Chemical Warfare Agents

Chemical warfare (CW) are developed chemical MCW by governments for the war effort, and include toxic agents (intended to cause serious injury or death) Incapacitating agents (are only temporary, non-life-threatening effects) as a non Although incapacitating agents sometimes deadly are called, these agents can cause serious injury or death at high doses. Toxic industrial chemicals (TICs) are chemicals for industrial applications, which are able to produce a large number of injured. Some chemicals (eg. Chlorine, phosgene, hydrocyanic acid compounds) may also be used as a CW both industrially and are referred to as substances having a dual use. Classification Toxic CW agents are divided into four main classes: lung means Systemic asphyxiants (blood-substances) to denLungenmitteln Vesicants (blistering warfare agents) nerve agents Because also include substances that are more about the upper respiratory tract instead of the lung parenchyma in the first place, some prefer expert the right to refer to this class as “agents with acute local effects on the respiratory system,” Since affect most TICs that can cause mass injuries, respiratory tract, it is discussed as choking agents. Systemic suffocating, especially cyanide and hydrogen sulfide, affect mitochondrial energy transport and block the cellular respiration. They are distributed in the blood (and therefore referred to as blood substances in military instructions) and thus affect most tissues. Vesicants damage the dermo-epidermal junction, which leads to pain and typically blistering. Many can, when inhaled, affect the lungs. Nerve agents inhibit the enzyme acetylcholinesterase, thereby causing excessive cholinergic stimulation and cholinergic crisis (diarrhea, urination, miosis, bronchorrhea, bronchoconstriction, vomiting, lacrimation, salivation z. B.). IHandlungsunfähig solubilizing agents may be divided into: Anticholinergic agents used in the riot control agents (often incorrectly called tear gas) may be as solid aerosols or distributed as solutions. (Note: The US military does not believe that substances used in riot control are chemical warfare agents.) In addition to their chemical names, most warfare agents have also have a “one-to three-letter North Atlantic Treaty Organization (NATO) code “. Fire substances designed to produce light and flame, and burns with a large number of casualties can cause. Hydrogen fluoride (HF) can also cause burns. Some of these burns require specific treatment, notwithstanding the otherwise typical treatment of burns. Pulmonary Chemical warfare agents pulmonary agents include traditional CW “strangulation” – substances such as chlorine, phosgene, diphosgene and chloropicrin and some necrotizing substances such as mustard gas, lewisite and Phosgenoxim (affecting the skin) as well as military fumes, combustion products, and many toxic industrial chemicals. Most of these compounds are gases or volatile liquids. Pathophysiology Toxic CW substances which affect the respiratory system may be divided into 2 types, depending on which part of the tract is largely influenced (see Table: Representatives of Type 1, Type 2 and chemicals with mixed effects with acute local effects on the respiratory tract ): type 1 compounds: Where the large airways type 2 substances: Where the terminal and respiratory bronchioles, alveolar sacs and alveoli substances with mixed effects: Where the large and small airways and the alveoli type 1 substances are usually the with inhaled particles (eg. as smoke), which tend to be before they reach the alveoli to settle or highly water soluble and / or highly reactive chemicals that dissolve in the mucous membrane of the respiratory tract before reaching the alveoli. Type 1 substances cause necrosis and detachment of the respiratory epithelium in the large airways, which can cause a complete or partial obstruction of the airways. Chemical pneumonitis and secondary bacterial pneumonia may occur as a consequence of Type 1 damage. High doses of type 2 substances can also cause effects of type 1 (large airways), even if the type 1 effects seem to be rather temporary. Type 2 substances have a lower solubility and / or less reactive chemicals that come before the resolution to the alveoli normally. This will damage the pulmonary capillary endothelium, resulting in fluid leakage into the interstitial spaces and alveoli; pulmonary edema can occur. Some type 2 substances (eg. As nitrogen oxides and HC-vapor [hexachloroethane and zinc oxide]) can follow acute pulmonary edema days to weeks later by