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Weapons of Mass Destruction

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Presentation on theme: "Weapons of Mass Destruction"— Presentation transcript:

1 Weapons of Mass Destruction
The Chemical Agents

2 Stevan Cordas DO MPH Consultant Bioterrorism - Chemical WMD - Texas Department of Health Local Emergency Planning Committee - Tarrant county (toxicology) Medical Reserve Corps oversight committee. Clinical Associate Professor TCOM Certified internal medicine, allergy immunology, occupational medicine



5 Nerve Agents Are related to organophosphate pesticides.
Are lethal in small amounts. Act as cholinesterase inhibitors at receptor sites. 5 nerve agents are currently recognized – GA or tabun, GB or sarin, GD or soman, GF and VX. Toxicology definitions LD50 is the dose that is lethal to 50% of the population. ID50 is the dose that is incapacitating to 50% of the population. LC50 is the concentration in air in a given period of time (usually one hour) that will kill 50% of the test animals. Ct is an estimate of dose.C is the concentration of vapor in air expressed as mg/m3 and t represents time.Thus the Ct is the product of the concentration per time. It does not indicate how much is retained or inhaled however. LCt50 is defined as the concentration of vapor per unit of time that is lethal to 50% of the population. Haber’s law states that the Ct to produce a given biological effect is usually constant over an interval of several minutes to several hours. As an example., an effect produced by 0.05mg/m3 for 100 minutes is also produced by 5mg /m3 for 1 minute. The Ct is 5mg.min/m3 in both cases. This is a way of discussing the dose response curve. Toxic chemicals can produce either a local or a systemic effect. Some local agents can later develop systemic effects.

6 Organophosphates and Carbamyl Agents
Diazinon (Spectracide) Malathion Parathion Chlorfenviphos Dimethoate Ronnel Nerve Gas Agents Pyridostigmine (Mestinon) Physostigmine (Antilirium) Neostigmine (Prostigmine) Cognex and others Sevin Dust, Carbaryl and many others

7 History of Nerve Gas First organophosphate –1854
Tabun (GA) - Schroeder – discovered 1936 Sarin (GB) – Schroeder – discovered 1937 Military production of tabun –nazi –1942 30,000 tons of tabun produced Soman (GD) – discovered 1944

8 History of Nerve Gas GF discovered Schroeder – 1944
VX discovered Port Down, England –1955 Russians captured tabun factories and start their own production-1946 United states and England start their own production. – Edgewood chemical and biologic center. –

9 History of Nerve Gas President Nixon orders all chemical and biologic agents destroyed. – 1969. Chemical stockpiles partially destroyed in the United States. Soviet union continued production – developed Novilchek agents - current production status uncertain.

10 History of Nerve Gas Iraq develops tabun and uses it against Iran – Iraq also used tabun against Kurdish dissidents. Iraq admits to placing sarin in scuds and artillery operation desert storm. Large amounts of chemical containers destroyed by U.S. forces 1991 – 98,900 low level exposures. – Gulf war syndrome emerges.


12 History of Nerve Gas First attack by Japanese cult using sarin gas – 7 dead and 200 injured. 1995 – Second attack – same cult using sarin in Tokyo subways – 12 dead and 6000 injured. 1998 – Traces of VX found in Iraqi warheads. 2001-London police find sarin plans –thwart attack. 2001- Insecticide bomb found on terrorist in Israel.

13 Sarin Also known as GB; phosphonofluoridic acid, methyl, isopropyl ester; Isoproposmethylphosphonyl fluoride Odorless and colorless Heavier than air – hovers near the ground More lethal in higher temperature Degrades faster with rise in humidity 26 times more deadly than cyanide gas

14 Basic Mechanism Nerve gases bind to an esterase (ChE) that breaks down acetylcholine after it is released from the nerve end plate. After a period of time this binding undergoes complex changes and cannot not be reversed – this is called “aging.” This results in an excess acetylcholine (ACh) syndrome which affects the muscarinic and nicotinic receptors. They are chemically similar to organophosphate pesticides and exert their biological effects by inhibiting acetylcholinesterase enzymes. G-type agents are clear,colorless, and tasteless liquids that are miscible in water and most organic solvents. GB is odorless and is the most volatile nerve agent; however, it evaporates at about the same rate as water. GA has a slightly fruity odor, and GD has a slight camphor-like odor. VX is a clear, amber-colored, odorless, oily liquid. It is miscible with water and soluble in all solvents. It is the least volatile nerve agent. Nerve agents alter cholinergic synaptic transmission at neuroeffector junctions (muscarinic effects), at skeletal myoneural junctions and autonomic ganglia (nicotinic effects), and in the CNS. Initial symptoms depend on the dose and route of exposure.

15 The ACh Goes to Muscarinic and Nicotinic Receptor Sites.
Muscarinic effects include pinpoint pupils; blurred or dim vision; conjunctivitis; eye and head pain; hypersecretion by salivary, lacrimal, sweat, and bronchial glands; narrowing of the bronchi; nausea, vomiting, diarrhea, and crampy abdominal pains; urinary and fecal incontinence; and slow heart rate. Nicotinic effects include skeletal muscle twitching, cramping, and weakness. Nicotinic stimulation can obscure certain muscarinic effects and produce rapid heart rate and high blood pressure. Relatively small to moderate vapor exposure causes pinpoint pupils, rhinorrhea, bronchoconstriction, excessive bronchial secretions, and slight to moderate dyspnea. Mild to moderate dermal exposure results in sweating and muscular fasciculations at the site of contact, nausea, vomiting, diarrhea, and weakness. The onset of these mild to moderate signs and symptoms following dermal exposure may be delayed for as long as 18 hours. Higher exposures (any route) cause loss of consciousness, seizures, muscle fasciculations, flaccid paralysis, copious secretions, apnea, and death.

