Armas de destrucción masiva

Presentación del tema: "Armas de destrucción masiva"— Transcripción de la presentación:

1 Armas de destrucción masiva
MAYLA ANDREA PERDOMO AMAR Urgentóloga Hospital Pablo Tobón Uribe Docente UPB – CES - UdeA

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3 ARMAS DE DESTRUCCIÓN MASIVA
Armas que son capaces de producir cantidad masiva de víctimas, usadas por terroristas.

4 TIPOS Biológicas Químicas Nucleares

5 HISTORIA 1346 Segunda plaga… Tártaros usaron catapultas para lanzar cuerpos infectados con plaga a la ciudad de Génova. Naturally occurring plague is a flea-borne zoonosis. It is caused by Yersinia pestis, a gram-negative coccobacillus that belongs to the Enterobacteriaceae family. Plague is known to have caused more than 200 million deaths worldwide during its numerous epidemics and three pandemics [8]. The most well-known pandemic was the second plague which started in 1346 and is known as the ‘‘Black Death.’’ This outbreak began in Europe and eventually claimed the lives of 20 to 30 million people, or close to one third of the European population. It is thought that the use of plague as a bioweapon started during the second plague. During that time, the Tartars used catapults to launch corpses infected with plague into a Genoese city. Reportedly, the attack was successful, although it is unknown whether the disease was caused by the ballistic corpses or by infected fleas [11]. More recently, attempts have been made to weaponize Yersinia pestis. During World War II, members of the Japanese Army are reported to have dropped plague-infected fleas over populated areas of China. During the Cold War, the United States and Soviet Union both worked to turn plague into a biologic weapon. Although the US efforts ended in 1970 when the offensive bioweapons program was terminated, Soviet scientists were able to manufacture large quantities of weapons-grade agents

6 HISTORIA Unión Soviética produjo Anthrax: guerra fría.
1979 Sverdlovsk, Unión soviética: inhalación Antrax, 66 muertes. Octubre 4, Anthrax correo, 1 muerte. Anthrax bacteria are easy to cultivate in the microbiology laboratory and can be readily induced to produce spores. The Soviet Union produced weaponized anthrax in ton quantities during the cold war era. An outbreak of inhalational anthrax occurred near a Soviet bioweapons facility at Sverdlovsk in 1979, resulting in 77 infections and 66 deaths, with some victims becoming ill up to 6 weeks after exposure [18]. The Japanese cult group Aum Shinrikyo attempted several attacks with anthrax in the 1990s but were unsuccessful [19]. Anthrax became the most notorious bioterrorism agent after October 4, 2001, when a 63-year-old man died of inhalational anthrax that was traced to intentional exposure through the United States mail [20,21]. This instance represented the first inhalation anthrax case in the United States since 1976 Kman NE. Emerg Med Clin N Am. 2008; 26:

7 HISTORIA 1980 Agentes nerviosos usados por militares Iraquíes contra tropas Iraníes y Kurdas. 1994, 1995 Grupo liberación del culto Aum Shinrikyo en Japón. Nerve agents were designed for use on the battlefield. Though rarely employed in warfare, recent documented use includes the Iraqi military’s use against Iranian troops and the Kurds in the 1980s [1] and the Aum Shinrikyo cult’s release in Japan in 1994 and 1995 [2]. Nerve agents are acetylcholinesterase enzyme inhibitors similar to organophosphate insecticides Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

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9 BIOLÓGICAS Bacterias, virus, toxinas Características
Fácil diseminación y transmisión. Potencial impacto en salud pública. Causar pánico, alteración social. Necesidad preparación sistema de salud pública. Sin olor, difíciles de detectar. Bozeman WP. Emerg Med Clin N Am. 2002;20:

10 BIOLÓGICAS ARMA BIOLÓGICA IDEAL
Capaz de producir gran cantidad de lesionados. Fácil y amplia diseminación. Estable e infecciosa a pesar de la exposición ambiental. Disponible para su producción en adecuadas cantidades. Moran G. Infect Dis Clin N Am. 2008;22:

11 BIOLÓGICAS: CATEGORÍAS
CATEGORÍA A Fácil diseminar. Alta morbimortalidad. Requiere diagnóstico y manejos específicos. Anthrax Plaga Viruela Fiebres hemorrágicas Botulismo Tularemia Moran G. Infect Dis Clin N Am. 2008;22:

12 BIOLÓGICAS: CATEGORÍAS
CATEGORÍA B Relativamente de fácil diseminación. Moderada morbilidad y baja mortalidad. Diagnósticos y manejos específicos. Fiebre Q : Coxiella burnetti Brucellosis: brucella especies. Alfa virus Encefalomielitis venezolana Enterotoxina estafilocóccica. Salmonella especies. Escherichia coli Cólera: Vibrio cholerae Moran G. Infect Dis Clin N Am. 2008;22:

13 BIOLÓGICAS: CATEGORÍAS
CATEGORÍA C Patógenos emergentes, podrían ser ADM. Fácil producción, diseminación. Potencial alta morbilidad y mortalidad. Hantavirus Fiebre amarilla TBC multiresistente Virus fiebre hemorrágica transmitida garrapatas. Virus encefalitis transmitida garrapatas Moran G. Infect Dis Clin N Am. 2008;22:

14 ANTHRAX Bacillus anthracis, G+
Contacto directo con esporas, ingestión, inhalación. Síntomas cutáneos, gi, respiratorios. No transmisión persona – persona. Incubación: 1-5d. Bacillus anthracis could be considered to be the perfect agent for bioterrorism. It occurs naturally as a zoonotic disease of persons who handle contaminated animal products, such as hair or hides. It forms spores that are stable over long periods and can withstand exposure to air, sunlight, and even some disinfectants. Anthrax can present as three distinct clinical syndromes in humans: cutaneous, inhalation, and gastrointestinal. Cutaneous anthrax, the most common naturally occurring form, is usually spread through contact with infected animals, particularly cows, sheep, and horses, or their products. Cutaneous anthrax (Fig. 1) typically produces large black eschars on the skin, but in early stages may appear as papules that progress to vesicles. Patients may also experience lymphadenopathy, fever, malaise, and nausea. Local cutaneous anthrax has a mortality rate of less than 1% if treated but can occasionally Kman NE. Emerg Med Clin N Am. 2008; 26:

15 ANTHRAX Cutáneo: pápula roja, úlcera, escara negra.
Inhalación: alta mortalidad. Fiebre, malestar, disnea, shock. Meningitis, mediastinitis. Gastrointestinal: ulceras, diarrea con sangre, linfadenopatía, sepsis. The first symptoms of inhalational anthrax are nonspecific, and making the diagnosis requires a high degree of suspicion. After a typical incubation period of 1 to 6 days, patients may describe fever, dyspnea, cough, headache, chills, vomiting, weakness, or chest pain [4]. In the attacks of 2001, malaise and fever were present in all patients who had inhalational anthrax. Cough, nausea, vomiting, diaphoresis, dyspnea, chest pain, and headaches were also common in these patients. Signs that were present included fever, tachycardia, and hypoxemia. Gastrointestinal anthrax results from the ingestion of bacilli from poorly cooked meat and can occur anywhere in the gastrointestinal tract. Oral-pharyngeal anthrax causes lip, oral, or esophageal ulcers and leads to lymphadenopathy, edema, and sepsis [4]. Anthrax infection of the lower gastrointestinal tract can present with nausea, vomiting, malaise, or bloody diarrhea. Infection can ultimately lead to ascites, acute abdomen, or fulminant sepsis. After the spore germinates in the skin, toxin production results in local edema. This edema subsequently develops into a black, coal-colored eschar for which anthrax is named (the Greek word for coal is anthrakis). The eschar is painless but often associated with extensive local edema, lymphangitis, and painful lymphadenopathy (Fig. 1). After 1 to 2 weeks, the anthrax eschar dries, loosens, and falls off Kman NE. Emerg Med Clin N Am. 2008; 26:

16 ANTHRAX Dx: Rx: mediastino
Bacilos G+, sangre, LCR, lesión piel, hemocultivos. Elisa: toxina TTO y profilaxis: Ciprofloxacina, doxicilina/ 60 días. Meningitis: Cipro + cloramfenicol /PNC/rifampicina. The working group on the management of anthrax as a biologic weapon now recommends a 60-day course with oral ciprofloxacin or Doxycycline. Inhalational anthrax can lead to rapid sepsis or death. Early antibiotic administration is crucial, and multidrug therapy is recommended. Antibiotic therapy should include either doxycycline or ciprofloxacin plus one or two other agents. The other agents could be rifampin, vancomycin, imipenem, clindamycin, or clarithromycin. There appears to be some resistance to b-lactamase inhibitors, which are not concentrated in phagocytes and should not be used as a lone agent. Early multidrug therapy would also be effective against the frightening possibility of a genetically engineered strain of drug-resistant anthrax. Once the correct treatment is determined, it should be continued for 60 days or longer if necessary. It is wise to draw blood cultures before antibiotic administration and then tailor treatment to organism susceptibility. In a limited casualty setting, intravenous antibiotics are indicated. In a mass casualty setting, this therapy may not be feasible, and oral antibiotics may need to be issued. Corticosteriods are recommended in all patients who have pulmonary edema, respiratory failure, and meningitis. If meningitis is suspected, ciprofloxacin with chloramphenicol, rifampin, or penicillin should be used over doxycycline to enhance cerebrospinal fluid penetration. The first suspicion of an anthrax illness should prompt notification of local and state health departments [12]. Routine hematologic and chemistry laboratory testing is typically not helpful, although elevated liver transaminase levels are common. Blood cultures should be performed on all suspected patients before the start of antibiotics. Cultures tend to show growth in 6 to 24 hours [11]. Aerobic blood culture growth of large, gram-positive bacilli provides preliminary identification of Bacillus sp. After preliminary identification, the isolate should be sent promptly to a level B or C laboratory in the Laboratory Response Network. Currently, 81 clinical laboratories in this network have diagnostic capabilities for bioterrorism pathogens [10]. A plain chest radiograph can be of great help in establishing the diagnosis. In the attacks of 2001, all ten patients had abnormal plain films of the chest. Seven had mediastinal widening, seven had infiltrates, and eight had pleural effusions. If inhalational anthrax is suspected, a chest CT scan should be obtained. As shown in Fig. 2, mediastinal widening or pleural effusions can help differentiate inhalational anthrax from communityacquired pneumonia [11]. In fact, any patient presenting to the emergency department with mediastinitis should prompt the physician to consider the diagnosis of inhalational anthrax. Kman NE. Emerg Med Clin N Am. 2008; 26:

17 PLAGA Plaga negra (muerte negra)…
Infección zoonótica: roedor – pulgas. History and significance Few illnesses carry as many terrifying connotations for the general public as plague, caused by the gram-negative bacillus Yersinia pestis. The ‘‘Black Death’’ killed millions of people throughout Europe in the fourteenth century. A more recent pandemic originated in China and spread worldwide at the turn of the twentieth century. Bubonic plague is the most common naturally occurring form. It is a zoonotic infection spread from the rodent reservoir to man through the bites of infected fleas. Plague, like anthrax, also has a pneumonic form, which can be transmitted through inhalation of droplets spread by cough or, in the event of a terrorist attack, through inhalation of an aerosol containing Y pestis. As with anthrax, the pneumonic form of the disease is far more dangerous. Left untreated, pneumonic plague is nearly always fatal within 2 days of onset of symptoms. Plague is more difficult to use as a biological weapon than anthrax because Y pestis is susceptible to drying, heat, and ultraviolet light. However, unlike anthrax, secondary cases may result from person-to-person transmission. Attempts to use plague as a biological weapon date back to the ancient practice of flinging plague-infected corpses over the walls of cities under siege. The Japanese attempted to use plague as a biological weapon by releasing infected fleas over cities in Manchuria during World War II, but dissemination attempts met with limited success. The United States did not develop plague as a potential weapon because of its persistence in the environment and the possibility of noncombatant and friendly casualties after an attack. The Soviet Union reportedly developed dry, antibiotic-resistant, environmentally stable forms of Y pestis that could be disseminated as an aerosol [38]. The Black Death earned its name from the gangrenous lesions that developed in the digits and nose of patients with advanced disease. These lesions are a late complication of septicemic plague; therefore, they do not aid in making the diagnosis. In patients with septicemic plague, disseminated intravascular coagulation, necrosis of small vessels, and purpuric skin lesions can develop. Septicemia can arise from Y pestis in two ways. When sepsis develops after a flea bite with no bubo, the disease is termed primary septicemic plague. Although case fatality is high, only 13% of the cases of plague occurring in the United States during the last 50 years have been septicemic plague. Septicemia can also result secondary to bubonic plague. This disease is termed secondary septicemic plague [8]. The clinical manifestations of weaponized plague would likely be different from those observed in nature [8]. It is believed that most patients would present with primary pneumonic plague, which is very rare in nature. The symptoms would occur rapidly. In about 2 to 4 days, patients would exhibit the sudden onset of a productive cough, chills, headache, body aches, and dyspnea. They would also likely show signs of gastrointestinal illness, including nausea, vomiting, abdominal pain, and diarrhea. Two recent cases of primary pneumonic plague secondary to cat pneumonic plague exposure resulted in fatalities. Indeed, this form of plague is the most severe and rapidly fatal, usually within 24 hours of symptom onset [23]. Naturally occurring plague is a flea-borne zoonosis. It is caused by Yersinia pestis, a gram-negative coccobacillus that belongs to the Enterobacteriaceae family. Plague is known to have caused more than 200 million deaths worldwide during its numerous epidemics and three pandemics [8]. The most well-known pandemic was the second plague which started in 1346 and is known as the ‘‘Black Death.’’ This outbreak began in Europe and eventually claimed the lives of 20 to 30 million people, or close to one third of the European population.