progressive and potentially irreversible pulmonary fibrosis. It is believed that the mechanism is immunologically. High doses of type 1 substances may also cause pulmonary edema. Substances with mixed effects acting in both large airways and the alveoli in low to moderate doses. Representatives of Type 1, Type 2 and chemicals with mixed effects with acute local effects on the respiratory tract Type Example Type 1 acetaldehyde acetic acid acrolein ammonia formaldehyde hydrochloric hydrofluoric ozone used in the riot control agents smoke products in sulfur mustard (H, HD) type 2 carbon tetrachloride, chloropicrin (PS ) diphosgene (DP) of methyl isocyanate nitrogen oxides perfluoroisobutylene (PFIB) of phosgene (CG) Phosgenoxim (CX) Mixed effect chloramines chlorine (CL) HC (hexachloroethane and zinc oxide) – smoke Lewisite (L) symptoms and complaints initial exposure to type 1 substances causes sneezing, coughing, laryngospasm and (eye irritation can occur). Patients with airway obstruction have hoarseness, wheezing and inspiratory stridor. With a high dose of a type 1 agent can then develop chest tightness or shortness of breath as a result of an incipient pulmonary edema. In type 2 substances, the symptoms and discomfort usually occur delayed many hours after exposure. Patients complain initially tightness in the chest or shortness of breath. Physical findings may be minimal, apart from rare expiratory crackles and dullness on percussion. Time of occurrence takes place shorter at higher doses; Development of dyspnea within 4 h after exposure suggests a potentially fatal dose hin.Diagnose Clinical examination Frequent revaluation due to deterioration Sometimes bronchoscopy, chest x-ray Clinical diagnosis is used to detect the exposure and to distinguish the type of damage (not necessarily the type of substance since both types can cause similar effects depending on the dose). In patients with breast anfänlichen noise and prominent symptoms there are probably a contribution from the type 1 (large airways). Delayed onset of shortness of breath with a relatively quiet breast suggests a type 2 damage. Although a high dose of type 2 substances can initially cause coughing, sneezing and wheezing, decrease these signs usually over time; the patient appears healthy until he developed a progressive shortness of breath. The chest x-ray findings may initially be unremarkable. Scattered turbidity due to chemical or pneumonia may develop secondary damage at type-1. Finally, if pulmonary edema is evident radiographically, Kerley-B lines and loosened interstitial infiltrates are visible due to damage caused by type. 2 A bronchoscopy can confirm type 1 damage, but early type 2 damage oversight. Laboratory tests are the first diagnosis is not helpful, but pulse oximetry and / or ABG measurements can help clinical deterioration aufzuzeichnen.Triage severity signs of type 1 damage (eg. As heavy wheezing, inspiratory stridor, soot around the nose or mouth due to smoke inhalation), the threshold for early intubation should lower. In one type-2 drug, it is important that often a new triage occurs at the patient. Initially asymptomatic patients should be monitored for worsening; even mild symptoms are reasons for rapid transport to a medical facility because of the condition of such patients often continued to deteriorate. Most patients with shortness of breath due to early pulmonary edema can be spotted delayed for medical treatment; They tolerate a slight delay in the rule if immediate victims require treatment. However, such patients should (urgently) have to evacuate top priority because they may be a final, life-saving treatment in a pulmonary intensive care benötigen.Therapie Supportive treatment Type 1: Early intubation and bronchodilators, sometimes inhaled corticosteroids and antibiotics in documented secondary bacterial infection, in type 2: O2 and positive-pressure ventilation (continuous positive airway pressure for patient is conscious, positive end-expiratory pressure in ventilated patients), bronchodilators and rarely corticosteroids It is important to treat the damage rather than the drug because some drugs both type 1 and type 2 reactions cause, even at very low doses and because at high doses both types of damage. Decontamination of steam or gas exposure is not displayed and there is no specific antidote for these funds. In type 1 effects give warm, humidified 100% O2 using a face mask. Bronchoscopy can be done both diagnostically and therapeutically, on the removal of necrotic debris from the large airways. Early intubation and