Guest guest Posted September 15, 2002 Report Share Posted September 15, 2002 ----- Original Message ----- From: " Kathi " <pureheart@...> Sent: Saturday, September 14, 2002 10:01 PM Subject: Toxicity, Phosgene > Toxicity, Phosgene > Last Updated: January 21, 2002 > > Author: Noltkamper, MD, Assistant Medical Director, Department of > Emergency Medicine, Naval Hospital of Camp Lejeune > > Coauthor(s): Burgher, MD, Department of Emergency Medicine, the > Woodlands Memorial-Herman Hospital, Memorial Hermann Southwest Hospital > Noltkamper, MD, is a member of the following medical societies: > American College of Emergency Physicians Editor(s): C Fernandez, > MD, Medical Director of South Texas Poison Center, Associate Clinical > Professor, Departments of Emergency Medicine and Toxicology, University > of Texas Health Science Center at San ; T VanDeVoort, > PharmD, DABAT, Manager, Clinical Assistant Professor, Pharmacy > Department, Regions Hospital; Fred Harchelroad, MD, FACMT, Chair, > Department of Emergency Medicine, Director of Medical Toxicology, > Associate Professor, Department of Emergency Medicine, Allegheny General > Hospital; Halamka, MD, Chief Information Officer, CareGroup > Healthcare System, Assistant Professor of Medicine, Department of > Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant > Professor of Medicine, Harvard Medical School; and J Roberge, > MD, MPH, FAAEM, FACMT, Research Director, Department of Emergency > Medicine, Ohio Valley Medical Center; Clinical Associate Professor, > Department of Emergency Medicine, University of Pittsburgh > > Background: > Phosgene (COCl2) is a highly toxic gas or liquid that is classified as a > pulmonary irritant. Synonyms for phosgene include carbonic dichloride, > carbon oxychloride, carbonyl dichloride, chloroformyl chloride, d-stoff, > and green cross. The military symbol for phosgene is CG, and its United > Nations/Department of Transportation number is UN#1076. The American > Chemical Society's Chemical Abstracts Service (CAS) registry number for > phosgene is #75-44-5. > > Sir Humphrey Davy first synthesized phosgene in 1812 by passing carbon > monoxide and chloride through charcoal. During World War I, it was used > in combination with chlorine gas for combat purposes by the German army. > This combination allowed phosgene emission to be hastened in cold > weather. The German army switched to mustard gas in 1917 because of the > development of effective gas masks. More effective agents and improved > personal protective equipment make phosgene an unlikely agent to be used > in future battles. > > Present day exposure occurs during the manufacture of aniline dyes, > polycarbonate resins, coal tar, pesticides, isocyanates, polyurethane, > and pharmaceuticals. Phosgene exposure also occurs in the uranium > enrichment process and during the bleaching of sand for glass > production. Exposures related to the heating or combustion of > chlorinated organic compounds, such as carbon tetrachloride, chloroform, > and methylene chloride, also occur. These products are found in common > household solvents, paint removers, and dry cleaning fluids. > Occupational exposure can occur when welders heat metals treated with > these chemicals and in organic chemistry laboratories that use > chloroform. Similarly, vehicle crashes involving trains or trucks > transporting phosgene (or chlorinated hydrocarbons, such as methylene > chloride, that could combust to form phosgene) could expose numerous > individuals to this toxin. > > Pathophysiology: > Phosgene is a colorless gas with the odor of newly mown hay or green > corn. Olfactory fatigue may occur with a large exposure. Exposure to > concentrations of 3 ppm may not cause noticeable symptoms for 12-24 > hours. Exposures to 50 ppm may be rapidly fatal. While an odor threshold > of 1.5 ppm has been reported in some humans, this does not protect > against toxic inhalation effects. > > Phosgene is considered to have poor warning properties and, hence, may > reach the lower airways before it is noticed. It is 4 times heavier than > air and is a gas above > 47°F (8°C). Because of hydrolysis from atmospheric water, it appears as > a white cloud