Scribd Logo
Upload

Welcome to Scribd!

  • 26 views

    Emergency and Disaster Nursing

    Uploaded by

    chupzpt
    Emergency and Disaster Nursing

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content

    You might also like

    Emergency and Disaster Nursing

    Uploaded by

    chupzpt
    26 views24 pages
    Emergency and Disaster Nursing

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Report this Document
    Emergency and Disaster Nursing

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    Download as pdf
    26 views24 pages

    Emergency and Disaster Nursing

    Uploaded by

    chupzpt
    Emergency and Disaster Nursing

    Copyright:

    © All Rights Reserved
    Download as PDF or read online from Scribd
    Flag for inappropriate content
    Download as pdf
    of 24
    When we accept tough jobs as. a and wade into them with joy and enthusiasm, miracles ‘challenge joy and en Harry $ Truman ON ELA aU LCA az aa rea (SI oO Emergency and Disaster Nursing Linda Bucher ‘LEARNING ‘OBJECTIVES. 1. Apply the sequential steps in tage, the primary survey andthe secondary survey to a patient in an emergency situation. 2. Describe the pathophysiology, assessment, and collaborative care of select environmental emergencies, including hyperthermia, hypothermia, submersion injury, and animal bites. 5. Describe the pathophysiology, assessment, and collaborative care of select toxcologic emergencies. 4 iferentiate between the various types and victims of volence 5 enti the agents mos likely to be used in a terrorist attack 6. Diferentate the esponsibilties of health care providers the community, and selec federal agencies in e emergency and mas casualty incident preparedness. Electronic Resources ‘Supplemental content related to Chapter 69 can be found Companion cD + Stess Busting Kt for Nursing Students + NCLEX Examination Review Questions : + Comprehensive Glossary Content Updates Key Points Printable and CO/MP3 Download) + + Concept Map Creator . KEY TERMS bioterrorism, p. 1838 ‘emergency . 1642 heat cramps, p. 1828 heat exhaustion, p. 1829, heatstroke, p. 1829 bypothermia, p. 1851 jaw-thrust maneuver, p. 1823, mass casualty incident, p. 1842 triage, p. 1822 Evolve Website @ZI0Z9 htp//evoleesevercom/Lewis/medsurg + Key Ter Flash Cards Electronic Caleulators Weblinks panded Aucio Glossary Most patients with lfeshreatening or potentially life-threatening problems arrive atthe hospital through the emergency department (ED). Many more patients report tothe ED for less urgent cond tions.! Over 80 million people visit EDs annually, and this number is increasing fora variety of reasons (@2., the inability to see a primary care provider, the aging population, shorter hospital stays resulting in fequentreadmissions, and lack of health insurance or primary care provider)? These factors have resulted in chronic overcrowding and long wait times in many EDs.! ‘Emergency nurses care for patients of all ages and with a vari ety of problems. However, some EDs specialize in certain patient populations or conditions, such as pediatric ED or trauma ED. The Emergency Nurses Assocation (ENA) is the specialty nursing or- ization aimed at advancing emergency nursing practice. The provides standards of care for nurses working inthe ED, as well asa certification process that allows nurses to become a ceti- fied emergency nurse (CEN).‘ This certification validates the knowledge that a nurse needs to provide competent care in emer- ‘gency settings. Emergency management of patients with various medical, sur gical, and traumatic emergencies is presented throughout this bbook. Tables that highlight emergency management of specific problems are presented in the related chapters. Table 69-1 lists each emergency management table by title, number, and page. ‘This chapter focuses on triage, initial assessment, and manage- ‘ment of the trauma patient and selected emergency conditions not addressed elsewhere in this book, including heat- and cold-related emergencies, submersion injures, bites, stings, and poisonings. In addition, an overview of issues related to violence and emergency and disaster preparedness is presented, Reviewed by Carlyn Cary, RN, MSN, CEN, Staff Nurse, Emergency Deparent, Virus West Jersey Hospital Marlon, Marton, NJ; and Virginia Crocker, RN MS, CEN, Clinical Nurse Specialist, Emergency Deparment, Winchester Hospi, Winchester, Mase. 1821 1822 Section 12 Nursing Care in Spec ized Settings CARE OF THE EMERGENCY PATIENT Recognition of life-threatening illness or injury is one of the ‘most important aspects of emergency care. Before a diagnosis ‘can