18 PLAGA Yersinia pestis, CBGN. Neumónica, septicémica, bubónica.
Fiebre, mialgias, neumonía fulminante 2-3 d. Meningitis. Dx: CBG- sangre, esputo, nódulo linfático aspirado. Tto efectivo, inicia 24h. Estreptomicina, gentamicina, doxiciclina, cloramfenicol. Profilaxis: Doxi o quinolona/6 días. Clinical manifestations In cases of naturally occurring plague, a flea bite causes direct inoculation of bacteria under the skin. The bacteria then follow the path of the cutaneous lymphatics to regional lymph nodes. In the regional lymph nodes, bacteria are phagocytosed, causing regional lymphadenopathy and abscess formation. The bacteria resist destruction and rapidly replicate. These areas of lymphadenopathy are clinically apparent as ‘‘buboes.’’ Later, the lymph nodes become necrotic, causing the bacteria to escape with subsequent pneumonia, bacteremia, and sepsis [23]. With naturally occurring bubonic plague, patients typically develop symptoms 2 to 8 days after a flea bite. Buboes typically develop 1 day after the onset of fever, chills, and weakness. A bubo is an acutely swollen, tender lymph node that tends to develop in the groin, axilla, or cervical region (Fig. 4). Buboes range in size from 1 to 10 cm, are extremely painful, erythematous, and associated with surrounding edema and warmth [8] and associated with surrounding edema and warmth Kman NE. Emerg Med Clin N Am. 2008; 26:

19 VIRUELA Virus viruela Erradicada 1970.
Fiebre, malestar, cefalea, síntomas gastrointestinales, rash papular, vesículas, pústulas sincrónicas. Mortalidad 30%. Alta transmisión persona – persona. Tto: soporte Smallpox Smallpox (variola) as a natural disease was eradicated in the 1970s by the use of the smallpox vaccine. Routine vaccination has not been performed for a quarter century and is no longer available. From 1 to 2 weeks after exposure to aerosolized smallpox virus, a smallpox victim becomes viremic and experiences an abrupt onset prodrome of malaise, fevers, headaches, and GI upset. This is followed in 2 to 3 days by an erythematous rash. Maculopapular lesions develop, and then progress through stages to vesicles and then pustules. The lesions heal over a period of approximately 2 weeks, leaving scars. The rash is centrifugal, involving first the face and extremities, then the trunk. It remains more prominent at the extremities, and vesicles in each body region remain synchronous (ie, at similar stages of development). These features allow identification of smallpox on clinical grounds, but only after appearance of the characteristic lesions [14]. Care for smallpox is supportive. Mortality of smallpox was approximately 30% prior to its eradication. Smallpox patients remain infectious until all lesions are fully healed, making potential for person-to-person transmission high and careful contact isolation and airborne precautions appropriate [12,14]. Immediate vaccination of all potentially exposed individuals is recommended after a possible BW event. Quarantine and supportive care should be provided. Newer antiviral agents may be useful [ Bozeman WP. Emerg Med Clin N Am. 2002;20:

20 BOTULISMO Clostridium botulinum
Toxina, liga unión presináptica, previene liberación de Acolina. Parálisis nervios craneales (oculares). Parálisis descendente. Falla respiratoria abrupta. No transmisión persona – persona. Antitoxina: previene mayor progresión. Botulinum toxins Produced by the bacterium Clostridium botulinum, the several botulinum toxins are the most toxic substances known. The toxins bind to the presynaptic neuromuscular junction and prevent the release of acetylcholine. This produces visual and swallowing difficulties 1 to 3 days after exposure, followed by descending symmetric skeletal muscle paralysis. Respiratory failure may be abrupt. Recovery from paralysis may take weeks or months [15]. Intubation and respiratory support may be necessary. Botulinum antitoxin is highly effective if given prior to symptoms and may prevent progression of paralysis if given early in the symptomatic phase Bozeman WP. Emerg Med Clin N Am. 2002;20:

21 BRUCELLOSIS Brucella especies, CBG-
Transmitida contacto con animales infectados, ingestión. Fiebre, malestar, compromiso respiratorio, hepático, urinario. Endocarditis, SNC. Mortalidad baja. Tto: doxiciclina, fluoroquinolona + rifampicina. Profilaxis: 6 semanas. Brucellosis Several closely related Brucella species, slow-growing gram-negative coccobacilli that normally infect cattle, swine, goats, and dogs, can also be human pathogens. Brucellosis is normally transmitted by contact with infected animals or ingestion of contaminated meat or dairy products. Several days to weeks after inhaling weaponized Brucella, victims will experience nonspecific symptoms of fever and malaise. Respiratory, hepatic, urinary, and bone and joint involvement may occur. Endocarditis and central nervous system (CNS) infections are unusual but associated with more severe cases when they do occur [9]. Mortality from brucellosis is low. Symptoms may be prolonged, but most patients eventually recover, even without antibiotic treatment. Resolution is sped by appropriate antibiotic treatment. A vaccine is not available Moran G. Infect Dis Clin N Am. 2008;22:

22 FIEBRES HEMORRÁGICAS Virus hemorrágicos, RNA. FAMILIA VIRUS Filovirus
Ebola Marbug Arenasavirus Lassa New World arenasavirus Bunyavirus Crimean – Congo Omsk fiebre hemorrágica Kyasanur enfermedad forestal In September of 2007, theWHO announced the current outbreak of a category A agent of bioterrorism. At the time of this writing, Ebola hemorrhagic fever virus in the Democratic Republic of the Congo has affected 372 people, killing 166 [20]. These numbers are expected to climb. Although not thought to be related to an intentional release, this endemic outbreak serves as a stern reminder of the lethality caused by viral hemorrhagic fevers. Several viruses that cause hemorrhagic fevers are listed by the CDC as category A agents. These viruses are Ebola, Marburg, Lassa, Junin, Machupo, Guanarito, and Sabia [21]. Viral hemorrhagic fevers are caused by RNA viruses from several families. Filoviruses (Ebola and Marburg), arenaviruses (Lassa and New World arenaviruses), bunyaviruses (Crimean- Congo hemorrhagic fever and Rift Valley fever), and flaviviruses (yellow fever, Omsk hemorrhagic fever, and Kyasanur Forest disease) are all potential agents of bioterrorism. These agents all cause fever, malaise, vomiting, bleeding diatheses, edema, and hypotension that can progress to death. As evidenced by the nearly 50% fatality rate of the current outbreak of Ebola in Africa, these viruses pose a terrible threat if used as a bioweapon. They are widely distributed in nature, many are spread by airborne transmission, and humans are highly susceptible [22]. These viruses are also difficult to clinically distinguish from other disease processes. With such a wide differential diagnosis, making the diagnosis requires a high index of suspicion and advanced laboratory resources. Similarly, treatment, isolation, and prevention are difficult, making these agents dangerous when used as Weapons Humans are infected by the bite of an infected arthropod (mosquitoes and yellow fever), via aerosol generated from infected rodent excreta, or by direct contact with infected animal carcasses, blood, or bodily secretions Filoviruses like Ebola and Marburg are spread by direct contact with blood, secretions, or tissues of infected patients, bats, or primates. New research points to bats as the most likely reservoir of Ebola virus, because it is the only animal able to tolerate high virus titers without causing disease [ Kman NE. Emerg Med Clin N Am. 2008; 26:

23 FIEBRES HEMORRÁGICAS Fiebre, postración, mialgias, inyección conjuntival, rash petequial, sangrados. Alta mortalidad. Trombocitopenia, alt coagulación. Tto: soporte, ribavirina. In September of 2007, theWHO announced the current outbreak of a category A agent of bioterrorism. At the time of this writing, Ebola hemorrhagic fever virus in the Democratic Republic of the Congo has affected 372 people, killing 166 [20]. These numbers are expected to climb. Although not thought to be related to an intentional release, this endemic outbreak serves as a stern reminder of the lethality caused by viral hemorrhagic fevers. Several viruses that cause hemorrhagic fevers are listed by the CDC as category A agents. These viruses are Ebola, Marburg, Lassa, Junin, Machupo, Guanarito, and Sabia [21]. Viral hemorrhagic fevers are caused by RNA viruses from several families. Filoviruses (Ebola and Marburg), arenaviruses (Lassa and New World arenaviruses), bunyaviruses (Crimean- Congo hemorrhagic fever and Rift Valley fever), and flaviviruses (yellow fever, Omsk hemorrhagic fever, and Kyasanur Forest disease) are all potential agents of bioterrorism. These agents all cause fever, malaise, vomiting, bleeding diatheses, edema, and hypotension that can progress to death. As evidenced by the nearly 50% fatality rate of the current outbreak of Ebola in Africa, these viruses pose a terrible threat if used as a bioweapon. They are widely distributed in nature, many are spread by airborne transmission, and humans are highly susceptible [22]. These viruses are also difficult to clinically distinguish from other disease processes. With such a wide differential diagnosis, making the diagnosis requires a high index of suspicion and advanced laboratory resources. Similarly, treatment, isolation, and prevention are difficult, making these agents dangerous when used as Weapons Humans are infected by the bite of an infected arthropod (mosquitoes and yellow fever), via aerosol generated from infected rodent excreta, or by direct contact with infected animal carcasses, blood, or bodily secretions Filoviruses like Ebola and Marburg are spread by direct contact with blood, secretions, or tissues of infected patients, bats, or primates. New research points to bats as the most likely reservoir of Ebola virus, because it is the only animal able to tolerate high virus titers without causing disease [ Once the diagnosis is suspected, laboratory confirmation can occur. Laboratory abnormalities are nonspecific and include leukopenia, anemia, thrombocytopenia, hemoconcentration, and elevated liver function tests. Coagulation abnormalities may include a prolonged bleeding time, prothrombin time, and activated partial thromboplastin time. Elevated fibrin degradation products and decreased fibrinogen may also be seen. If the diagnosis is suspected, laboratory samples need to be sent to a biosafety level 4 facility. Two capable facilities are the CDC in Atlanta, Georgia, and the US Army Medical Research Institute of Infectious Diseases in Frederick, Maryland [7]. This sample collection should be done only after suspected cases are reported immediately to local and state health departments. These health departments would then report directly to the CDC. Treatment Therapy for viral hemorrhagic fever is aggressive support. Fluids, electrolytes, and blood products are likely necessary in large quantities. Invasive procedures, although often necessary, should be limited secondary to the risk of needle stick infections which carry high morbidity and mortality. Currently, no antiviral drugs have been approved for the treatment of viral hemorrhagic fever by the FDA; however, ribavirin, a nucleoside analogue, has had some activity in treating viruses causing hemorrhagic fever [7]. Recent studies have shown that ribavirin is effective against arenaviruses (Lassa and New World arenaviruses) and bunyaviruses (Rift Valley fever, Crimean-Congo hemorrhagic fever, and Hantavirus Kman NE. Emerg Med Clin N Am. 2008; 26:

24 BIOLÓGICAS: evitar contagio
AGENTE AISLAMIENTO BACTERIAS Anthrax Brucellosis Plaga Fiebre Q Tularemia Gotas VIRUS Viruela Encefalitis Fiebre hemorrágica Aéreo, contacto Kaufman KM. Ann Emerg Med. 1999;34:

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26 QUÍMICAS 429 DC Thucydides, ateniano: uso humo de carbón encendido + sulfuro para incapacitar civiles en las barricadas. History Thucydides, an Athenian, documented the use of smoke from lighted coals and sulfur to incapacitate civilians inside barricaded forts in 429 BC [16]. Since that time, sulfur-laden ships have been supplanted by a variety of agents designed to erode both the physical and psychologic strength of the target. Specialized agents such as nerve gases, pulmonary irritants, and chemical asphyxiants were developed during the 20th century specifically for use as chemical warfare agents (CWAs). Reminiscent of the events of antiquity, sulfur (in the form of sulfur mustard) has produced the greatest known number of chemically induced human casualities by far [17]. Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

27 QUÍMICAS CLASES Agentes nerviosos Series G Tabun Sarin Soman, VX
Vesicantes Sulfuro de mostaza Lewisite Asfixiantes químicos Cianuro Cianógeno cloruro Irritantes pulmonares Cloro Fosgene Difosgene Agentes controladores multitudes Cloroacetofeno Types of chemical warfare agents Chemicals that have been developed as WMDs fall into five classes: 1. nerve agents (tabun, sarin, soman, VX) 2. vesicants (sulfur mustard, lewisite) 3. chemical asphyxiants (hydrogen cyanide, cyanogen chloride) 4. pulmonary irritants (chlorine, phosgene, and diphosgene) 5. riot-control agents (chloroacetophenome, CS) The clinical characteristics, mechanism of action, physical decontamination and available treatment modalities are reviewed for each of these classes of agents. In general, CWAs have a high potential for secondary contamination from victims to rescuers. Therefore, special personal protective equipment should be used by rescuers caring for CWA victims until thorough decontamination has been performed or the agent is identified as one that requires a lower level of protection. Level A gear, which provides the highest level of protection, is appropriate for most agents until this occurs, whereas level B equipment is the minimum required for an unknown hazardous material (Table 3). During decontamination, victims’ clothing should be fully removed. Where cutaneous exposure to a CWA has occurred, the affected areas should be washed well with soap and water. Eyes should be irrigated copiously with water or saline for 15 to 20 minutes, if affected. These guidelines are general. Additional or special decontamination and protective requirements are noted after each agent described in the following sections Bozeman WP. Emerg Med Clin N Am. 2002;20:

28 QUÍMICAS Alto potencial de segunda contaminación. Descontaminación:
Remover ropa Lavar agua, jabón Irrigación ocular 15-20min. In general, CWAs have a high potential for secondary contamination from victims to rescuers. Therefore, special personal protective equipment should be used by rescuers caring for CWA victims until thorough decontamination has been performed or the agent is identified as one that requires a lower level of protection. Level A gear, which provides the highest level of protection, is appropriate for most agents until this occurs, whereas level B equipment is the minimum required for an unknown hazardous material (Table 3). During decontamination, victims’ clothing should be fully removed. Where cutaneous exposure to a CWA has occurred, the affected areas should be washed well with soap and water. Eyes should be irrigated copiously with water or saline for 15 to 20 minutes, if affected. These guidelines are general. Additional or special decontamination and protective requirements are noted after each agent described in the following sections. Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