in an outside environment. > > Damage caused by phosgene is due to the presence of a highly reactive > carbonyl group attached to 2 chloride atoms. The gas dissolves slowly in > water, but when this occurs, it hydrolyses to form carbon dioxide and > hydrochloric acid. This slow dissolution allows phosgene to enter the > pulmonary system without significant damage to the upper airways. > However, in the lower airways and alveoli, the tissue undergoes necrosis > and inflammation. After the first few hours of exposure, the carbonyl > group attacks the surface of the alveolar capillaries, causing leakage > of serum into the alveolar septa. The tissue fills with fluid, causing > hypoxia and apnea. Massive amounts of fluid (up to 1 L/h) leak out of > the circulation, leading to a noncardiogenic pulmonary edema, with > associated hypoxemia and volume depletion. > > Researchers in the past decade have discovered 2 important facts that > may lead to improved therapy. First, phosgene stimulates the synthesis > of lipoxygenase-derived leukotrienes. Second, phosgene combines with > glutathione to form diglutathionyl dithiocarbonate. When the glutathione > stores become depleted, phosgene binds to the cellular macromolecules, > causing cell necrosis in the renal and hepatic tissues. > > Frequency: > In the US: Clinically significant phosgene exposure occurs infrequently. > Sporadic exposures in recent years are related to industrial accidents > or isolated. > > Internationally: In view of currently available war gases, which are > much more lethal than phosgene, and improved respiratory protection, > phosgene is no longer considered a significant threat. > > Mortality/Morbidity: > The Occupational Safety and Health Administration permissible exposure > limit (OSHA PEL) for the workplace is 0.1 ppm (0.4 mg/m) as an 8-hour > time weighted average. The level immediately dangerous to life or health > (IDLH) is 2 ppm. Even a short exposure to 50 ppm may result in rapid > fatality. > > During World War I, from December 1915 to August 1916, casualties from > phosgene exposure occurred in 4.1% of gas-exposed troops. Fatality from > phosgene exposure occurred in 0.7% of gas-exposed troops. Total > casualties from chemical gas exposure occurred in 1.2 million troops and > caused 100,000 deaths. Phosgene accounted for an estimated 80% of these > cases. > > According to OSHA, millions of kilograms of phosgene are produced > annually, with 10,000 workers at risk of exposure. This does not include > the large number of people that may have mild-to-moderate exposures in > their homes from using solvents (eg, methylene chloride) with heat guns > to remove paint. > > Morbidity and mortality are related to the degree of pulmonary insult > and subsequent hypoxemia. Delayed diagnosis may result from delayed > signs and symptoms. Underlying medical conditions contribute to the > patient's ability to withstand the hypoxic insult. > > Race: > No evidence has demonstrated that outcome of phosgene toxicity is > dependent on race. > > Sex: > No sex predilection exists. Historically, most exposures have occurred > in men because of their military roles. Women were exposed during World > War I from developing and testing gas masks at the home front. > > History: Diagnosis of phosgene toxicity depends largely on history of > exposure. Consider phosgene toxicity in patients involved in the > manufacture of dyes, resins, coal tar, and pesticides. Query patients > regarding occupation and any exposure to chemicals, especially around > sources of heat. In the work setting and at home, phosgene can be > produced by the combustion of methylene chloride (paint remover) or > trichloroethylene (a degreasing solvent). Patients typically have an > asymptomatic period of > 30 minutes to 72 hours, but most significant exposures have a latent > period less than 24 hours. The duration and concentration of exposure > determine the time to symptom onset. > > Pulmonary > Cough (initially nonproductive, later frothy white-to-yellow sputum) or > hemoptysis > Dyspnea (exertional early on, subsequently becomes resting dyspnea) > Chest tightness or discomfort (may be pleuritic but frequently is > described