be made, recognition of dangerous clinical signs and symp- toms with initiation of interventions to reverse or prevent a crisis Bvt EMERGENCY MANAGEMENT CSI Emergency Management Tabl Title Chapter ‘Redominal aura a Page 7018 ‘Acute abdominal pain a 1035, Acute sot tissue jury 63 692 Anaphylactic shock 4 230 Chemical urns 2 489 Chest pain x 806 Chest wauma 2 586 Cocaine and amphetamine toxicity 2 175 Depressant drugs, overdose of 2 178 Diabetic ketoacicis 4 1280 Dysthytnis 36 848 Eloctrcal burns 25 480 Eye iniuy 2 221 Fractured extremity 63 r612 Head injry 87 1484 Hypertnermia 6 1890 Hypothermia 69 1832 Inhalation njcy 25 480 Sexual assaut| 54 1810 Shock 6 1785; Spinal cord injury et 1596 Stroke 58 1511 ‘Submesion injuries eo 1833 Thermal burns 25 490 Thorac injures a 586 Tonie-cloni eezures 59 1837 is essential, This process begins with the first patient contact ‘The emergency nurse is usually confronted with multiple py tients who have a variety of problems. Prompt identification patients requiring immediate treatment and determination of propriate treatment area are essential nurse competencies in a busy ED. Triage Triage, « French word meaning “to sor,” refers to the process of rapidly determining patient acuity, tis one of the most important skills needed by the emergency nurse. The triage process is based on the premise that patients who have a threat 10 life, vision, or limb should be treated before other patients, {A triage system identifies and categorizes patients so that the ‘most critical are treated first. The ENA and American College of Emergency Physicians support the use of a five-level triage sys tem.’ The Emergency Severity Index (ESI) is a five-level triage system that incorporates concepts of illness severity and resource utilization (e.g., electrocardiogram, laboratory work, radiology studies, intravenous fluids) to determine who should be treated firs’ (Table 69-2), The ESI includes a triage algorithm that the ‘nurse uses to assign an ESI level to patients presenting to the ED (Fig, 69-1), Initially, patients are assessed for any threat (eg. Is the patient apneic?), Patients who do not meet the criteria for ESI-1 or ESI-2 are next evaluated for the number of anticipated resources they may need. Patients are assigned to ESI level 3, 4, or 5 based on this determination. Vital signs are required for patients assigned to ESI level 3, Patients with abnormal vital signs may be reassigned fo ESI level 2° The use of triage systems such as th ESI can provide a mechanism for EDs to predict short-term hos} tal resource and stating needs.* After the emergency nurse completes the initial assessment 0 determine the presence of actual or potential threats folie, appro- priate interventions are initiated forthe patient’s condition. A his to life TABLE 69-2 We ee ek) gy, diseuptive pyohiate patient Tevel Definition ESI-1 ESL? ESI-3 ES-4 ESI-S Staiy ofvtat Unstable “Treatened Sable Stable Sable function (ASC) Life treat oF organ Obvious Let but not aways Untely but pssile No No ‘throat ‘covous How soon patent immediatly Mites Upto the Cod be delayed Cou be delayed should bo seen by physician Expected resource High resource High resource intensty; Medumiigh resource Low resource Low source intonsty intensity tat ‘rule ofen com: intensity mula iter one intensity, exam 2 bedsioe plex dagrostic Gagosie studies Simple agnostic. nation only ominously; often Stusils fequent or re obser study ora simple mobilization of Conautation conie- on er compiex procedure team response ‘ous pemete) proceaure mmentonng Exomples Consac ares Cet pain probaby _Abominl pain or Closed exvemity Cod symptoms, Tnubate trauma reslteg fom ynecologe trauma, simple roe burn, patent severe ischemia, miele sorter unlessinn—_laveration,cytiis, recheck ‘overdose, SOS ‘rouma ress severe dates, ‘ype mgane (eg, wound) response eid ip acre ‘wih feverandietn- —_eldery patent ‘Reims wih pormison, Copyright 190, Richard C, Woe, MD, and David R Eel MD. ACs, Aiceay, behing, ciclaton SIDS, sdlen nl death syndrome. Tio nendan | Sl ee) e Ne ! High-Fek shootin? Conhse/lathogic/ doit? Severe poin/ direst Yes <3mo />180/ >50/ e AGIA Emergency Severity index Tage Agorhm, version 4 tory is obtained simultaneously with the assessment. A systematic approach to the inital patient assessment decreases the time re- 4uired to identify potential threats and minimizes the risk of over: looking a life-threatening condition. Two systematic approaches, primary survey and a secondary survey, were initially developed for use with the trauma patient, but these can be easily applied to assessment of any emergency patie Primary