16 Signs and symptoms of Nerve Gas
Miosis, dim vision, pain in eyes Severe rhinorrhea, lacrymation Bronchorrhea Nausea, Vomiting Diaphoresis Memory, fatigue, anxious, impaired judgment Nerve agents are readily absorbed from the respiratory tract. Rhinorrhea and tightness in the throat or chest begin within seconds to minutes after exposure. Nerve agent vapors are heavier than air. Odor does not provide adequate warning of detection. The estimated LCt50 (the product of concentration 50 times time that is lethal to 50% of the exposed population by inhalation) ranges from 10 mg-min/m3 for VX to 400 mg-min/m3 for GA.

17 Signs and symptoms of Nerve Gas
Increased airways resistance. Diarrhea and involuntary micturition. Local or generalized muscle fasciculations. Muscle fatigue then flaccid paralysis. Convulsions and Coma. DUMBELS Nerve agent liquids are readily absorbed from the skin and eyes. Vapors are not absorbed through the skin except at very high concentrations. Ocular effects may result from both direct contact and systemic absorption. The nature and timing of symptoms following dermal contact with liquid nerve agents depend on exposure dose; effects may be delayed for several hours. As little as one drop of VX on the skin can be fatal and 1 to 10 mL of GA, GB, or GD can be fatal.

18 Clinical Picture When Exposed to Nerve Gas Vapor
In mild cases, miosis, rhinorrhea, slight tightness in chest or bronchospasm,slight dyspnea, increased secretions, ocular pain and frontal headaches. In moderate cases. An exaggeration of the above symptoms with marked dyspnea, nausea and vomiting. There are three routes of exposure and many agents have different symptoms dependant upon the exposure route. They are oral, inhalational and cutaneous. Some agents have more than one route of entry at the time of exposure. Factors related to toxicity: Factors related to the chemical. Composition, physical characteristics, presence of impurities or breakdown products. Factors related to the exposure. Dose concentration, route of exposure, duration Factors related to the person exposed. Heredity, immune status, nutritional status, hormones, age, sex, health status. Factors related to the environment. Media (air, water or soil), additional chemicals present, temperature, air pressure. The LCt50 for tabun is 400 mg.min/m3, for sarin vapor it is 100 mg.min/m3, for soman is is 50 mg.min/m3 and for VX it is 10 mg.min/m3.

19 Clinical Picture In severe cases the same symptoms as for moderate but also confusion, unconsciousness, muscular fasciculations (generalized), involuntary micturition and defecation, apnea, flaccid paralysis, convulsions, arrhythmias.

20 Case 1 27 year old male exposed to unknown substance that was lethal to others in the area. Subjective: Anxiety, nausea, rhinorrhea, mild chest tightness. Objective: Miosis, diaphoresis, elevated BP, regular heart rate, short onset time, seems stable. RBC cholinesterase 30% of normal.

21 Hazard to Health Professionals
Persons whose skin or clothing is contaminated with nerve agent can contaminate rescuers by direct contact or through off-gassing vapor. Persons whose skin is exposed only to nerve agent vapor pose no risk of secondary contamination; however, clothing can trap vapor.

22 Protect Yourself Nerve agent vapor is readily absorbed by inhalation and ocular contact and produces rapid local and systemic effects. The liquid is readily absorbed thorough the skin; however, effects may be delayed for several minutes to up to18 hours.

23 Respiratory Protection: Pressure-demand, self-contained breathing apparatus (SCBA) is recommended in response situations that involve exposure to any nerve agent vapor or liquid. Skin Protection: Chemical-protective clothing and butyl rubber gloves are recommended when skin contact is possible because nerve agent liquid is rapidly absorbed through the skin and may cause systemic toxicity.

24 Chemical casualty triage is based on walking feasibility, respiratory status, age, and additional conventional injuries. The triage officer must know the natural course of a given injury, the medical resources immediately available, the current and likely casualty flow, and the medical evacuation capabilities.

25 Category Effects Clinical Signs Immediate Moderate to severe effects in two or more systems (e.g., respiratory, GI, muscular, CNS) Seizing or post-ictal, severe respiratory distress or apneic. Recent cardiac arrest. Delayed Recovering from agent exposure or antidote Diminished secretions, improving respiration

26 Minimal Walking and talking Miosis, rhinorrhea, mild to moderate dyspnea Expectant Unconscious, Cardiac/respiratory arrest of long duration. Not expected to survive

27 Treat ABC Quickly ensure that the victim has a patent airway. Maintain adequate circulation. If trauma is suspected, maintain cervical immobilization manually and apply a decontaminable cervical collar and a backboard when feasible. Apply direct pressure to stop arterial bleeding, if present.