as retrosternal burning) > Head, ears, eyes, nose, and throat > Mucosal irritation - More common with intense exposure > Eye irritation and tearing > Nasal irritation (irritation and burning of the nasal passages) - Occurs > with phosgene concentrations higher than 3 ppm, but, with lower > respiratory tract disease, may occur at even lower concentrations > Throat irritation extending to the retrosternal area - Common with > exposures more than 5 ppm and may be described as a burning sensation > Sudden death secondary to laryngospasm with large exposures > Cardiovascular (caused by volume depletion or hypoxemia) > Lightheadedness, palpitations > Angina > Headache (thought to be secondary to the hypoxemia and the inflammatory > response initiated in the pulmonary parenchyma) > Anorexia, nausea, and vomiting > Flat metallic taste when smoking cigarettes or overall altered taste > sensation > Weakness > Anxiety and sense of impending doom (likely from the hypoxemia and > tachycardia) > Skin burning if the patient has been sweating or if clothing is wet > (caused by the breakdown to hydrochloric acid) > > Physical: Physical examination is useful with patients with active > symptoms. Patients who relate a recent exposure may be in the latent > phase and have no specific findings related to the exposure. > > Pulmonary > Tachypnea and bronchorrhea > Wheezes, crackles, or rales on auscultation > Cyanosis > Apnea (late finding) > Head, ears, eyes, nose, and throat (Upper airway findings are not good > prognostic indicators because significant injury may occur to the lower > airways without upper airway involvement.) > Conjunctival injection and lacrimation > Oropharyngeal hyperemia and salivation > Nasal mucosa hyperemia associated with rhinorrhea > Cardiovascular > Tachycardia > Hypotension > Skin > Cyanosis from pulmonary injury and resultant hypoxemia > Chemical burns from liquefied phosgene (Although it also is considered a > frostbite hazard in the compressed liquid form) > > Causes: > The major risks are occupational exposure and close proximity to an > industrial incident. > > Present day exposures described in literature are caused by the > combustion products from chlorinated chemicals (eg, methylene chloride, > trichloroethylene). > > Welding metals recently treated with degreasers, such as > trichloroethylene, may produce phosgene. > > Use of methylene chloride, a commonly used chemical paint remover, near > a heat source allows the release of phosgene. > > Carbon monoxide is released in vivo as a metabolic product of methylene > chloride. > > Phosgene is a breakdown product of chloroform that is stored for more > than 6 months, even if the chloroform is stabilized with amylene. > > > DIFFERENTIALS > Acute Coronary Syndrome > Acute Respiratory Distress Syndrome > Altitude Illness - Pulmonary Syndromes > Bronchitis > CBRNE - Chemical Warfare Agents > Congestive Heart Failure and Pulmonary Edema > EMS and Terrorism > Hantavirus Cardiopulmonary Syndrome > Hazmat > Pneumonia, Bacterial > Pneumonia, Mycoplasma > Pneumonia, Viral > Pulmonary Embolism > Respiratory Distress Syndrome, Adult > Smoke Inhalation > Toxicity, Ammonia > Toxicity, Carbon Monoxide > Toxicity, Chlorine Gas > Toxicity, Cyanide > Toxicity, Hydrocarbon Insecticides > Toxicity, Hydrogen Sulfide > Toxicity, Organophosphate and Carbamate > Toxicity, Phosgene > > Other Problems to be Considered: > > Phosphorus pentoxide exposure (white phosphorus weaponry) > Sulfur dioxide exposure > > WORKUP > Lab Studies: > > ABG with carboxyhemoglobin and methemoglobin levels > > ABG demonstrates the degree of hypoxemia. A partial pressure of oxygen > (pO2) as low as 23 mm Hg on 8 L/min of oxygen by face mask has been > reported. > > Typical presenting pO2 levels are 50-60 mm Hg while breathing room air. > > The carboxyhemoglobin level is important for cases involving exposure to > methylene chloride or when carbon monoxide exposure is suspected. > Methemoglobinemia may suggest other causes. > > CBC > > CBC may be obtained as a baseline level or if pneumonia is high on the > differential diagnosis list. An elevated WBC count is not specific > because it may result from hypoxemic stress or