ventilation hönnen be required. Bronchodilators can help by increasing the degree of airways. Inhaled corticosteroids may the inflammation that often accompanies damage to the large airways, decrease. For treatment of smoke inhalation, burns: smoke inhalation. In type 2 effects, patients should be moved to an intensive care unit. O2 should “continuous positive airway pressure (CPAP) in patients with consciousness or” positive end-expiratory pressure “(PEEP) are given in intubated patients. Positive pressure ventilation can help to guide the fluid from the alveolar spaces back into the pulmonary capillaries. A central management can help monitor lung pressures so that they can be controlled without a hypovolemic shock for guidelines for hospital treatment of pulmonary edema, pulmonary edema. treatment Although there is evidence that bronchodilators mainly expand the large airways in cases of type 1 damage. , suggest recent evidence suggests that they act through independent ways to alleviate type 2 damage. corticosteroids do not relieve pulmonary edema, but oral corticosteroids may be early indicated for patients, the HC smoke or nitrogen oxides have been exposed to late-onset prevent lung fibrosis. A vorb eugende treatment with antibiotics helps in either of the two types of injury. Antibiotics should be given only after the diagnosis of bacterial infection, including isolation of an organism and determination of antibiotic sensitivity. Systemic asphyxiants systemic asphyxiants are cyanide compounds hydrogen sulfide systemic asphyxiants were also called blood agents because they are systemically distributed via the blood. However, their site of action is not the blood, but the cellular level throughout the body. Although cyanide salts were used to murder on their income, a large number of injured would take place rather as a result of inhalation of hydrogen cyanide or cyanogen chloride, which are highly volatile liquids or gases at ambient temperatures. Cyanides are also products of combustion of many household and industrial content, and patients with smoke inhalation can have cyanide poisoning. Cyanide has a characteristic bitter almond odor, but the ability to detect this odor, is possible by a single gene, which is missing half the population. Hydrogen sulfide is always a gas at ambient temperatures. The exposure is thus usually through inhalation. Hydrogen sulfide may be produced by mixing the sulfur-containing household chemicals with acids; this combination of suicide (called “detergent suicide”) used and residual gas may affect Savior, resulting in several casualties. Hydrogen sulfide is also generated when manure decomposes. Large cesspools of farms often contain lethal amounts of the gas, which can lead to several deaths, if any rescuers without appropriate protective equipment succumb to this. Hydrogen sulphide has a characteristic odor of rotten eggs, but high concentrations damage the olfactory fibers so that the smell is not perceived in the most deadly environments. Pathophysiology cyanides and hydrogen sulfides penetrate both into the mitochondria, where they inactivate cytochrome oxidase, an enzyme responsible for the oxidative phosphorylation (cell breathing) is required. The suppression of oxidative phosphorylation leads to cellular anoxia, with ATP deficiency; Inability to extract oxygen from the blood that was released into the tissue and lactic acidosis caused by the attempts of the body to produce energy nonoxidative. Organs and tissues are affected, but neurons are more sensitive than muscles; Central apnea is the usual mechanism of Todes.Symptome complaints and cyanides initially cause wheezing, tachycardia and hypertension. Loss of consciousness and convulsions may occur in less than 30 seconds. Tetanus-like characters, including lockjaw (tetanus), risus sardonicus (grimacing) and opisthotonos (arching neck) may occur. The skin can be rinsed, but about half of the victims are cyanotic. Apnea is usually preceded by bradycardia and hypotension and Dekortikationshaltung can be detected before death. Hydrogen sulfide in high doses also causes sudden loss of consciousness with cramps. Direct damage to the heart muscle can prominently be Prolonged exposure to initially sublethal concentrations may cause eye irritation with conjunctivitis and corneal erosions and ulcerations ( “gas eye”), irritation of the nose and throat, headache, weakness, ataxia, nausea, vomiting, chest tightness and cause hyperventilation. Some of these revelations seem to be a reaction to the unpleasant smell of the connection. A