28 General Principles of Triage for Chemical Exposure
Check triage tag/card for any previous treatment or triage. Survey for evidence of associated traumatic/blast injuries. Observe for sweating, labored breathing, coughing/vomiting, secretions. Severe casualty triaged as immediate if assisted breathing is required.

29 General Principles of Triage for Chemical Exposure
Blast injuries or other trauma, where there is question whether there is chemical exposure, victims must be tagged as immediate in most cases. Blast victims evidence delayed effects such as ARDS, etc. Mild/moderate casualty: self/buddy aid, triaged as delayed or minimal and release is based on strict follow up and instructions.

30 Treatment of Nerve Gas Agents
Hold your breath. Get fresh air as soon as possible. If you have a respirator, put it on. In the military there are three kits – use them all. In the civilian sector the same first three rules apply. If the patient only has miosis 5 or 10 minutes after removal from agent, they probably don’t need treatment. The first rule in a military setting is to hold your breath, put on your gas mask and inject with one or more MARK1 kits either by yourself or your buddy. Nerve gas vapor can kill after you inhale only one or two breaths of it. Once masked (with an M40 or M17A2 respirator), immediate detoxification is important. In the military, self decontamination is taught as a vital second step along with giving the atropine. An M291 kit contains charcoal and sorptive resins and the M258A1 kit contain absorptive material in the form of two towelettes. One is for G agents and the other for VX. After a few minutes, a nerve agent penetrates the skin (10-20 minutes at most) and only the liquid type of agent, which is more persistent but still subject to evaporation, will need to be decontaminated. Skin decontamination is not required after nerve gas vapor exposure. Remove their clothes which may be contaminated. With liquid agents after you remove their garments, wash them down with Clorox diluted 1 to 10. Scrape any thick material off and place it in a sealed bag. Make sure the hair is washed. Wash the Clorox off with running water to complete detoxification. If adsorbents are not available flour or tissue paper may help absorb some of the material. Protect yourself or you may be a casualty. If is a liquid agent, such as VX, make sure you are adequately protected if you have the potential to be exposed to the agent. MOPP 4 or Level A protection is required. If it is a non-persistent vapor, a respirator and butyl or Neoprene gloves are required. In the medical setting you usually do not have the opportunity to help those exposed to the highest concentration of the gas or liquid. They will fatalities unless they are in a military setting and well trained and equipped to help themselves or their buddy. Thus you will be seeing individuals with a lesser amount of exposure. They may divided into mild , moderate and severe signs and symptoms (see slide) Decide if further treatment is required and if you are seeing them early or late after exposure. If they seem to be getting worse give Atropine and 2-PAM. In the military, there are three MARK I kits each containing 2 mg of atropine. Current military policy is to give all three followed by an autoinjector with 10 mg of Valium. The 2-Pam is given if clinical symptoms develop on a prn basis.

31 Mark I Kit If the military Mark I kits containing autoinjectors are available, they provide the best way to administer the antidotes. One autoinjector automatically delivers 2 mg atropine and the other automatically delivers 600 mg 2-PAM Cl.

32 Decontaminate as a Priority
Rapid decontamination is critical to prevent further absorption by the patient and to prevent exposure to others. Decontaminable gurneys and back boards should be used if possible when managing casualties in a contaminated area. Decontaminable gurneys are made of a monofilament polypropylene fabric that allows drainage of liquids, does not absorb chemical agents, and is easily decontaminated.

33 If water supplies are limited, and showers are not available, an alternative form of decontamination is to use 0.5% sodium hypochlorite solution, or absorbent powders such as flour, talcum powder, or Fuller's earth If exposure to vapor only is certain, remove outer clothing and wash exposed skin with soap and water or 0.5% sodium hypochlorite. Place contaminated clothes and personal belongings in a sealed double bag.

34 Specific Therapy for Nerve Gas
Give atropine sulfate 2mg IV and 2 mg IM stat. Manage Airways, breathing and circulation. Early intubation and ventilatory support with oxygenation. Repeat atropine 2mg IM every 5 or 10 minutes and watch for return of copious secretions and increasing dyspnea. For severe sx, 6 mg is given initially. Follow atropine with Pralidoxime (2-PAM) Protopam in I g vials. 15 to 25 mg/kg or given over 15 minutes IV. 15 mg/kg IM for mild to moderate cases None of these agents is a truly specific antidote but the atropine acts by blocking the effects of the excess acetylcholine at muscarinic receptor sites. This agent does not block the effect of the nerve agent as it binds to the acetylcholinesterase. The 2-PAM (pyridine –2- aldoxime chloride) helps to reactivate the organophosphate inhibited cholinesterase. In the civilian sector it is best to give one vial (I gram) of Protopam (Wyeth-Ayerst), which is 2 PAM Cl, IV over a 15 to 20 period of time. Hypertension will result which lasts several hours. It will help the fasciculations (nicotinic effect) but do not give too often. No more than 2.5 g for the first 1.5 hours. If the organophosphate ChE complex ages or becomes fixed, then oximes will not work. Soman fixes rapidly so that drug therapy is relatively ineffective for this agent. Physostigmine used preventively is the best treatment for agents that fix rapidly. Physostigmine is a carbamate that reversibly attaches to the ChE receptor and acts as a competitive inhibitor for GD. Sarin takes about 5 hours to fix. Tabun is longer. VX does not age.