an infectious process. > > CBC may reveal hemoconcentration late in the disease process. > > Electrolytes may be obtained as baseline studies because of the > anticipated large fluid shifts that occur. > > Cardiac enzymes (eg, creatine kinase-MB [CK-MB], troponin T, troponin I) > may be obtained if cardiogenic pulmonary edema is high on the > differential. > > Continue pulse oximetry and cardiac monitoring in patients suspected of > phosgene toxicity. > > Investigation on a blood test that measures exposure to phosgene is > being pursued. Most likely, This test will be used in laboratory > settings. > > Imaging Studies: > > Chest x-ray > > Initial findings may be normal; however, as the disease progresses, the > chest x-ray (CXR) may demonstrate bilateral, diffuse interstitial > infiltrates. > > Heart and pulmonary vessel sizes are usually normal unless the patient > has baseline cardiomegaly. > > CXR findings may precede the clinical presentation. > > Procedures: > > Perform endotracheal (ET) intubation and mechanical ventilation based on > the degree of respiratory failure and overall clinical picture. > > > TREATMENT > Prehospital Care: > > To avoid further exposures, hazardous materials (Hazmat) prehospital > providers should always ensure that the environment is safe. > > A self-contained breathing apparatus (SCBA) should be worn at the > exposure site. Remove the patient's clothes to prevent further > contamination. > > If the eyes and skin are exposed, begin irrigation onsite. > > In the field, standard management of ABCs usually is sufficient. Severe > exposures may require ET intubation and suctioning. If a significant > bronchospastic component is present, bronchodilators may be used with > caution. > > Past wartime experience has demonstrated that, in a mass casualty > situation, phosgene exposures should be classified as immediate because > of the impending need for intubation and positive end-expiratory > pressure (PEEP) to maintain distal airway opening. > > Emergency Department Care: > Always consider the need for decontamination in any toxic exposure to > minimize the risk of poisoning hospital personnel. Inhalational exposure > of phosgene should not occur unless in the proximity of the gas. If > external decontamination has not been performed in the field, use > personal protective equipment, as necessary, including dermal, eye, and > facial protection. A decontamination shower unit may be used. > > Initiate humidified oxygen supplementation. Intubation with continuous > positive airway pressure (CPAP) ventilation and pressure support is > usually required to improve oxygenation. Frequent suctioning may improve > conditions. > > Bronchodilators may improve existing bronchospasm. In animal studies, > beneficial effect has been shown with the administration of numerous > drugs, including leukotriene antagonists, ibuprofen, colchicine, > cyclophosphamide, terbutaline, aminophylline, and N-acetylcysteine. > Nebulized sodium bicarbonate treatment theoretically may be beneficial; > however, consider it as second line after the drugs noted above. > > Avoid excessive fluid administration. Pulmonary artery catheter > monitoring may be required to maintain appropriate fluid balance while > treating hypotension caused by fluid shifts. > > In severe cases, extracorporeal membrane oxygenation (ECMO) may be > considered refractory to supportive care. > > Minimize fluid administration except when it is needed to correct > hypotension. Avoid diuretics because the patient typically is > volume-depleted from fluid shifts. > > Avoid exertion during treatment and for several weeks after recovery. > > Prophylactic antibiotics have been recommended by some authors based on > the findings of pneumonia and bronchitis in virtually all autopsy > specimens. > > Corticosteroid administration within 15 minutes postexposure has been > shown to reduce the degree of pulmonary edema. > > No specific antidote or effective elimination process exists. During > both world wars, the Germans and Russians believed that hexamethylene > tetramine was the antidote. Subsequent studies have shown some > preexposure benefit but no definite postexposure