Survey The primary survey (Table 69-3) focuses on airway, breathin circulation, and disability and serves to identify life-threatening conditions so that appropriate interventions can be initiated Life-threatening conditions related to airway, breathing, circula- tion, and disability (Table 69-4) may be identified at any point during the primary survey. When this occurs, interventions are started immediately and before proceeding to the next step of the survey. A= Airway with Cervical Spine Stabilization and/or Immobilization. Nearly ll immediate trauma deaths occur be- cause of airway obstruction, Saliva, bloody secretions, vomitus, laryngeal trauma, dentures, facil t ‘can obstruct the airway. Patients at risk for airway compromise in- clude those who have seizures, near-drowning, anaphylaxis, for- body obstruction, oF cardiopulmonary arrest. fan airway is ou ‘obstruction of ulow occurs and hypo, aid and death may result Primary signs and symptoms in a patient with a compromised airway include dyspnea, inability to vocalize, presence of foreign 1ma, fractures, and the tongue Chapter 69 Emergency and Disaster Nursing 1823 body in the airway, and trauma to the face or neck. Airway maine- nance should progress rapidly from the least 10 the most invasive method. Treatment includes opening the airway using the jaw- thrust maneuver (avoiding hyperextension ofthe neck) (Fig. 69. suctioning and/or removal of foreign bedly, insertion of a nasopha: ryngeal oF an oropharyngeal airway (wil use gagging if patent is conscious), and endotracheal intubation. If unable to intubate be- cause of airway obstruction, an emergency cricothyridotomy or tracheotomy should be performed (see Chapter 27), Patients should be ventilated with 100% oxygen using a bag-valve-mask (BVM) Debycration + Tachycardia fds, + Thyrotoxcose Weak, thready pulse + Obtain ECs. * Diabetes + Tampere 09 6"F (975° G)10 104° F + Obtain blond for eecrlyes and CBC. oc) * Insen uray cathter Drugs +" Phenothiazines Heatstroke Ongoing Monitoring + Treyeleantiseprossants Hot, dy skin "Motor A, aligns, level of Diretee + Atered mental stats (9, ranging from consciousness. + Montor cardiac rhythm, O» saturation, + BeAdrenerge Blockors + Hypotension lectrottes, and urinary output. | + Antnistemnes © Taenyoaraa ‘+ Monitor uire for development of © Weakness rmyogiobinua, Other Temperature >104° F140") + Monitor clting studies for development of lisseminatod intravascular coagulation. ACs, Airway, rcahng, Scan, BV, agave mks CRC. compete ioe coun; CNW cena serous ater, CG. elececaioga IV IHvaNenOw hot weather and physical exercise is imperative, Patients should also be instructed on the early signs of and interventions for heat: related stress. COLD-RELATED EMERGENCIES Cold injuries may be localized (Frostbite) or systemic (hypother: ‘mia Contributing factors include age, duration of exposure, envi ‘ronmental temperature, homelessness, preexisting conditions (e.. diabetes mellitus, peripheral vascular disease), medications that ‘suppress shivering (opioids, heroin, psychotropic agents, and anti femeties), and alcohol intoxication, which causes peripheral vaso- dilation, increases sensations of warmth, and depresses shivering, ‘Smokers have an increased risk of cold-related injury asa result of the vasoconstrictive effects of nicotine. Frostbite Frostbite can be described as “true tissue freezing.” which results in the formation of ice crystals in the tissues and cells. Peripheral ‘vasoconstriction isthe initial response 10 cold stress and results in 1 decrease in blood flow and vascular stasis. As cellular tempera- ture decreases and ice crystals form in intracellular spaces. intra cellular sodium and chloride inerease, the cell membrane is de- stroyed, and organelles are damaged. These alterations result in edema, Depth of frostbite is the result of ambient temperature, length of exposure, type and condition (wet or dry) of clothing, and contact with metal surfaces. Other factors that affect severity include skin color (dark-skinned people are more prone to frost- bite). lack of acclimatization, previous episodes, exhaustion, and poor peripheral vascular st ‘Superficial frostbite involves skin and subcutaneous tissue, usu- ally the ears, nose, fingers, and toes. The skin appearance will (BIGGS ema ad ter formation 24 hus ater site in occur sgn an aca covred bya thy ed boot n of tingling Bea ‘Gangrenous necross 6 weeks atter the frostbite injury shown in rg 693. cof deep thermal injury with mottling gradually progressing to gangrene (Fig. 69-4) The affected extremity is immersed in a circulating water bath (102° to 108” F [38.9° to 42.2° C)) until distal flush occurs. After rewarming, the extremity should be ele- vated to reduce edema Significant edema may begin within 3 hours, with blistering in 6 hours to days. Intravenous analgesia is always required in severe frostbite because ofthe pain associ- ated wit tissue thawing. Tetanus prophylaxis should be given, and the patient should be evaluated for systemic hypothermia, ‘Amputation may be required ifthe injured area is untreated or treatment is unsuccessful. The patient may be admitted to the ital for observation over 24 to 48 hours with bed rest, eleva- ‘ofthe injured part, and prophylactic antibiotics if tbe wound at rsk for infection Hypothermia ‘Hypothermia, defined a a core temperature less than 95°F (35°C), ‘occurs when heat produced by the body cannot compensate for heat lost to the environment. From 55% to 60% of all body beat i lost as radiant energy, with the greatest loss from the head, thorax, and Jungs (with each breath). Wet clothing increases evaporative heat Joss 5 times greater than normal; immersion in cold water increases beat loss by a factor of 25. Environmental exposure to freezing tem- peratures, cold winds, and wet, damp terrain in the presence of physical exhaustion, inadequate clothing, and/or inexperience pre- disposes individuals to hypothermia. Near-drowning and water immersion are also associated with hypothermia, ‘The elderly are more prone to hypothermia due to decreased body fat, diminished energy reserves, decreased basal metabolic rate, decreased shivering response, decreased sensory perception, chronic medical conditions, and medications that ater body de- fenses. In addition, certain drugs, alcohol, and diabetes are consid- eed risk factors for hypothermia. ‘Hypothermia mimics cerebral or metabolic disturbances caus- ing ataxia, confusion, and withdrawal, so the patient may be mis- diagnosed. Peripheral vasoconstriction is the body's first attempt to conserve heat. As cold temperatures persist, shivering and movement are the body's only mechanisms for producing heat. results when core temperature falls below 82.4° F (28° C), death usually occurs when core temperature falls below 78° F O* Core temperature below 86° F (30° C) is severe and potentially life threatening. Assessment findings in hypothermia are variable sand dependent on core temperature (Table 69-9). Patients with Chapter 69 Emergency and Disaster Nursing 1831 ‘mild hypothermia (93.2° to 96.8° F [34° to 36° C}) have shivering, lethargy, confusion, rational to irrational behavior, and minor heart rate changes. Shivering disappears at temperatures less than 92°F (G3.3° ©). Moderate hypothermia (86° to 93.2° F [30° to 34° C}) causes rigidity, bradycardia, slowed respiratory rate, blood pres- ‘sure obtainable only by Doppler, metabolic and respiratory acido- sis, and hypovolemia. ‘As core temperature drops, basal metabolic rate decreases two or three times. The cold myocardium is extremely irritable, mak- ing it valnerable to dysrhythmis (e.g, atrial and ventricular fibril- lation). Decreased renal blood flow decreases glomerular filtration rate, which impairs water reabsorption and leads to dehydration, ‘The hematocrit increases as intravascular volume decreases. Cold blood becomes thick and acts asa thrombus, placing the patient at risk for stroke, myocardial infarction, pulmonary emboli, acute tu- bular necrosis, and renal failure. Decreased blood flow leads to lactic acid accumulation from anaerobic metabolism and subse- quent metabolic acidosis, Profound hypothermia (less than 86° F (30° C}) makes the per- son appear dead. Metabolic rate, heart rate, and respirations are so slow that they may be difficult to detect. Reflexes are absent and the pupils fixed and dilated. Profound bradycardia, asystole, or ventricular fibrillation may be present. Every effort is made to warm the patient to at least 90° F (32.2° C) before the person is pronounced dead. The cause of death is usually refractory ventric- ‘lar fibrillation, Care. Treatment of hypothermia focuses on managing and maintaining ABCs, rewarming the patient, correcting dehydration and acidosis, and treating cardiac dysthythmias (see ‘Table 69-9), Passive or active external rewarming is used for mild hypothermia. Passive external rewarming involves moving the pa- tient to a warm, dry place, removing damp clothing, and placing warm blankets on the patient. Gentle handling is essential to prevent stimulation ofthe cold myocardium. Active external rewarming in- volves body-to-body contact, uid- or air-filled warming blankets, ‘or radiant heat lamps. The patient should be closely