green discoloration or darkening of worn by the patient coins should Clinical to increased suspicion of hydrogen sulfide poisoning führen.Diagnose study patients Severely affected must be treated before a test is available, the diagnosis is v. a. clinically. Laboratory findings include a reduced arteriovenous O2 difference (due to a higher than usual O2 content in the veins) and Azedemie high anion gap with increased Laktat.Triage All unconscious patients with a pulse are potentially save and should for immediate medical treatment be spotted. Since the condition of patients does not deteriorate with inhalation exposure usually when they were removed from the contaminated environment, patients can be delayed with decreasing symptoms conscious sighted (ie they are able to tolerate a short delay while immediate victims are treated) .Therapie respiratory support and 100% O2 When cyanide antidotes specific attention should be paid to airway, breathing and circulation. Water with or without soap suffice for decontamination of the skin; Patients who were only exposed to steam or gas, do not require decontamination in general. Cyanide victims need a fast antidote therapy with inhaled amyl nitrite 0.2 ml (1 ampoule) for each 30 s min; 3% Na nitrite in 10 ml of 2.5 to 5 ml / min i.v. (In children, 10 mg / kg), then 25% sodium thiosulfate i.v. 25 to 50 ml at 2.5 to 5 ml / min If available, may instead hydroxocobalamin 5 to 10 g I.V. are given. In addition antidotes can also be effective in apneic patients. If no antidote is available, ventilation and administration of 100% O2 can be lifesaving. However, unprotected mouth-to-mouth resuscitation may expose the first responders cyanide in the breathing of the patient. Cyanide victims due to smoke inhalation and carbon monoxide poisoning may include; Earlier concerns about the administration of nitrites in this situation were probably overrated. There is no evidence that hyperbaric O2 improves results when poisoned with cyanide patients. Hydrogen sulfide victims are treated with supportive, including administration of 100% O2. Amyl nitrite and v. a. Na nitrite can be useful, but there are no signs of sodium thiosulfate or hydroxocobalamin. Hyperbaric O2 has not proven to be useful. Vesikantien Vesikantien are substances that produce on the skin blisters and include mustards, including mustard gas and nitrogen mustards Lewisite Phosgenoxim (technically more of a muslin and a corrosion agent as a vesicant, although it is classified as a vesicant) These funds also have effects on the respiratory system: Mustards are predominantly type 1 substances Phosgenoxim is a type-2 medium and lewisite is a mixed agent (representative of type 1, type 2 and chemicals with mixed effects with acute local effects on the respiratory tract). Mustard gas was variously described as if it smells like mustard, garlic, horseradish or asphalt. Lewisite can have a geranium-like smell and Phosgenoxim was simply described as irritating. The perception of these odors are so subjective that they are not a reliable indicator of the presence of these compounds. Pathophysiology mustard gas and nitrogen mustards alkylate many cellular components, including DNA and release inflammatory cytokines. They have similar acute local effects on the skin, eyes and respiratory tract; in fatal concentrations they suppress the bone marrow. Damage to cells in the basal layer of the epidermis give a separation of the epidermis from the dermis or, in high doses, a direct necrosis and replacement of the epidermis. Blister fluid containing no active mustard gas. Type 1 damage to include the large airways detachment of the mucosa of the respiratory tract such as Pseudomonas membranes. Pulmonary edema (type 2 damage) may occur at high doses. Mustard can also induce nausea, presumably via a cholinergic mechanism. Bone marrow suppression can lead to sepsis, a week or two after exposure. Among the long-term effects of ocular abnormalities (e.g. chronic keratitis) and skin cancer and cancer of the respiratory tract may belong. Lewisite cause skin damage similar to those of mustard gas, although the mechanism of injury is different and includes the effects of both glutathione and sulfhydryl groups of enzymes as well as the inhibition of pyruvate dehydrogenase. In the airways, the arsenic content of Lewisite in leakage of the pulmonary capillaries and pulmonary edema leads; at high doses, a systemic hypotension – called Lewisite shock -. occur. Unlike the mustards, Lewisite not result in immunosuppression. Phosgenoxim caused urticaria and tissue