benefit. > > Tomelukast, a leukotriene receptor antagonist, prevents pulmonary edema > in phosgene-exposed rabbits. Experimentally, ibuprofen has been shown to > reduce phosgene-induced pulmonary edema. Colchicine and cyclophosphamide > reduce neutrophil influx when administered to mice 30 minutes following > phosgene exposure. These drugs reduce lung injury and mortality in mice. > > Intratracheal dibutyryl cyclic adenosine monophosphate (DBcAMP), a > cyclic adenosine monophosphate (cAMP) analogue, inhibits the release of > leukotrienes that contribute to the disease process. In phosgene-exposed > rabbits, terbutaline and aminophylline (cAMP enhancers) limit the > pulmonary capillary leakage. Also, intratracheal N-acetylcysteine (NAC), > administered to rabbits 45 minutes postexposure, reduces leukotriene > formation and pulmonary edema. Theoretically, nebulized NAC also should > be effective. > > Consultations: > > Consult the regional poison control center and a medical toxicologist > for additional useful information and patient care recommendations. > > Prolonged critical care management often is required for the pulmonary > complications of phosgene exposure. > > MEDICATION Section 7 of 11 Author Information Introduction > Clinical Differentials Workup Treatment Medication Follow-up > Miscellaneous Pictures Bibliography > > Management of phosgene toxicity is supportive. Oxygen, corticosteroids > (inhaled, systemic), leukotriene inhibitors, IV fluids, and prophylactic > antibiotics are recommended. The recommended steroid dose is much higher > than the dose conventionally used in asthma. Prophylactic antibiotics > and antifungals may be required because of the risk of superinfection. > Pressor agents may be required to treat hypotension, bradycardia, and > renal failure. > > Drug Category: > Corticosteroids -- Reduce inflammatory response. Whether early > administration of corticosteroids can prevent development of > noncardiogenic pulmonary edema is unknown. The decision to administer > corticosteroids must be made on clinical grounds. > > Treatments lasting more than 1 week may require a taper to prevent > abrupt steroid withdrawal. > > Drug Name > Dexamethasone (Decadron) -- Decreases inflammation by suppressing > migration of polymorphonuclear leukocytes and reducing capillary > permeability. > Adult Dose 4 puffs immediately followed by 1 puff q3min until any sense > of irritation is gone; then 5 puffs q15min until 1 inhaler is exhausted; > followed by a daily regimen of 1 puff qh during the day and 5 puffs > q15min for 90 min before sleep; repeat for at least 5 d > Pediatric Dose Not established > Contraindications Documented hypersensitivity Interactions Effects > decrease with coadministration of barbiturates, phenytoin, and rifampin; > decreases effect of salicylates and vaccines used for immunization > Pregnancy C - Safety for use during pregnancy has not been established. > Precautions Increases risk of multiple complications, including severe > infections; monitor adrenal insufficiency when tapering drug; abrupt > discontinuation of glucocorticoids may cause adrenal crisis; > hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, > hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, > growth suppression, and infections are possible complications of > glucocorticoid use > > Drug Name > Beclomethasone (Beclovent, Vanceril) -- Inhibits bronchoconstriction > mechanisms, producing direct smooth muscle relaxation; may decrease > number and activity of inflammatory cells, in turn decreasing airway > hyperresponsiveness. > Adult Dose > 10 puffs immediately followed by 5 puffs qh for 10 h; then 1 puff qh for > at least 5 d Pediatric Dose Not established > Contraindications Documented hypersensitivity; bronchospasm, status > asthmaticus, and other types of acute episodes of asthma Interactions > Coadministration with ketoconazole may increase plasma levels but does > not appear to be clinically significant Pregnancy C - Safety for use > during pregnancy has not been established. > Precautions Weight gain, increased bruising, cushingoid features, > acneiform lesions, mental disturbances, and cataracts may occur (taper > medication slowly if