monitored for ‘marked vasodilation and hypotension during rewarming. ‘Active core rewarming is used for moderate to profound hypo- thermia and refers to heat applied directly tothe core. Techniques include heated (107.6° to 148° F [42° to 46° C), humidified oxy- ‘gem; warmed IV fluids (109.4° F [43° C); and peritoneal, gastric, or colonic lavage with warmed fluids. Hemodialysis or cardiopulmo- nary bypass may also be considered in profound hypothermia ‘Core temperature should be carefully monitored during re- ‘warming procedures. Warming places the patient at risk for afer- drop, a further drop in core temperature, which occurs when cold peripheral blood returns to the central circulation. Rewarming shock can produce hypotension and dysrhythmias. Thus patients with moderate to profound hypothermia should have the core ‘warmed before the extremities. Rewarming should be discontinued ‘once the core temperature reaches 95° F (35° C): Patient teaching should focus on how to avoid future cold- related problems. Essential information includes dressing in layers for cold weather, covering the head, carrying high-carbohydrate foods for extra calories, and developing a plan for survival should an injury occur. SUBMERSION INJURIES ‘Submersion injury results when a person becomes hypoxic due to submersion in a substance, usually water. Approximately 8000 deaths occur from submersion injuries annually in the United 1832 Section 12 _ Nursing Care in Specialized Settings r i i potital EMERGENCY MANAGEMENT oo ea Hospital Acquired © Cold fats ‘in to com) Etiology ‘Assessment Findings Interventions Environmental + Core body temperature: Initial Prolonged exposure to old Mid hypothermia: 95.2"-96.8° F G4"-96"C) + Remove patient from cold envionment. Prolonged submersion Moderate hypothermia: 86°-88.2"F Manage and mantain ABC. + Inadequate clthing fr environmental (00-34 6) + Provise righsow Oz via non-rebreathor temperature Profound hypothermia: <86"F (30° 0) mask or BVM, ‘+ Shivering, diminished or absent at core body + Anticipate intubation fr eminished or Metabolic temperature =92"F (333° 0) absent gag refs. + Hypostycemia + Hypoventation + Faowam patent: + Hypotnyroism * Hypoiension Passive: Remove wet clothing, apply dry ‘Altered mental status (ranging from contu- + ofoxia (absence of reflexes) ‘Active extemal: Use body-to-body contact, © Blood administration © Pale, cyanotic skin apply eating devices (e.g, alec * Inadequate warming or rewarming inthe ED + lve, white, or frozen extremities warming blankets) or radiant ight or sugery * Dysthymias: bradycardia, ail Fixllaion, Active core warming: Administer warmed + Adminstration of peuromuscular blocking ventricular filation, aystole 'V us; heated, humicied 0: agents Fixed, cated pups pertoneal, gastric, or colonic lavage wit warmed fu. Other * Anticipate the need for hemodialysis + Phenethiazines Ccarciopulmonary bypass. + Barbiturates| * Warm central trunk frst in patients with pro + Alcohol found hypothermia to mit rewarming shock. : Tama + Establish IV access with two large-bore Clothing and warm blankets, administer warm fds, catheters for fui resustation. ‘Assess for othe injuries. ‘Keop patients head covered with warm, dy ‘owes, or stocking cap to limit los of hoat ‘Treat patient gently to avoid increased car ac imtabity, Ongoing Monitoring Monitor ABCs, level of consciousness, temperature, vital sans. Monitor O, saturation, cardiac rythm. Monitor electrolytes, glucose. ABCs, Away, being culation, BVM, fag valve-nask: ED. emergency depart, V7, invavenow. States. Forty percent of these victims are children under 5 years of age. The primary risk factors for submersion injury include inabil- ity to swim, use of alcohol or drugs, trauma, seizures, hypother- ‘mia, and stroke Drowning is death from suffocation after submersion in water or other fluid medium. Near-drowning is defined as survival from potential drowning. Jmmersion syndrome occurs with immersion in cold water, which leads to stimulation of the vagus nerve and potentially fatal dysrhythmias (e.., bradycardia). Death from a submersion injury is caused by hypoxia secon dary to aspiration and swallowing of fluid, usually water. Swal- lowed water may cause vomiting and additional aspiration. A ma- jority of drowning victims aspirate water into the pulmonary tree and develop pulmonary edema. Victims who do not aspirate fluid develop intense bronchospasm and airway obstruction, the cause of death in “dry drowning.” Regardless of what fluid is aspirated into the pulmonary tree, the ultimate result is pulmonary edem: ‘The osmotic gradient caused by aspirated fluid