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30 QUÍMICAS: EQUIPO PROTECTOR
NIVEL CARACTERÍSTICAS A Encapsulado totalmente, resistente químicos traje, botas, guantes, equipo respirador autocontenido (SCBA). Máxima protección salpicaduras, vapor. B Resistente químicos traje, guantes, botas con externa presión positiva o respirador. Mínima protección para sustancias desconocidas o agentes químicos conocidos. C Resistente químicos con respirador (máscara de gas presión negativa o dispositivo presión positiva con baterías). Solo uso con sustancias seguras. D Estándar. No respirador. Levels and characteristics of chemical personal protective equipment [29] Level Characteristics A Fully encapsulated chemical-resistant suit/boots/gloves over positive-pressure self-contained breathing apparatus (SCBA). Provides maximal splash and vapor protection. Use requires special training. B Chemical-resistant suit/boots/gloves with externally worn positive-pressure SCBA or positive-pressure supplied air respirator. Minimum protection level for an unknown substance or known chemical warfare agent prior to decontamination. C Chemical-resistant suit/boots/gloves with supplied air respirator. (Respirator may be a negative-pressure gas mask or battery-powered positive-pressure device.) For use with known substances at safe levels. D Standard work clothes, no respirator (eg, a hospital care provider with scrubs and universal precautions in place). Bozeman WP. Emerg Med Clin N Am. 2002;20:

31 AGENTES NERVIOSOS Series G: inhibidores acetilcolinesterasa.
Letales inhalación, volátiles. Manifestaciones 2min post inhalación, 20-30min post contacto dérmico. Síntomas colinérgicos, falla respiratoria. Series V: derivados ácido fosfonotioico, inhibidor colinesterasa. Induce muerte pocas gotas dérmicas. G series Nerve agents Developed by the Germans during World War 2 and therefore named the ‘‘G’’ series, the nerve agents tabun, sarin, and soman are acetylcholinesterase inhibitors. By binding to and inactivating acetylcholinesterase, these agents affect the transmission of nerve impulses in both the central and peripheral nervous system in a fashion similar to organophosphate pesticide poisoning. Symptoms resulting from exposure are directly related to an accumulation of excessive acetylcholine at postsynaptic cholinergic receptor sites. Manifesting severe lethal effects rapidly after exposure, the G series of nerve agents notoriously have the most rapid onset of all the chemical warfare agents Under normal conditions, tabun, sarin, and soman exist as clear, colorless liquids. In addition, they are distinctly volatile and evaporation limits their persistence on skin and in the environment. Sarin, soman, and tabun exhibit progressively decreased volatility, respectively [20]. These properties make the G nerve agents lethal by inhalation, and to a lesser degree, cutaneous exposure, while allowing minimal re-entry risk into the affected environment after their dissipation. Symptoms produced by the G agents are dependent on the route, concentration, and duration of exposure. Patients may have an asymptomatic period of 20 to 30 minutes after a dermal exposure to a nerve agent, whereas onset of symptoms following inhalation may occur 2 minutes to 18 hours postexposure. Clinical effects are caused by an excess of acetylcholine, resulting in a cholinergic syndrome. Symptoms related to dermal exposure may be initially localized to the contact site, followed by GI and then other systemic manifestations. Mild exposures can result in localized sweating and muscle twitching in the contaminated area, abdominal cramping, nausea, increased salivation, rhinorrhea, miosis, and visual impairment and/or headache [19]. Patients may also complain of chest tightness, difficulty breathing, and fatigue. Moderate exposures progress to weakness, muscle fasciculations, slurred speech, and hallucinations. With severe dermal exposure or inhalation, respiratory distress secondary to bronchospasm and increased secretions are likely. Miosis, vomiting, and involuntary urination and defecation are also seen, and may progress rapidly to seizures, coma, and respiratory failure. Respiratory muscle paralysis and suffocation are the most common causes of death [20]. V series The V series nerve agents are derivatives of phosphonothioic acid developed by the British after World War II. The VX nerve agent (O-ethyl-S- [2(diisopropylamino)ethyl]methylphosphonothioate), like those of the G series, is an acetylcholinesterase inhibitor with a rapid onset. Unlike the G series, VX may induce death from just a few drops deposited dermally [20]. It is approximately 10 times more toxic than agents in the G series. VX is a colorless, essentially odorless liquid possessing the consistency of heavy lubricating oil. It has low volatility and can persist on equipment and terrain for long periods of time (Table 4). Although dermal absorption is the most likely route of exposure, VX may also be dispersed as an aerosol. Oral exposure following the consumption of contaminated liquids or foods will also cause toxicity. Effects of VX poisoning are typically seen rapidly, but may be delayed for up to 18 hours depending on the dose and route. The effects are identical to those of the G series nerve agents [20]. Treatment Level A personal protective equipment (see Table 3) is preferred for all of the nerve agents until full decontamination is accomplished or evaporation/ Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

32 AGENTES NERVIOSOS TRATAMIENTO
Atropina, revierte síntomas muscarínicos. Pralidoxima, restaura actividad enzima. Diazepam, convulsiones required for victims. If intubation is required, depolarizing neuromuscular dissemination is confirmed [21]. Airway and ventilatory support may be blockade with succinylcholine should be avoided to prevent excess release of acetylcholine [21]. Several specific antidotes are available for nerve agents: Atropine blocks excess acetylcholine at peripheral muscarinic sites. In sufficient doses, it can reverse the signs of muscarinic poisoning (ie, bronchospasm, bradycardia, excessive salivation, diaphoresis, diarrhea and vomiting). Atropine will not reverse the nicotinic effects (muscle weakness and paralysis) of nerve agent poisoning. A dose of 2 mg should be administered intravenously (IV) every 3 to 5 minutes (0.01–0.05 mg/kg in children) until excessive respiratory secretions have resolved and ventilation has improved. Miosis may not be reversed and should not be used as a clinical endpoint. If necessary, atropine can be administered intramuscularly or by endotracheal tube. High doses are often required. Cases requiring 10 to 20 mg of atropine in the first several hours and cumulative doses up to 100 mg have been reported [21]. Pralidoxime (2-PAM) can release a nerve agent’s attachment from acetylcholinesterase, and restore the enzyme’s activity, reversing the effects of nerve agents; however, 2-PAM must be administered before the nerve agent-acetylcholinesterase complex undergoes ‘‘aging’’ to become an irreversible covalent bond, permanently destroying the enzyme. In clinical practice, therapy should not be withheld from late-presenting patients on the premise that the aging process has been completed [21]. Doses of 1 to 2 g of 2-PAM (20–40 mg/kg in children) should be administered, preferably as an IV bolus over a period of 5 to 10 minutes. Additional doses may be administered as needed every 4 to 6 hours, or a continuous infusion of 500 mg per hour can be initiated if muscle weakness or fasciculations are not relieved in 1 hour [20]. Diazepam may be administered in 5- to 10-mg IV doses initially and repeated every 5 to 10 minutes as needed for seizure activity. Other benzodiazepines may be substituted. Atropine, 2-PAM, and diazepam are available in autoinjector kits through the US military. The MARK I kit contains 2 mg of atropine and 600 mg of 2-PAM in two intramuscular autoinjectors. The CANA IM autoinjector kit contains 10 mg of diazepam. One MARK I kit should be used if a patient exhibits symptoms such as severe rhinorrhea, miosis, and/or nausea and vomiting after CWA exposure. Two MARK I kits should be used if there is mild to moderate dyspnea and/or progression of nausea and vomiting. Three MARK I kits, with the added empiric use of 1 CANA IM kit, are used to manage copious secretions, severe dyspnea, muscular twitching/ fasciculations, seizure, or coma. Laboratory investigations have limited value in cases of nerve agent exposure. Red blood cell cholinesterase levels can confirm exposure but are typically unavailable in time to impact clinical treatment. Furthermore, theamount of enzyme inhibition does not always correlate with the degree of toxicity. Acetylcholinesterase is known to regenerate at approximately 1% each day, and a postexposure level may allow a rough estimate of recovery time [21]. Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