these changes occur) > > Drug Name > Methylprednisolone (Solu-Medrol) -- Decreases inflammation by > suppressing migration of polymorphonuclear leukocytes and reversing > increased capillary permeability. > Adult Dose Day 1: 1000 mg IV Days 2-3: 800 mg IV Days 4-5: 700 mg IV Day > 6: Reduce dose quickly if chest x-ray remains clear > Pediatric Dose Not established > Contraindications Documented hypersensitivity Interactions > Coadministration with digoxin may increase digitalis toxicity secondary > to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin > and rifampin may decrease levels (adjust dose); monitor patients for > hypokalemia when taking medication concurrently with diuretics Pregnancy > C - Safety for use during pregnancy has not been established. > Precautions Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, > hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, > myopathy, and infections are possible complications; caution in viral, > fungal, or tubercular skin infections > > Drug Name > Betamethasone (Celestone, Soluspan) -- Decreases inflammation by > suppressing migration of polymorphonuclear leukocytes and reversing > increased capillary permeability. > Adult Dose Begin with 20 mg IV; repeat q6h IV/IM for 24 h; reduce dose > over next 5 d > Pediatric Dose Not established > Contraindications Documented hypersensitivity Interactions Effects > decrease with coadministration of barbiturates, phenytoin, and rifampin; > dexamethasone decreases effect of salicylates and vaccines used for > immunization Pregnancy C - Safety for use during pregnancy has not been > established. > Precautions Increases risk of multiple complications, including severe > infections (caution in tubercular or systemic fungal infections); > monitor adrenal insufficiency when tapering drug; abrupt discontinuation > of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, > osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, > osteoporosis, euphoria, psychosis, myasthenia gravis, growth > suppression, and infections are possible complications > > Drug Category: > Vasopressors -- Used to treat hypotension, bradycardia, or renal > failure. > Drug Name > Dopamine (Intropin) -- Stimulates adrenergic and dopaminergic receptors. > Hemodynamic effect is dependent on the dose. Lower doses predominantly > stimulate dopaminergic receptors that, in turn, produce renal and > mesenteric vasodilation. Use low dose to protect renal function; use > high dose to combat severe hypotension unresponsive to fluid > administration. > Adult Dose 2-20 mcg/kg/min IV; titrate to effect > Pediatric Dose Administer as in adults > Contraindications Documented hypersensitivity; pheochromocytoma or > ventricular fibrillation Interactions Phenytoin, alpha- and > beta-adrenergic blockers, general anesthesia, and MAOIs increase and > prolong effects Pregnancy C - Safety for use during pregnancy has not > been established. > Precautions Closely monitor urine flow, cardiac output, pulmonary wedge > pressure, and blood pressure during the infusion; before infusion, > correct hypovolemia with whole blood or plasma prn; monitoring central > venous pressure or left ventricular filling pressure may be helpful in > detecting and treating hypovolemia > > Drug Category: > Leukotriene antagonists -- Reduce the inflammatory response elicited by > the leukotriene cascade. Leukotriene antagonists are approved by the > Food and Drug Administration (FDA) only for chronic asthma management. > Drug Name > Zafirlukast (Accolate) -- No human studies have evaluated the efficacy > and safety of zafirlukast in patients exposed to phosgene. Nevertheless, > given the known effects of leukotriene stimulation by phosgene, the > results from animal studies, and the drug's safety profile, should be > considered first line. In the presence of food, bioavailability of oral > zafirlukast is decreased by 40%. Administer on an empty stomach. > Adult Dose 20 mg q12h PO asthma; however, given the pharmacokinetic > profile and the exaggerated response caused by phosgene, an increased > dosage can be assumed (consider 40-80 mg PO q12h for the initial 48 h) > Pediatric Dose Not established > Contraindications