35 2 PAM 2-PAM Cl solution needs to be prepared from the ampoule containing 1 gram of desiccated 2-PAM Cl: inject 3 ml of saline, 5% distilled or sterile water into ampoule and shake well. Resulting solution is 3.3 ml of 300 mg/ml. Mild/Moderate symptoms include localized sweating, muscle fasciculations, nausea, vomiting, weakness, dyspnea. Severe symptoms include unconsciousness, convulsions, apnea, flaccid paralysis.

36 Effect of Atropine

37 Treatment (contd.) Little effect of 2 PAM treatment on Soman (GD) due to rapid aging. Pyridostigmine pretreatment is most helpful here and has some value with GA. Given orally 30mg every 8 hours. If the individual is alive 5 minutes after inhaling the vapor they probably can make it with your help.

38 RBC Cholinesterase Levels
With minor adverse effects there is no correlation with RBC-ChE levels. With vomiting one can suspect that at least inhibition of 50 to 90% of the baseline ChE has occurred. Often used to verify organophosphate poisonings. Only decreased by pernicious anemia. There are three cholinesterases in the human body. (a) Tissue cholinesterases which cannot be readily measured, (b) butyrochloineserase (BuChE). BuChE is present both in tissue and blood. It is produced in liver with a replacement time of about 50 day. (c) RBC cholinesterase (RBC-ChE). BuChE is relevant because it is sometimes found to be low or abnormal in the population and if so will adversely influence individuals receiving succinylcholine with anesthesia causing prolonged paralysis. About 0.3% of the population is homozygous for low BuChE activity. Since RBC-ChE levels are more stable than BuChE this test is considered more reliable and is used to monitor a organophosphate poisoning. RBC have a life of 120 days. Recovery after a poisoning occurs only with production of new RBCs –about 1% per day. The blood ChE will be inhibited before the tissue CheE. Though BuChE activity is significantly more affected than RBC-ChE by such common insecticides as malathion and parathion, nerve gases cause the reverse with RBC-ChE rapidly reversed.

39 Late effects of Nerve Gas Attacks
Generally no serious adverse effects 6 months late. With convulsions and apnea, inability to learn new tasks, memory impairment and retrograde amnesia has occurred. No clear evidence of peripheral neuropathy or intermediate syndrome.

40 Resource for more information
Agency for Toxic Substances and Disease Registry Division of Toxicology 1600 Clifton Road NE, Mailstop F-32 Atlanta, GA Phone: ATSDR ( ) FAX:   (770)


42 Blister Gases HD, H, HN2, HN3, CX, L
Blister gases are HD for sulfur mustard, H for impure sulfur mustard, which originally stood for Hun. HN1, HN2, HN3 were discovered after the war by substituting nitrogen for the sulfur. HN3 is in some nations chemical inventory as a vesicant and respiratory irritant. HN2 later became known as Mustargen and was used as a mainstay for early cancer treatment as it is an alkylating agent. CX is Phosgene Oxime, an immediate reacting vesicant and L is Lewisite which contains arsenic instead of sulfur.

43 2,2, - Di (Chloro-ethyl)-sulfide
Sulfur Mustard, 2,2, - Di (Chloro-ethyl)-sulfide

44 H and HD Pure Mustard Gas is HD, impure is H.
Sulfur Mustard is a vesicant and a respiratory irritant. It was the most effective chemical agent in WWI accounting for 85% of the chemical injuries. Besides being a severe respiratory irritant, it affected the skin like a burn with painful blisters,. The eyes, axilla and scrotum were especially sensitive. HD is 2,2 di(chloroethyl) sulfide. In high dose it can be lethal however in 85% of cases it produces prolonged morbidity, not mortality. It would easily tie up a civilian hospital group if a large amount of casualties occurred from this agent. The only military casualty in the Gulf War was burned by HD in a captured bunker. He was left with some scars. No actual mustard was used on U.S.troops in that war but we know that Sadam had deployed this agent in the front line. The Iraqis used this agent against Iran in their war and also on their own Kurdish citizens. It is estimated that 17 nations have this type of chemical agent.

45 History of Blister Gas 1822- First discovered.
1860- Ability to produce burns and vesicles proven. 1917 – Used by Germans for the first time at Ypres, France. Called Yperite by French. Lost by Germans. Called yellow cross by the allies and later H and HD. H stood for Hun. HD produced 85% of chemical casualties in WWI.

46 History of Blister Gas French quickly followed as did English. The US troops used French blister canisters and shells. Captain Lewis’ team discovers lewisite 1918. US production after WWI begins Pine Bluff and Aberdeen Proving Ground as chemical warfare department under war department forms in latter days of WWI. Especially from 1950 to 1969.

47 History of Blister Gases
No use in WWII, Korea or Viet Nam of blister gases. Bari incident Dec 1981 Iraq uses HD against Iran. 1984 Iraq uses HD against Kurds. 1991 Iraq deploys HD but doesn’t have a chance to use them.


49 WWI Mustard Casualties and % Death
Germany 200,000 4.5 France 190,000 4.2 Britain 189,000 U.S. 73,000 2 Russia 475,000 11.8

50 Physical Properties Thick oily amber to brown liquid which freezes/melts at 58° F. Heavier than air (vapor) or water (liquid). Persistent. Penetrates skin in 2 minutes. Causes cellular damage in 5 minutes. Delayed onset of clinical effects hours.