33 VESICANTES Produce ampollas cutáneas. Sulfuro de mostaza
Liga enzimas intracelulares, ácidos nucleicos, daño celular irreversible. Eritema, vesículas, bullas, , necrosis de coagulación piel axilas, región inguinal, cuello. Compromiso vía aérea, ocular, gi, falla respiratoria, muerte. Manejo: soporte. Vesicants As their name implies, the vesicant agents produce prominent blistering of the skin (in addition to other effects) after dermal exposure. The infamous ‘‘mustard gas’’ was developed and used during World War I and continues to be stored to the present day [17,22]. Sulfur mustard and lewisite are the most common of the vesicant agents. Sulfur mustard Following exposure, sulfur mustard rapidly breaks down in the extracellular water of the body. The resulting compounds quickly bind to intracellular enzymes and nucleic acids, causing irreversible cell damage. Protease digestion of anchoring filaments in the epidermal-dermal junction results in the formation of blisters several hours after exposure. Hematopoietic suppression effects of sulfur mustard are similar to those of ionizing radiation, and occur within 1 to 2 hours of exposure. The exact mechanism of these effects is unknown. Once sulfur mustard reacts with body tissues, it is no longer an intact molecule; therefore, one cannot become exposed from contact with body fluids or tissues after successful decontamination [17,20]. Sulfur mustard is an oily liquid ranging from light brown to yellow and has an odor similar to garlic, onion, or mustard. The form sulfur mustard takes is temperature dependent. Under temperate conditions, sulfur mustard evaporates slowly, posing primarily a liquid hazard for over a week after dispersal [23]. At temperatures of 100F or greater, sulfur mustard can evaporate within a day, but may present a vapor hazard. Sulfur mustard freezes at 57F and is often mixed with substances with a lower freezing point so that the mixture will remain liquid at lower temperatures [24]. Skin effects typically appear within 12 to 24 hours following exposure to sulfur mustard [24]. Time of onset is dependent on concentration, ambient temperature and humidity, and skin area exposed. More sensitive dermal areas include the axillae, groin, and neck. Erythema is seen initially. Small vesicles can develop within erythematous areas, which may later coalesce to form bullae. Fluid within the blisters does not contain sulfur mustard and is not a vesicant. Exposure from higher doses, such as those from liquid contact, may result in lesions with a central area of coagulation necrosis [24]. Early respiratory effects following a sulfur mustard vapor exposure may be irritation or burning of the nares, epistaxis, sinus pain, and irritation or soreness of the pharynx. Larger concentrations and prolonged exposure may lead to progressive injury and involvement of the lower airways. Symptoms may progress to severe cough, dyspnea, and rarely, hemorrhagic Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

34 VESICANTES Lewisite Síntomas inmediatos, permb capilar.
Síntomas respiratorios, ceguera. Tto: lavado con hipoclorito de sodio + agua+jabón Dimercaprol, BAL (British Anti-Lewisite) 2-4mg/kilo IM may occur with later damage to the musculature of the airways. Death from pulmonary edema. Necrosis of the laryngeal and tracheobronchial mucosa sulfur mustard poisoning is typically caused by respiratory failure, superimposed bacterial infection, and/or bone marrow suppression [20,23]. Ocular effects may be prominent after sulfur mustard exposure. Patients may present with pain and miosis secondary to cholinergic activity. Conjunctivitis, photophobia, blepharospasm, and corneal damage are seen with larger doses. Scarring and synechiae formation may occur, restricting pupillary movement and predisposing the victim to glaucoma [24]. More severe eye damage is caused by liquid sulfur mustard from airborne droplets. The mucosa of the GI tract is susceptible to sulfur mustard, although severe GI effects are infrequent. Nausea is common; diarrhea (rarely bloody) and vomiting may occur after high-dose exposure and imply a poor prognosis. Animal studies suggest that mustards (particularly nitrogen mustards) are proconvulsant, although CNS effects are poorly defined in humans [20]. Treatment. Level A personal protective equipment is preferred until full decontamination is accomplished. There are no specific antidotes for sulfur mustard exposure. Management is primarily supportive. Erythema may be treated with topical calamine or other soothing lotion to reduce burning and itching. Denuded areas should be thoroughly cleaned and treated with a topical antibiotic. Fluid loss is typically not of the magnitude seen with thermal burns, though fluid and electrolytes should be carefully monitored [23]. Eyes should be thoroughly irrigated, followed by regular application of a mydriatic, to prevent future synechiae formation, and a topical antibiotic [20]. Mild upper airway symptoms may respond to cough suppressants. Symptoms that suggest bronchitis may appear 12 to 24 hours following exposure and are usually secondary to a sterile pneumonitis [20]. Increasing fever, dyspnea, and pulmonary infiltrate on X ray may indicate infection and should be treated with appropriate antibiotics. Intubation may be necessary in those with severe pulmonary effects. Lewisite Lewisite is another vesicant agent that damages the eyes, skin, and airways by direct contact. After absorption, it causes an increase in capillary permeability to produce hypovolemia, shock, and organ damage. Its exact mechanism of biologic activity is unknown. Unlike sulfur mustard, lewisite has no latent time; symptoms appear immediately [25]. Lewisite is a colorless to brown or violet oily liquid with poor water solubility. It has a fruity or geranium-like odor. Common routes of exposure include ocular, cutaneous, and inhalation. Immediate burning and stinging occurs after dermal exposure to lewisite, with erythema appearing within 30 minutes and painful blister formation in 2 to 3 hours. Ocular effects include immediate burning and stinging with blepharospasm and edema. Iritis and corneal haziness occur over a few hours. Blindness may occur if eyes are not decontaminated within 1 minute [25]. Systemic signs of exposure include the following: diarrhea, restlessness, weakness, hypothermia, pulmonary edema, hypotension, hemolysis, focal liver necrosis, kidney damage, and necrosis of respiratory and GI mucosa. Treatment. Level A personal protective equipment is appropriate until full decontamination is accomplished. Alkaline solutions will degrade lewisite. Therefore, a dilute sodium hypochlorite (household bleach) solution should be used in addition to standard soap-and-water decontamination if this agent is suspected [25]. British Anti-Lewisite (BAL or dimercaprol) is a specific antidote that may alleviate systemic effects related to lewisite exposure by acting as a chelator. Indications for BAL administration include pulmonary edema, skin burns on more than 1% of body surface area (BSA) that were not decontaminated within 15 minutes, or skin burns on more than 5% of BSA [25]. BAL is supplied in 3 mL ampules containing 100 mg/mL. The initial dose is 2 to 4 mg/ kg, up to 400 mg administered intramuscularly. This dose may be repeated every 4 to 12 hours. Patients with a peanut allergy should not receive BAL because its vehicle is peanut oil. Chemet (Succimer, or 2,3-dimercaptosuccinic acid [DMSA] ) has also been successful in animal studies [25]. Bozeman WP. Emerg Med Clin N Am. 2002;20:

35 ASFIXIANTES QUÍMICOS Cianuro
Liga hierro hemoglobina, mioglobina, mitocondria. Inhibe fosforilación: metabolismo anaeróbico. Falla respiratoria, convulsiones, colapso cardíaco. Tto: kit cianuro IV Nitrito de sodio 3% Tiosulfato de sodio 25% Opción: hidroxicobalamina (vit B12) 2.5-5g. Chemical asphyxiants Cyanide Cyanide is available in a wide variety of forms and used in many industrial settings; it also can be used as a CWA [26]. Cyanide binds to oxidized or ferric iron present within the hemoglobin of red blood cells, myoglobin of the heart, and the mitochondria’s cytochrome oxidase. Inhibition of this enzyme inhibits oxidative phosphorylation with resultant anaerobic metabolism ensuing. Hydrogen cyanide and cyanogen chloride are clear liquid industrial solvents that become gases at temperatures more than 26F. Although not a reliable indicator, cyanide may be recognized by the smell of bitter almonds. These agents can rapidly kill at concentrations of 150 to 200 ppm. High concentrations of cyanide may cause respiratory distress and seizures in seconds, respiratory arrest within 3 to 5 minutes, and cardiovascular collapse/ death within 10 minutes. Lower concentrations may temporarily incapacitate victims, causing anxiety, dyspnea, hyperventilation, giddiness, headache, dizziness, nausea, palpitations, and flushed skin [20]. Treatment. Level A or B protective garments are appropriate (depending on concentration of cyanide) until full decontamination is accomplished. Airway Proper and timely use of the commercially available cyanide antidote kit can be critical for patients exhibiting severe cerebrovascular, cardiotoxic, or metabolic effects of cyanide. Each kit contains two 300-mg ampules of 3% sodium nitrite and two 50-mL ampules of 25% sodium thiosulfate. Sodium nitrite induces methemoglobinemia, which preferentially binds cyanide and prevents its attachment to cytochrome oxidase. Sodium thiosulfate is then administered to serve as a sulfur donor. This aids in the hepatic metabolism of cyanide to nontoxic thiocyanate, which is then renally excreted. One ampule of sodium nitrite is administered IV over a period of 5 to 20 minutes, followed by one ampule of sodium thiosulfate to complete the therapy [20]. Hydroxycobalamin (vitamin B12a) in concentrated form is an alternative cyanide antidote that is available in Europe but not in the United States. Hydroxycobalamin binds directly with ionized cyanide to form nontoxic cyanocobalamine (vitamin B12). Doses of 2.5 to 5 g of this safe and inexpensive agent have been recommended for prehospital and in-hospital use [27]. Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

36 Kit de Cianuro Nitrito de sodio al 3%. Ampolla de 1.5 gr en 50 ml. ( 30mg/ml) Dosis Adultos. Uso IV. Se pasan 10 ml (300mg) en un período de 5 minutos. Podría pasarse directa sin diluir o se podría diluir en 50 – 100cc para pasar durante 5 minutos. Niños – 0.33 ml /Kg en 5 minutos. OJO: tener cuidado en pasar máximo solo 10 ml de la ampolla por dosis, puesto que la formación de metahemoglobina en exceso podría ser letal para el paciente. Formación de Tiocianatos para la eliminación del tóxico: Hidroxicobalamina. (Las ampollas disponibles en nuestro medio son de 1mg/ml y la dosis inicial es hasta de 4 gr. No contamos con la ampollas disponibles en el Cyanokit, con 2 ampollas de 2.5 gr c/una). Tiosulfato de sodio o Hiposulfito de sodio al 25%. Ampolla de 12.5 gr en 50 ml (250mg/ml). Adultos. Uso IV. Se pasan 50 ml (12.5 gr) si diluir de forma rápida y directa (en bolo), Luego de 5 a 10 minutos de pasar el nitrito de sodio o amilo. Niños ml/Kg OJO: en este caso si se pasa la ampolla completa, ya que el hiposulfito o tiosulfato de sodio es atoxico.