Documented hypersensitivity Interactions Aspirin > increases plasma levels; erythromycin decreases plasma levels; > theophylline may decrease levels and may increase plasma theophylline > levels; warfarin may result in clinically significant increases in > half-life of warfarin Pregnancy B - Usually safe but benefits must > outweigh the risks. > Precautions Severe liver disease; concomitant warfarin therapy; systemic > eosinophilia, and symptoms consistent with Churg-Strauss syndrome have > been reported during reduction in oral steroid therapy; efficacy and > safety in humans exposed to phosgene have not been validated in clinical > trials > > FOLLOW-UP > Further Inpatient Care: > > Admit patient to an intensive care setting for continued monitoring and > supportive care. Improvement typically occurs within 48-72 hours. > > Further Outpatient Care: > > In a case of suspected exposure to phosgene, monitor the patient for a > minimum of 12-24 hours because of the potential for delayed-onset > pulmonary edema. (The patient must remain asymptomatic and have no chest > x-ray changes or hypoxemia after observation to be released from the ED > or inpatient ward.) > > Instruct patients discharged from the hospital after recovery from > pulmonary edema to avoid exertion and any pulmonary toxins that may > precipitate a recurrence. Also, instruct patients to avoid circumstances > similar to their exposure and to warn others of the same dangers. > > Transfer: > > Provide supplemental oxygen and/or bilevel positive airway pressure > (BiPAP) and immediately transfer patients to an appropriate facility if > they present to clinics or hospitals without endotracheal intubation > capability, ventilator capability, or ICU monitoring. > > Deterrence/Prevention: > > A standard field protective mask or gas particulate filter provides > adequate protection. > > Personnel working with chlorinated hydrocarbon compounds should ensure > adequate ventilation and avoid exposing the compounds and the vapors to > heat. > > Complications: > > Recurrence of pulmonary edema because of exertion, re-exposure, or > exposure to other pulmonary toxins > Pneumonia > Development of reactive airway disease > > Prognosis: > > The prognosis of acute phosgene exposure is good with early > intervention. Few significant long-term sequelae occur after recovery. > > Studies involving combat personnel and workers involved in the uranium > enrichment process have shown increased morbidity and mortality with > high level exposure because of the development of pneumonitis, chronic > bronchitis, emphysema, and impaired pulmonary function. > > The degree of the patient's cyanosis provides a rough estimate of > survivability. Historically, patients with a mouse grey cyanosis have a > worse prognosis than those with a plum blue cyanosis (quantitative > assessment of hypoxemia was not routinely available at the time of these > historical observations). To estimate the time until respiratory > failure, double the length of time from exposure to the development of > crackles. > > Patient Education: > > Instruct patients to avoid future exposures and to educate others > involved in similar practices. Patients should minimize exertion for > several weeks. Determining factors for return to the ED should include > the symptoms of cough recurrence, dyspnea (especially resting dyspnea), > and chest discomfort. > > MISCELLANEOUS > Medical/Legal Pitfalls: > > Failure to consider the asymptomatic period and delayed onset of > symptoms associated with phosgene toxicity and discharging the patient > from the ED without an adequate period of observation > > Failure to ascertain a history consistent with phosgene exposure > > Failure to recognize phosgene as a combustion product of certain > chemicals, especially chlorinated compounds (eg, methylene chloride, > trichloroethylene) > > Failure to associate phosgene with the manufacturing process of common > chemicals (eg, methyl isocyanate) > > Failure to consider phosgene toxicity in patients who present dyspnea or > chest discomfort and who have occupations (eg, welding, refinishing) > with increased risk of exposure > > Delay in the administration of corticosteroids