51 Diagnosis Delayed onset of clinical symptoms.
Urinary thiodiglycol levels elevated. Possible chemical pneumonia manifestations on x-ray. Mainly a clinical diagnosis depending on the circumstances. M8, M9 ( paper if liquid Mustard). CAM.

52 Although it is a nonspecific finding, leukopenia can indicate vesicant exposure. It usually begins 3 to 5 days after exposure. With a white blood cell count < 500, the prognosis is poor.

53 Effects of Mustard Mustard enter the skin rapidly and convert to cyclic agents that are alkylating agents. They are mutagenic, teratogenic, cytotoxic, and ultimately carcinogenic. DNA adducts are formed and cross linkage damage occurs. The incidence of lung cancer is increased slightly in Mustard survivors than controls. The gas is really a oily liquid that vaporizes easily.. It is colorless and odorless in the pure state but in the impure state on the battlefield, it appeared brown to yellowish with a smell of garlic. It vaporized with increasing temperature so the Germans (and later the Allies) would deploy it at night and the thick vapor would roll with the prevailing wind low to the ground and drop into the trenches. The troops would expect that it was all right to remove their gas masks hours later when daylight occurred. As the temperature increased so did the volatility of Mustard so that those troops without a gas mask were poisoned. It readily penetrates clothing and the gas masks of those days did not offer much protection.

54 Clinical Aspects of Mustard
Mild cases –the eyes will develop an irritating conjunctivitis that lasts approximately two weeks. Respiratory symptoms do not occur. The skin will turn reddish and itch or burn. There is always a latent period of 4 to 12 hours before clinical symptoms occur with Mustard even though the damage occurs quickly. In slightly more severe cases the skin will look like scarlet fever. With modest exposure after a latent period of at lest 2 hours, the eyelids would swell and close, more conjunctival and corneal swelling and temporary blindness would occur though permanent blindness with mustard is uncommon. Upper respiratory symptoms begin with hoarseness leading to aphonia. There may be actual vocal cord damage. Rhinorrhea occurs with thick discharge and chest pain, bronchitis with increasingly abnormal pulmonary function tests noted. Late pulmonary effects continue to plague many Mustard survivors and there were continuing deaths in the 1920s, will after the war ended from emphysema and bronchitis symptoms, recurrent respiratory infections including pneumonia. In moderate doses frank blisters form on the skin. The blisters are not tender, they are thin walled and the fluid is not toxic. With higher amounts of agent or direct liquid contact the blisters may become necrotic. Pigmentation of the skin is common after Mustard burns even if vesicles don’t form.

55 Clinical Aspects of Mustard
High doses will increase mortality, usually from delayed toxic pulmonary edema. CNS effects including convulsions occur. Severe neutropenia and thrombocytopenia can occur. Those who recover are often hospitalized for months even in the more recent poisonings.

56 Differential diagnosis
Barbiturates Chemotherapeutic agents Carbon monoxide Stevens-Johnson syndrome Staphylococcus scalded skin syndrome Toxic epidermal necrolysis Bullous pemphigoid Pemphigus vulgaris Other chemical burns (such as with strong acids, bases, or corrosives)

57 Gassed by John Singer Sargent
Gassed by John Singer Sargent. The bandages over their eyes indicate that they were gassed by Mustard.

58 Treatment of Mustard Gas Casualties
Decontaminate the eyes with water, saline or a weak sodium bicarbonate solution. Remove clothes and bag properly. Decontaminate the skin with 0.5% (1 to 10 dilution) Clorox. Wash this off after 4 or 5 minutes with soap and water. Antibacterial eye drops. Systemic narcotics prn. Provide general supportive care. It is possible for the physician to become poisoned by the patient so follow level A regulations as published in Managing Hazardous Materials Incidents as published by the Department of HHS, ATSDR. This can be obtained free. It will direct you in how to set up the emergency room, how to protect yourself and how to detoxify and protect the patient. Various military sources are available as well. There is no specific antidote to this compound. The same treatment principles apply to the nitrogen mustards that are reviewed for sulphur or sulfur mustard. Nontoxic pulmonary edema is treated aggressively with oxygen, PEEP or intubation and ventilation. Steroids are often used but may have little effect. Anorexia, fever depression, malaise occur as systemic effects.

59 Management Eyes – Avoid topical anesthetics or analgesics.
Use mydriatics, topical antibiotics. Vaseline on lids (Don’t use eye patch. Sunglasses.

60 Skin Unroof blisters. Fluid is non-toxic. Debridement of burns.
Soothing lotions. Frequent irrigations. Systemic analgesics. Electrolyte and fluid replacement but not like that for burns.

61 Airways Steam, Cough suppressants. Oxygen. Bronchodilators, Steroids.
Early intubation may be required. Specific antibiotic administration. Avoid prophylactic antibiotics, Assisted ventilation.

62 Marrow May need to use: Reverse isolation. Hormonal therapy.
Marrow transplants. Cellular replacement i.e. platelet transfusions etc.

63 Death Usually pulmonary with higher exposure concentrations.
Secondary infection common and can be fatal. Radiomimetic effect of HD depresses immunity.