necrosis by mechanisms sind.Symptome still unclear and complaints mustard compounds cause intense and increasing skin pain, redness and blistering after a latency period. The latency period is inversely proportional to the dose, but is generally at least a few hours (and up to 36 h). Bubbles caused by mustard gas, sometimes resemble a pearl necklace around a central, pristine region; Bubbles caused by nitrogen mustard, show this pattern less likely. Bubbles can zuwerden large and continuous. A painful chemical conjunctivitis, which causes a blink reflex, occurs earlier than skin symptoms, but still after a delay of many hours. The cornea may be tarnished. Symptoms of respiratory diseases are cough, laryngospasm, hoarseness, wheezing, and inspiratory stridor. Tightness in the chest and dyspnea may occur with serious exposure. Nausea may occur after a moderate to high doses. Lewisite caused pain within about one minute of exposure to skin. Erythema is often after 15 to 30 minutes noticeable, and bubbles form after several hours. The bubbles form usually in the middle of the erythematous area and spread peripherally located. The pain is not as strong as a rule, such as that caused by mustard and begins to decline after bubbles form. Irritation of the mucous membranes and the large airways occurs soon after breathing and leads to coughing, sneezing and wheezing. Later, after a few hours, kicking, type 2 symptoms (chest tightness, and dyspnea) on. Skin contact with Phosgenoxim causes severe, “stinging” pain and bleach within 5 to 20 seconds. The affected skin is then gray with reddened border. Between 5 and 30 min after exposure the edema resulting wheals (urticaria). In the next 7 days, the skin is dark brown and then black when necrosis of the skin and the underlying subcutaneous tissue and muscles occurs. If the lesion is not surgically removed, it can persist for more than 6 Monte. In the airways, causing pulmonary edema Phosgenoxim, even at low Dosierung.Diagnose Clinical examination pain that occurs at or shortly after exposure, suggest that Lewisite or Phosgenoxim are the active ingredient; the early onset of skin lesions differs phosgene oxime. Delayed onset of pain (sometimes up to one day after challenge) suggesting mustard gas. The clinical diagnosis can be confirmed by laboratory tests, but these tests are only in specialized laboratories. In patients who were exposed to mustard, regular blood counts should be performed in order in the first two weeks changes in lymphopenia and neutropenia überwachen.Triage All accidents with possible skin or eye exposure to Vesikantien should be prioritized for immediate decontamination. Decontamination of the skin within 2 minutes is ideal, but a decontamination up to 15 or 20 minutes after the exposure, the size of any bubbles may decrease. However, patients who arrive later should be decontaminated yet as soon as possible, to stop ongoing absorption and accumulation of a lethal dose, which is about 3 to 7 grams of mustard and lewisite. However, with the exception of patients with impending airway compromise, most patients who were exposed to Vesikantien tolerate a short delay in treatment, while more urgent injuries stabilized werden.Therapie decontamination Treat skin lesions similar to burns respiratory support as needed eyes – and skin decontamination should be done as soon as possible, preferably using a reactive skin decontamination lotion (RSDL®). A 0.5% solution of sodium hypochlorite is less effective, but still useful if RSDL® is not available. A physical or mechanical decontamination can be attempted, but water and soap are minimally effective. are skin lesions such as burns treated (burns: first wound care). However, since the fluid loss in patients who were exposed to Vesikantien is lower than in patients with burns, less liquid should be used as it is listed in the Brooke- or parkland fluid replacement formulas. Scrupulous hygiene is important to prevent secondary infections. Antibiotic ointments should be applied to the edges of the eyelids to prevent Lidadhäsion. Supporting ventilation with attention to airway and breathing is indicated for patients with respiratory manifestations (pulmonary Chemical warfare agents: therapy). Since nausea is cholinergic origin, those with atropine (eg., 0.1 to 1.3 mg i.v. every 1 to 2 hours as needed) can be treated. A bone marrow depression requires reverse isolation and treatment with colony stimulating factors. Nerve agents There are two types of nerve agents: agents of the G-series active ingredients of the V-series