates found in some plants)

A

i. Hypocalcemia and renal failure

85
Q

e. Paraquat (herbicide)

A

i. Pulmonary fibrosis

86
Q

f. Potassium Permanganate (found in some fungal skin infections preps and antiseptic mouth washes)

A

i. Methemoglobinemia

87
Q

g. Phenol

A

i. Seizures, coma, hepatic and renal damage

88
Q

h. Phosphorus

A

i. Hepatic and renal injury

89
Q

i. Picric acid (military explosive, as a yellow dye, and as an antiseptic)

A

i. Renal injury

90
Q

j. Silver nitrate (cauterize infected tissues around a skin wound and for wart and skin tag removal)

A

i. Methemoglobinemia

91
Q

k. Tannic acid (chestnut and oak trees)

A

i. Hepatic injury

92
Q

Treatment

A
  1. Protect airway
  2. Dilute (water or milk)
  3. Lavage (ok for some substances)
  4. Charcoal
    a. consider if agent can cause systemic toxicity
  5. Irrigate for dermal or eye exposure
    a. Goal eye pH 7.4
  6. Antiemetic to decrease aspiration risk and repeat esophageal injury
  7. Endoscopy to assess for damage
93
Q
  1. Hydrofluoric Acid
A

a. corrosive ingestion and systemic toxicity
b. ex rust cleaners, brick cleaners, glass etching, jewelry cleaners, rim cleaners
c. pain out of proportion to visible injury
d. may be delay of 1-24 hrs before symptom onset depending on concentration of acid

94
Q

e. s/s - Hydrofluoric Acid

A

i. hypocalcemia
1. muscle spasms, tremors, headache, sz, hyperreflexia, prolonged QT

ii. hypomagnesemia
1. prolonged QT

iii. hyperkalemia
1. peaked T-waves, widened QRS, AV block, bradycardia

95
Q

f. Treatment - Hydrofluoric Acid

A

i. Estimated toxic dose 5-10 mg/kg
ii. correct electrolyte abnormalities
iii. correct acidosis with bicarb
iv. consider gastric emptying with NG aspiration
v. calcium carbonate; magnesium/aluminum antacids or milk to stomach
vi. topical calcium gel (calcium gluconate)
vii. SQ, IV infusion, or intra-arterial infusion of calcium gluconate
viii. Eye irrigation with saline or 1-2% calcium gluconate solution
ix. Nebulized 2.5% calcium gluconate

96
Q
  1. Cyanide
A

a. Primary effects
i. Chemical asphyxiant
ii. Blocks the aerobic utilization of oxygen

b. Methods of exposure
i. Inhalation
ii. Dermal (solution well absorbed dermally)
iii. Ingestion
iv. possible secondary exposure to healthcare workers

97
Q

c. S/S - Cyanide

A

i. Elevated lactate (>10), elevated anion gap; elevated venous pO2 (>40) (ie. minimal difference between ABG and VBG O2)

ii. Abrupt onset of profound toxic effects after exposure
1. Headache, nausea, dyspnea, confusion, syncope, seizures, coma, agonal respirations, cardiovascular collapse
2. *severe lactic acidosis
3. *elevated venous oxygen saturation
4. *anion gap metabolic acidosis

98
Q

d. Treatment - Cyanide

A

i. Cyanide kits
ii. Hydroxycobalamin
iii. Charcoal

99
Q

Cyanide kits

A
  1. Amyl nitrate
    a. Pearl to inhale
    b. Produce cyanide-scavenging methemoglobinemia
    c. May cause hypotension and worsening cellular hypoxia if CO toxicity
    d. Contraindicated in smoke exposure
  2. Sodium nitrate
    a. 300mg IV (6mg/kg pediatric max of 300mg)
    b. Produce cyanide-scavenging methemoglobinemia
    c. May cause hypotension & worsening cellular hypoxia if CO toxicity (methemoglobinia)
    d. Contraindicated in smoke exposure
  3. Sodium thiosulfate
    a. 12.5g IV
    b. Accelerates conversion of cyanide to thiocyanate
100
Q

Hydroxycobalamin

A
  1. 5g IV over 15 min (70mg/kg pediatric)
  2. Creates vitamin B6
  3. Does not create hypotension
  4. Turns skin/urine red
101
Q

Nitrogen Dioxide (NO2)

A
  • Silo gas
  • Often yellow to reddish brown in color
  • Heavier-than-air
  • The nitrogen dioxide combines with water in the lungs to form highly corrosive nitric acid

Symptoms:
Pulmonary edema, pneumonitis, bronchitis, bronchiolitis, emphysema and possibly methemoglobinemia. Usually, no symptoms occur, except a slight cough, fatigue, and nausea. However, potentially fatal pulmonary edema can occur following minimal early symptoms.

1) Acute effects may or may not develop within one to two hours after exposure, and include tachypnea, tachycardia, fine crackles and wheezing, and cyanosis. Another acute scenario involves dyspnea and coughing which subside over two to three weeks.
2) The second stage involves abrupt development of fever and chills, more severe dyspnea, cyanosis, and pulmonary edema. There is no correlation between severity of the first and second stages.
3) Recovery may be either complete or may involve some degree of impairment of pulmonary function.

Mike (17 decks)

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