65 Lewisite Lewisite or L (NATO) an immediate reacting vesicant that closes the eyes with blepharospasm quickly and produces vesicles. And respiratory effects including pulmonary edema circulatory effects and death can result from this agent. Lewisite is a dark brown liquid in the preparation used in munitions. It smells like geraniums but is instantly very irritating to the eyes, skin and respiratory tract.It is 2-chlorovinyl dichloroarsine. With strong alkalis it becomes a non-vesicant. It is soluble in solvents and hydrolyzes rapidly. It is stored at only one facility at Toole Army Depot in Utah and is or has been slated for destruction by treaty. There is a delay at destroying our stockpile of chemical weapons as mandated by Presidential order in 1969. It can produce systemic effects as it contains arsenic and interferes with lipoic acid, sulfhydryl radicals and other enzyme systems. These effects are usually not as significant as the burning eye and skin pathology or the severe respiratory symptoms. The blisters start in about 1 to 2 hours last about 72 hours. In more severe cases, besides pulmonary edema, severe bronchial damage may occur, capillary leakage with anasarca leading to hypovolemia and renal compromise.

66 Treatment of Lewisite Poisoning
Decontamination is critical and must be performed rapidly as the number one priority. Remove form the agent, Remove the clothes, Make sure you decontaminate the hair. Give BAL, DMPS or DMSA to act as an antidote to this agent. Lewisite was named after Capt. W.L.Lewis who led an Allied team who synthesized it in It was not used in the war. British–Anti Lewisite (BAL) can be made in topical ointments, dilute eye drops, and given systemically at 3 mg deep IM, of the 10% in oil solution, every 4 hours for 2 days. 50% of recipients get sick from the BAL but the treatment is not worse than the disease. Newer agents such as meso-dimercaptosuccinic acid (DMSA) or dimercapto-1-propanesulfonate (DMPS) are more efficient in removing arsenic, safer, and can reduce the intracerebral arsenic level whereas BAL causes it to rise. Detoxification can be carried out with a 10% sodium carbonate solution since the agent is neutralized by alkaline material. Follow this in 5 minutes with soap and water.

67 Phosgene Oxime Dichlorformoxime is a colorless powder that is not a vesicant but an urticant. It commonly produces deep necrosis of the skin and muscle as well and is one of the most severe irritants known. It is termed CX by NATO. It will vaporize at room temperatures. Can cause pulmonary edema and death. One drop of this agent on the eye will cause coagulation necrosis with penetration of the cornea. One drop on the skin will cause it to turn white from immediate coagulation necrosis. There is no battlefield use of this agent that I am aware of. There is no specific antidote. Treat the eye as a corrosive injury, treat the lungs as you do for a toxic or noncardiac pulmonary edema. In decontaminating this agent, use sodium bicarbonate and not a chlorinating agent.

68 As a review of signs and symptoms as pertain to different vesicants the following slides are offered as a review of systems.

69 Respiratory signs and symptoms
Clear rhinorrhea Nasal irritation/pain Sore throat Cough Dyspnea (shortness of breath) Chest tightness Tachypnea Hemoptysis

70 Dermal signs and symptoms
Itching Immediate blanching (phosgene oxime) Erythema (immediate with lewisite and phosgene oxime, may be delayed for 2 to 24 hours with mustards) Blisters (within 1 hour with phosgene oxime, delayed for 2 to 12 hours with lewisite, delayed for 2 to 24 hours with mustards) Necrosis and eschar (over a period of 7 to 10 days)

71 Ocular signs and symptoms
Conjunctivitis Lacrimation Eye pain/burning Photophobia Blurred vision Eyelid edema Corneal ulceration Blindness

72 Cardiovascular signs Hypotension (with high-dose exposure to lewisite) Atrioventricular block and cardiac arrest (with high-dose exposure) Gastrointestinal signs and symptoms (prominent if ingestion is a route of exposure) Abdominal pain Nausea and vomiting Hematemesis Diarrhea (sometimes bloody)

73 Central nervous system signs and symptoms (with exposure to high doses)
Tremors Convulsions Ataxia Coma

74 Because no antidote exists for mustard exposure, the best thing to do is avoid it. If the nitrogen mustard release was indoors, get out of the building. If the release was outdoors, move away from the area of the release, stay upwind if possible, and seek higher ground. Quickly moving to an area where fresh air is available is highly effective in reducing the possibility of death from exposure to nitrogen mustard.

75 Remove Clothing If you think you may have been exposed, you should remove your clothing, rapidly wash your entire body with soap and water, and get medical care as quickly as possible. Quickly take off clothing that has nitrogen mustard on it. Any clothing that has to be pulled over the head should be cut off the body instead of pulled over the head.

76 Washing yourself: As quickly as possible, wash any nitrogen mustard from your skin with large amounts of soap and water. Washing with soap and water will help protect people from any chemicals on their bodies. If your eyes are burning or your vision is blurred, rinse your eyes with plain water for 10 to 15 minutes. If you wear contacts, remove them and put them with the contaminated clothing. Do not put the contacts back in your eyes (even if they are not disposable contacts). If you wear eyeglasses, wash them with soap and water.

77 Dispose Place your clothing inside a plastic bag. Avoid touching contaminated areas of the clothing. If you can't avoid touching contaminated areas, or you aren't sure where the contaminated areas are, wear rubber gloves or put the clothing in the bag using tongs, tool handles, sticks, or similar objects. Anything that touches the contaminated clothing should also be placed in the bag.