agents of the G-Series, or G-agents, GA (tabun), GB (sarin), GD (soman) and GF (cyclosarin) which were developed before and during world war II by Nazi Germany. Active ingredients of the V-series include VX; these compounds were synthesized after the Second World War. All nerve agents are organophosphorus esters as well as organophosphate (OP) – pesticides (poisoning with organophosphates and carbamates). However, nerve agents are much stronger; the LD50 (the amount that is required to the death of half of the those receiving this dose to cause amount) of VX equivalent to about 3 mg. At room temperature G-agents are aqueous liquids having high volatility and provide both skin contact and inhalation hazards represents. VX is a liquid with the consistency of engine oil, which evaporates relatively slowly. None of these agents has a distinct odor or causes local skin irritation. Pathophysiology nerve agents inhibit the enzyme acetylcholinesterase (AChE), which hydrolyzes the neurotransmitter acetylcholine (ACh) as soon as ACh completed to activate receptors in the neurons, muscles and glands. ACh receptors in the CNS, autonomic ganglia, skeletal muscle, smooth muscle and exocrine glands present. Binding of nerve gas to AChE is essentially irreversible without treatment; a treatment with an oxime can regenerate the enzyme as long as the binding was not further stabilized over time (a process called aging). Most nerve agents, such OP insecticides or require hours to age, but GD (Soman) may be substantially completely within 10 min after aging of the bond. Inhibition of AChE leads to an excess of ACh at all of its receptors (cholinergic crisis) and first causes increased activity of the affected tissue, then in the central nervous system and skeletal muscle fatigue and failure of the Gewebes.Symptome and complaints The clinical manifestation depends on the state of the drug , route of exposure and dosage. Steam exposure to the face causes local effects such as miosis, rhinorrhea and bronchoconstriction within seconds and proceeds to the full range of systemic manifestations of cholinergic excess. However, when steam is inhaled, a collapse will occur within seconds. Liquid exposure to the skin causes first local effects (local twitching, fasciculations, sweating). Systemic side effects take place after a latency period which can last up to 18 h after exposure to a very small droplets; even at lethal doses, it usually takes up to 20 to 30 minutes until the symptoms and complaints, which include sudden collapse and convulsions without warning occur. Patients have part or all of the cholinergic Toxidroms on (Common toxic syndromes (Toxidrome) and symptoms and treatment of specific toxins). Sensory overload and eventual fatigue of the CNS cause agitation, confusion, loss of consciousness and seizures, to failure of the respiratory center in the medulla. Reizüberflutung und eventuelle Ermüdungs der Skelettmuskeln verursachen Zucken und Faszikulationen, die zu Schwäche und Lähmung fortschreiten. Überstimulation der cholinerg aktivierten glatten Muskulatur führt zu Miosis, Bronchospasmus, und Hyperperistaltik (mit Übelkeit, Erbrechen, und Krämpfen), und Reizüberflutung der exokrinen Drüsen verursacht übermäßiges Reißen, Nasensekret, Speichelfluss, Bronchialsekret, Verdauungssekrete und Schwitzen. Der Tod erfolgt in der Regel aufgrund zentraler Apnoe, aber direkte Lähmung des Zwerchfells, Bronchospasmus, und Bronchorrhö können auch dazu beitragen.Diagnose Klinische Untersuchung Die Diagnose wird klinisch gestellt, auch wenn Laboranalyse von Erythrozyten-Cholinesterase-oder Plasma-Cholinesterase-Spiegel sowie speziellere Labortests eine Nervenmittel- Exposition bestätigen können.Triage Alle Menschen mit verdächtiger Flüssigkeit auf der Haut müssen zur umgehenden Dekontamination der betroffenen Stelle priorisiert werden. Die Patienten können dann zur medizinischen Behandlung gesichtet werden, basierend auf ihren Symptomen und Beschwerden. Alle Patienten, die Nervengiften ausgesetzt waren und die erhebliche Atembeschwerden oder systemische Wirkungen haben, sollten unmittelbar zur medizinischen Behandlung gesichtet werden.Therapie Anticholinergika (Atropin, 2-PAM) Benzodiazepinen Atmungsunterstützung nach Bedarf Aufmerksamkeit auf die ABCDDS – Airway (Atemweg), Breathing (Atmung), Circulation (Zirjulation), Immediate Decontamination (sofortige Dekontamination) und Drugs (Medikamente) sind von größter Bedeutung. Eine Bronchokonstriktion kann so schwerwiegend sein, dass die Beatmung unmögl

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