in patients with phosgene > exposure > > Administering diuretics to a volume-depleted patient, causing further > circulatory collapse > > Failure to consider secondary pneumonia in patients not responding after > 2-3 days of aggressive therapy > > Failure to recognize early signs of significant respiratory distress and > document either a pO2 or oxygen saturation via pulse oximetry > > Failure to monitor the patient in a setting where respiratory support is > immediately available or failure to transfer the patient to a facility > with appropriate respiratory support capability > > Failure to consider carbon monoxide poisoning from exposure to methylene > chloride > > Failure to evaluate and treat possible angina or myocardial infarction > > Special Concerns: > > The views expressed in this article are those of the authors and do not > reflect the official policy or position of the Department of the Navy, > Department of Defense, or the US government. > BIBLIOGRAPHY Section 11 of 11 Author Information Introduction > Clinical Differentials Workup Treatment Medication Follow-up > Miscellaneous Pictures Bibliography > Balmes J: Phosgene. In: Olson KR, ed. Poisoning and Drug Overdose. 2nd > ed. Appleton & Lange; 1994: 256. British War Office: Medical Manual of > Chemical Warfare. London; 1941: 31-38. Ellenhorn MJ: Chemical warfare. > In: Ellenhorn's Medical Toxicology. 2nd ed. Lippincott & > Wilkins; 1997: 1301-2. Kennedy TP, JR, Hoidal JR, et al: > Dibutyryl cAMP, aminophylline, and beta-adrenergic agonists protect > against pulmonary edema caused by phosgene. J Appl Physiol 1989 Dec; > 67(6): 2542-52[Medline]. LS: Simple asphyxiants and pulmonary > irritants. In: Goldfrank L, ed. Goldfrank's Toxicologic Emergencies. 6th > ed. New York: McGraw-Hill; 1998: 1530. Ng TP, Tsin TW, O' FJ: An > outbreak of illness after occupational exposure to ozone and acid > chlorides. Br J Ind Med 1985 Oct; 42(10): 686-90[Medline]. Noort D, > Hulst AG, Fidder A, et al: In vitro adduct formation of phosgene with > albumin and hemoglobin in human blood. Chem Res Toxicol 2000 Aug; 13(8): > 719-26[Medline]. Schelble DT: Phosgene and phosphine. In: Haddad LM, > MW, Winchester J, eds. Clinical Management of Poisoning and Drug > Overdose. 3rd ed. Philadelphia: WB Saunders; > 1998: 960-3. Sciuto AM, Strickland PT, Kennedy TP, Gurtner GH: > Protective effects of N-acetylcysteine treatment after phosgene exposure > in rabbits. Am J Respir Crit Care Med 1995 Mar; 151(3 Pt > 1): 768-72[Medline]. Sciuto AM, Strickland PT, Kennedy TP, Gurtner GH: > Postexposure treatment with aminophylline protects against phosgene- > induced acute lung injury. Exp Lung Res 1997 Jul-Aug; > 23(4): 317-32[Medline]. Sciuto AM, Stotts RR: Posttreatment with > eicosatetraynoic acid decreases lung edema in guinea pigs exposed to > phosgene: the role of leukotrienes. Exp Lung Res 1998 May-Jun; 24(3): > 273-92[Medline]. Sciuto AM: Assessment of early acute lung injury in > rodents exposed to phosgene. Arch Toxicol 1998 Apr; 72(5): > 283-8[Medline]. Sciuto AM, Strickland PT, Kennedy TP, et al: > Intratracheal administration of DBcAMP attenuates edema formation in > phosgene-induced acute lung injury. J Appl Physiol 1996 Jan; 80(1): > 149-57[Medline]. Sciuto AM, Stotts RR, Hurt HH: Efficacy of ibuprofen > and pentoxifylline in the treatment of phosgene- induced acute lung > injury. J Appl Toxicol 1996 Sep-Oct; 16(5): 381-4[Medline]. Selden A, > Sundell L: Chlorinated solvents, welding and pulmonary edema. Chest 1991 > Jan; 99(1): 263[Medline]. Sidell FR, Takafuji ET, Franz DR: Toxic > inhalation injury. In: Textbook of Military Medicine: Medical Aspects of > Chemical and Biological Warfare. Walter Army Medical Center; 1997: > 257-60. Sjogren B, Plato N, sson R, et al: Pulmonary reactions > caused by welding-induced decomposed trichloroethylene. Chest 1991 Jan; > 99(1): 237-8[Medline]. Snyder RW, Mishel HS, Christensen GC 3d: > Pulmonary toxicity following exposure to methylene chloride and its > combustion product, phosgene. Chest 1992 Mar; 101(3): > 860-1[Medline]. > > > > > Quote Link to comment Share on other sites More sharing options...
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