79 Cyanogen chloride (CK) and hydrogen cyanide (AC)
Cyanogens Cyanogen chloride (CK) and hydrogen cyanide (AC) Cyanides have been used extensively in this country for manufacturing purposes. It is used in electroplating, gold and silver processing, tanning, metallurgy, chemical processing and other compounds. It has been used in executions, suicides and poisonings for many years. Cyanide poisoning has been reported from eating chokecherries, bitter almonds and apricot pits. It is a component of Laetrile. Cassava, a staple, is blamed for a high incidence of tropical ataxic neuropathy due to its amount of cyanide. Cigarette smoke contains cyanide so that the smoker has about 17 g/mL. (Controls average about 0.06 g/mL.) The gas chamber utilizes the principle of generating Hydrogen Cyanide (HCN). Dropping a cyanide salt into a strong acid produces it. Numerous international terror attempts have used HCN release. Most recently the Aum Shinrikyo cult used cyanide salt and acid in several restrooms in the Tokyo subway several weeks after the sarin nerve gas attacks in March 1995. Cyanogen chloride has a strong pungent odor. It does not dissolve in water well but does in organic solvents. It vapor is heavier than air (2.10 vapor density) and unlike hydrogen cyanide, it is very irritating to the eyes and mucous membranes and can produce pulmonary edema. This compound is usually non-persistent. CK’s boiling point is 12.9 C, vapor pressure is 1,010 mg Hg, and in a pure form it is a colorless gas or liquid. The LCt is 11,000 mg.min/m3.

80 Sources of Cyanide Available without a prescription
Rodenticides, Insecticides Silver and metal polishing solutions Fumigating products Photographic development solutions Tanning and electroplating industries Metallurgy - jewelers

81 History of Cyanides Used as a potion to kill “friends and enemies” since ancient Rome. Isolated and identified by Sheele 1784. Continues to be used in the “gas chamber” as potassium cyanide dropped into dilute sulfuric acid. Still popular in murder and suicide. Used by France as hydrogen cyanide gas. Called AC by military.

82 History of Cyanide Cyanogen chloride, also called CK by the military, introduced September 1916. Austrians tried cyanogen bromide about the same time. In WWII millions of civilians and captured soldiers died from hydrocyanic acid adsorbed on a dispersible base (Zyklon B), a rodenticide. Aum Shinrikyo 1995 attempt to kill more in Tokyo.

83 History of Cyanide Iraq felt to have used cyanide against Iran, the Kurds and a village in Syria in 7 killed from poisoned Tylenol A major cause of death from fires is cyanide from the combustion products of plastics and other man made material. Cassava, low grade CN poisoning, causes tropical ataxic neuropathy.

84 Additional History Who will forget the Jonestown massacre or the Tylenol deaths? Cause of toxic amblyopia for tobacco originated cyanide. Congenital flaw in cyanide metabolism lead to Leber’s Optic Atrophy.

85 Facts About Cyanides 50 mg of the gas and 500mg of the sodium or potassium salts is lethal. Cigarette smoke contains g/ml whole blood g/ml in Controls. Inhalation of gas kills in seconds. Longer period with the soluble > insoluble> cyanogen salts. Skin absorption is possible with this agent. Italian authorities arrested a Al Quaeda Cell it Italy with 9 lbs of potassium cyanide intending to poison the water of the US Embassy.

86 Pathophysiology Rapidly enters the blood through breath, intestine or skin. Cases histotoxic hypoxia by interfering with the respiratory cytochrome oxidase system. Greatest affinity for oxidized Iron at the cytochrome a-a3 complex. TWA 8 hours in US is 10 ppm. 100 ppm will kill in one hour. 300 ppm will kill in minutes. CN is an important killer in fires.

87 Clinical Aspects of Cyanide Poisoning
If not fatal, we see weakness of the legs, vertigo, headache and nausea. This may be followed by convulsions and death. At a high Ct, death will occur in 20 seconds. It is unlikely that you will encounter any of those cases. The survivors should be observed and if symptomatic treated. If symptoms are mild. one may defer the treatment since there is some risk with producing methemoglobin. Other clues to cyanide poisoning are a cherry red skin coloration since it causes a peripheral vasodilation, and a burnt almond smell which is only detectable to portion of individuals due to genetic traits. Blood cyanide levels must be performed on whole blood since most of the cyanide is rapidly within the red blood cell. It tends to fall in stored samples due to it’s short half life. Levels of 0.5 to 1.0 gm/mL are associated with early symptoms. Levels of 2.5 to 3 g/mL are associated with coma and levels over 3 are associated with death. One will not have the luxury of a cyanide level to make the diagnosis however and must rely on clinical circumstances.

88 Clinical Manifestations of Cyanide Poisoning
Gasping for air, hypertensive, bradycardic. Bulging eyes. Odor of bitter almonds - faint % can’t smell it. Cold clammy skin May have cherry red skin. Cyanosis late. Venous blood the same color as arterial blood – bright red or cherry pink. May look inebriated, confused, dizzy, nauseated. Chest pain.