37 IRRITANTES PULMONARES Cloro, fosgeno, difosgeno.
Se convierten ácido hidrocloruro en presencia agua. Lesionan ojos, nariz, faringe, pulmones. Tto: soporte. CONTROLADORES MULTITUDES Lacrimógenos. Dolor ocular, lagrimación, blefarospasmo. Raro: broncoespasmo, edema pulmonar. Tto: soporte Pulmonary irritants Chlorine, phosgene, and diphosgene Chlorine, phosgene, and diphosgene are pulmonary and mucous membrane irritants. These agents are converted into hydrochloric acid in the presence of water, causing injury to the eyes, nose, throat, and lungs [28]. Because of the difference of water solubility between the agents, the onset of toxicity differs among the pulmonary irritants. Chlorine (highly water soluble) is immediately hydrolyzed to hydrochloric acid, and its effects are almost instant. Conversely, phosgene and disphosgene (both poorly water soluble) have delayed toxicity that may go unrecognized for 30 minutes to 8 hours or more. The agents also have different odors. Whereas chlorine may be identified by the smell of concentrated bleach, phosgene and diphosgene are typified by the smell of freshly mown hay (see Table 4). Initial signs of exposure to all of these agents include a generalized burning sensation of mucous membranes, including the eyes, nose, throat, and the upper respiratory tract. More severe exposures progress to the development of a croupy cough, wheezing and stridor, dyspnea, hypotension, and noncardiogenic pulmonary edema [19]. Exposure to these pulmonary irritants may result in the development of residual pulmonary impairment [28]. Treatment. Level A or B protective garments are appropriate (depending on concentration of the CWA) until full decontamination is accomplished. Presently, there are no specific antidotes for exposure to pulmonary irritant CWAs. Management is primarily supportive. Supplemental humidified oxygen iswith severe pulmonary symptoms. Mild and moderate bronchospasm may be treated with nebulized bronchodilators, such as albuterol. Systemic steroids may be added for severe wheezing. Symptoms that suggest bronchitis may appear 12 to 24 hours following exposure and are usually secondary to a sterile pneumonitis. Superimposed bacterial infections may occur and should be treated with antibiotics. Eyes should be thoroughly irrigated, followed by a mydriatic, to help prevent future synechiae formation, and topical antibiotics. Last, in patients with possible exposure to phosgene or diphosgene, monitoring for a minimum of 12 hours is appropriate because of the possibility of delayed symptoms following exposure. Riot-control agents CN and CS Several agents collectively known as riot-control agents or lacrimators are currently used by law enforcement agencies and available to the public. These relatively nontoxic agents cause temporary incapacitation by inducing eye pain, lacrimation, and blepharospasm. Exposure to these agents may also result in difficulty breathing, burning sensations in the chest, nausea, vomiting, and skin irritation. At high concentrations, injury to the skin and mucous membranes can occur. These agents include CN (chloracetophenon, or Mace) and CS (named after its creators, Corson and Stoughton) [20]. CN and CS are white or gray solids at room temperature, with a sharp irritating odor (see Table 4). They are dispersed as an aerosol in the form of a white cloud. They are not water soluble, but can be washed off the skin with regular soap and water. Riot-control agents cause almost instantaneous ocular pain, lacrimation, and blepharospasm [19]. This interference with vision is the primary mechanism for incapacitation and the reason for their common collective name, ‘‘tear gas.’’ Inhalation may cause a burning sensation in the mouth, throat, and chest. Nausea and vomiting are also common. Mild irritation of the skin occurs at lower concentrations and more severe burns can occur with concentrated or prolonged exposure. Treatment. Exposed persons should be removed from the offending source to fresh air. If rescuers need to enter an area that still contains high levels of CN or CS, level A or B personal protective equipment is appropriate. At lower levels, level C protection with an appropriate air-filtering gas mask approved for riot-control agents is adequate. Washing the skin with water will remove the residue but will not inactivate it. Removal of contaminated clothing will aid in preventing re-exposure. Treatment is supportive. Effects on the eyes and respiratory system generally dissipate within 15 to 30 minutes after cessation of exposure [20]. Although most exposures do not result in life-threatening emergencies, bronchospasm and noncardiogenic pulmonary edema have been seen. The rare exposure resulting in respiratory distress should be treated with supplemental oxygen and inhaled bronchodilators. Severe cases may require intubation with mechanical ventilation [20]. Rinsing the eyes with copious amounts of water will speed recovery. It is important not to rub the irritated eyes because this may cause mechanical corneal abrasions in addition to the chemical irritation. Significant ophthalmologic injury should be evaluated by an ophthalmologist [19]. Delayed skin erythema, if severe, can be treated with topical corticosteroids. Bozeman WP. Emerg Med Clin N Am. 2002;20:

38

39 NUCLEARES Agentes radioactivos.
Armas nucleares, sabotaje planta nuclear, detonaciones. Yoduro potasio: tto prevenir cáncer de tiroides en exposiciones radioactivas. Uso niños, embarazadas, mujer lactando, dósis 32 – 130mg. Azul de Prusia: tto radiocesio 3g orales/12h/30 días. Perhaps the most feared terrorist attack is one involving a radioactive agent. Exposure to radioactive material can occur from discharge of a nuclear weapon, sabotage of a nuclear power plant, or detonation of a dirty bomb. The overall management of victims of a radioactive weapon attack is out of the scope of this article, but several excellent references are available [136–138]. Issues related to antidotes that may be beneficial in reducing long-term consequences in those exposed are addressed here. Potassium iodide Potassium iodide (Fig. 7) is indicated to help prevent the development of thyroid cancer in those exposed to radioactive iodine [139]. It functions by preventing thyroid uptake of radioactive iodine [140]. To provide a protective effect, it must be administered within a few hours of exposure [137]. Unfortunately potassium iodide does not provide total protection from radioactive iodine [140]. The FDA and the World Health Organization have similar guidelines on the administration of potassium iodide [141]. These guidelines take into Therefore, adults over 40 are generally not advised to take potassium iodide unless there is a projected thyroid dose of over 5 Gy [137]; children and pregnant or lactating women should receive prophylaxis for projected exposure of over .05 Gy [142]. The doses recommended by the FDA are: adults, 130 mg; children between 3 and 18 years, 65 mg; infants and children, 32 mg; and newborns up to 1 month, 16 mg [143] Daily dosing should continue until the risk of exposure is eliminated [142]. Potassium iodide is indicated for events such as a nuclear blast or a reactor meltdown. A dirty bomb would expose victims to gamma radiation and other radioactive agents for which potassium iodide provides no protection Radiocesium (cesium-137) is readily available because of widespread use in radiotherapy and other medical and commercial devices. It is a principal constituent of radioactive fallout and is a likely source of contamination from a dirty bomb because of its ready availability [137,144]. Cesium contamination would cause a prolonged environmental hazard because it has a radioactive half-life of 30 years [144]. After being absorbed, cesium closely follows potassium, becoming uniformly distributed throughout the body. It is eliminated primarily through the kidney, with only approximately 10% normally excreted fecally [144]. The physiologic half-life varies, ranging from 50 to 150 days [128]. Victims generally present first with nausea, vomiting, and diarrhea. Dermal exposure can cause irritation, blistering, or necrotic lesions. Eventually exposure can lead to bone marrow suppression causing infection, hemorrhage, and death [128,144]. Prussian blue treats radiocesium exposure by a similar mechanism as for thallium poisoning. It binds to cesium secreted into the gut lumen, traps it, and allows it to be eliminated fecally. One study showed that patients urine/ feces excretion ratio of 4:1 was reversed to 1:4 after administration of Prussian blue. Also, this study showed the half-life was reduced by approximately 43% [144]. The minimum effective dose for Prussian blue is 3 g/day. Larger doses, up to 10 g/day are well tolerated and may be more effective. The FDA recommends 3 g orally two times a day for adults and adolescents and 1 g three times a day for children 2 to 12 years old. The treatment should continue for at least 30 days [137]. The patient’s serum potassium should be monitored. Also, Prussian blue can cause constipation, so it should be given with mannitol, and prophylactic administration of a laxative should be considered to prevent constipation and minimize the amount of time the radioactive matter in the feces is in contact with the intestines [144]. Lawrence DT. Emerg Med Clin N Am.2007;25: 567–595

40 CONCLUSIONES Muchos agentes potenciales existen para propósitos terroristas. Sospechar, conocer y tratar. Fundamental: PREVENCIÓN, mayor contaminación. Many potential agents exist that can be used for the purpose of chemical terrorism. Recognizing the toxicity is the first step in assisting victims of such an attack. Careful decontamination and supportive care will be the most important steps along with recognizing the particular syndrome to guide antidotal treatment. Also, using antidotes appropriately and assuring access to safe antidotes is extremely important. It is also important to realize that that the four toxins listed are more likely to be encountered in a nonterror-related incident (eg, pesticide exposure [organophosphates], exposure to improperly preserved foods [botulism], or smoke inhalation victims [cyanide]). Therefore, familiarity with these toxins’ manifestations and antidotes is useful for general emergency medicine

41 GRACIAS!! “La gente apasionada se entrega a lo que ama y nunca se dá por vencida”