89 Diagnosis of Cyanide Poisoning
Clinical diagnosis mainly. CYANTOSNO paper. Blood cyanide of 0.2 g/ml –Clinical toxicity begins. Blood cyanide of 1.0 to 2.5 g/ml stupor and agitation. Levels over 2.5 g/ml potentially fatal. Pulse oximetry not useful. Draw arterial and venous oxygen saturation. If less than 10 mm Hg suspect cyanide. Look for elevated lactate and metabolic acidosis. Plasma lactate > 6 mmol/L.

90 Treatment of Cyanide Poisoning
Use Lilly cyanide antidote kit. Manage ABC of emergency care. Remove from agent and remove any liquid cyanide that is present. But skin contamination is not required for the gas. First you must rapidly bind or fixate the cyanide ion either by creating methemoglobin or fixing it with cobalt compounds. Any person who is conscious and breathing normally more than 5 minutes after being exposed to and removed from cyanide agents will recover without any treatment as this substance is rapidly detoxified by the body. In those with symptoms, remove the patient from the source while wearing PPE. There are four methods used to fixate cyanide. (a)   Amyl nitrite is often used if there is a respiratory positive pressure present. Do not use amyl nitrate with oxygen as an explosion may occur. Follow this with sodium thiosulphate. In the military amy nitrate is used less than in the civilian sector. More meaningful and predictable levels of methemoglobin can be produced by the latter. If there is impairment with breathing, IV sodium nitrate should be used (10 cc of a 3% solution, 300mg over 3 minutes). This will produce methemoglobin, which binds the cyanide. Keep the patient flat or their blood pressure will fall from the nitrite. Try to obtain a little cyanosis to indicate methemoglobinemia A newer agent, 4-Dimethylaminophenol-hydrochloride (DMAP), is very effective in treating cyanide poisoning. If available, give it instead of the nitrites at a dose of 250 Mg IV slowly every hour until sodium thiosulphate is made available. The dose must be adjusted for children. Administer the sodium thiosulphate at a dose of 12.5 Gms (50 cc of a 50% solution over a 10 minute period of time.) The DMAP can be stopped once the sodium thiosulphate is given. This used by the German military and 3 mg/kg IV can produce a methemoglobin level of 15% in one minute. Disadvantages of 4-DMAP are necrosis in the area if given IM, increases in pain, fever and elevated muscle enzymes can be seen. Very high levels of methemoglobin are undesirable. Another alternative way to initially bind cyanide is with intravenous hydroxycyanocobalamine. This is commercially available but large amounts (4 g) IV slowly should be used as compared to the IM route. The cobalt will act to bind a portion of the cyanide and complex it until the thiosulphate is employed to finish the job. HydroxyB12 is relatively safe. Disadvantages include rare allergic reaction, high cost for the amounts required, short half-life as it decomposes in light. Remember that sodium thiosulphate must always be given to complete the medical detoxification of cyanate by converting the free and bound cyanide to thiocyanates under the influence of the enzyme rhodenase. The relatively nontoxic thiocyanates can be metabolized. There are four methods in the human to detoxify cyanide. The most effective of these is via rhodenase but it is rate limited by a rapid decline in sulfur containing substrate. Thiocyanate is the natural product of this process. The addition of more thiocyanate helps improve this process by adding sulfur molecules.

91 Treatment of Cyanide Poisoning
First you must rapidly bind or fixate the cyanide ion either by creating methemoglobin or fixing it with cobalt compounds. Any person who is conscious and breathing normally more than 5 minutes after being exposed to and removed from cyanide agents will recover without any treatment as this substance is rapidly detoxified by the body.

92 Treatment of Cyanide Poisoning
Amyl nitrite is often used if there is a respiratory positive pressure present. Do not use amyl nitrate with oxygen as an explosion may occur. Follow this with sodium thiosulphate. In the military, amyl nitrate is used less than in the civilian sector. More meaningful and predictable levels of methemoglobin can be produced by sodium nitrate.

93 Treatment of Cyanide Poisoning
If there is impairment with breathing, IV sodium nitrate should be used (10 cc of a 3% solution, 300mg over 3 minutes). This will produce methemoglobin, which binds the cyanide. Keep the patient flat or their blood pressure will fall from the nitrite. Try to obtain a little cyanosis to indicate methemoglobinemia.

94 Treatment of Cyanide Poisoning
Administer the sodium thiosulphate at a dose of 12.5 Gms (50 cc of a 50% solution over a 10 minute period of time. Remember that methemoglobin levels higher than 10% usually indicate that further nitrates are not needed. Cardiac complications with higher doses.

95 Treatment of Cyanide Poisoning
Remember that sodium thiosulphate must always be given to complete the medical detoxification of cyanate by converting the free and bound cyanide to thiocyanates under the influence of the enzyme rhodenase. The relatively nontoxic thiocyanates can be metabolized.

96 Summary of Cyanides There is generally a favorable prognosis for survivors of a cyanide attack who have residual symptoms. Aggressive care is required to ensure a good outcome including cobaltous agents or nitrates followed by sodium thiocyanate.

97 Odors of Some Chemical Weapons
Nerve gas – None to fruity or paint-like. Mustard –Garlic or Horseradish. Lewisite – Fruity to germanium. Phosgene – New mown hay or green corn. Cyanide – Bitter almond (faint).

98 If In Doubt Regional poison control center (1-800-222-1222)
Centers for Disease Control and Prevention Public Response Hotline (CDC) English (888) Español (888) TTY (866)


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