causes fuid imbal- ances in the body. Hypotonic fresh water is rapidly absorbed into the circulatory system through the alveoli, Fresh water may be contaminated with chlorine, mud, and algae, causing the break down of lung surfactant, fluid seepage, and pulmonary edema Hypertonic salt water draws protein-rich fluid from the vascular space into the alveot in hypoxia, Fig, 69 freshwater aspiration, ‘The body attempts to compensate for hypoxia by shunting blood to the lungs. This results in inereased pulmonary pressures and deteriorating respiratory status. More and more blood is shunted through the alveoli. However, the blood is not adequately oxygenated, so the hypoxemia worsens. Anaerobic metabolism. ‘occurs, which leads to lactic acidosis. The assessment findings of a patient with a submersion injury are listed in Table 69-10. Aggressive resuscitation efforts and the ‘mammalian diving reflex improve survival of near-drowning vic~ tims even after submersion in cold water for long periods of time?” old water lowers the body's metabolic rate and oxygen demand. ‘The mammalian diving reflex causes apnea, bradycardia, and pe- ripheral vasoconstriction and further decreases metabolic ate. Blood flow is redistributed to the most vital organs (ie., heart, lungs, brain). impairing alveolar ventilation and resulting shows the pulmonary effects of saltwater and Collaborative Care @ Treatment of submersion injures focuses on conecting hypo eel alec uloareefocpearing | ae lps lgie Renae rewaralag whos lypetarala i pre Chapter 69 Emergency and Disaster Nursing 1833 cnt. Initial evaluation involves assessment of airway, cervical spine, breathing, and circulation, Other interventions are listed in Se 69-10, ‘Mechanical ventilation with positive end-expiratory pressure or ‘Continuous positive airway pressure may be used to improve gas FIG. 6925 Pulmonary effects of water aspiration exchange across the alveolar-capillary membrane when significant pulmonary edema is present. Ventilation and oxygenation are the primary techniques used to treat respiratory acidosis. Mannitol (Osmitrol) or furosemide (Lasix) may be given to decrease free water and treat cerebral edema, Deterioration in neurologic status suggests cerebral edema, worsening hypoxia, or profound acidosis. Near-drowning vietims may also have head and neck injuries that cause prolonged altera tions in level of consciousness. All victims of near-drowning should be observed in a hospital for a minimum of 4 to 6 hours. Additional observation is needed for patients who have preexisting comorbidities (e.g., cardiovascular disease). Peumonia and cere= bral edema have been reported in patients who were essentially free of symptoms immediately after the near-drowning episode but later developed problems. Delayed pulmonary edema (also known as secondary drowning) can occur and is defined as delayed death from drowning due to pulmonary complications, ‘Teaching should focus on water safety and minimizing the risks for drowning. Swimming poo! gates should be locked: life jackets should be used on all watercraft, including inner tubes and rafts and water survival skills (eg, swimming lessons) should be a pri- ority. The dangers of combining alcohol and drugs with swimming and other water sports should be emphasized” BITES AND STINGS ‘Animals, spiders, and insects cause injury and even death by biting or stinging. Morbidity is a result of either direct tissue damage or lethal toxins. Direct tissue damage is a product of animal size, characteristics ofthe animals teth, and strength of the jaw. Tissue may be lacerated, crushed, or chewed while toxins released RUC EMERGENCY MANAGEMENT CST submersion Injuries Etiology ‘Assessment Findings Interventions aby to swim or exhaustion wile Pulmonary Initial swimming + infective breathing “Manage and martan ABCs * Entrapment or entanglement wih objects in Oyspnaa Assume cervical spine injury nal rowing water + Respratory dstoss Victims and sabize andlor mmebitze * Loss of ability to move secondary to trauma, + Respiratory arrest carvieal spine. stroke hypothermia, myocartal infarction” + Crackles, ones + Provide 100% O, via non-roreathr mask or + Poor judgment du to alcohol or drugs * Gough with pink-fothy sputum BVM © Seaure whe n water + Gyanosis + Anticipate need for intubation gag retex's absent. Cardiac + Estabish IV access with wo large-bore + Tachycardia ‘catheters fr fa esusctation and ise * Bradyearia ‘warmed fui if appropriate + Dystythmia + Assess for other ines + Hypotension * Remove wet dthing and cover wih warm + Garda: arest blankets + Obtain temperature and begin rewarming it Other pacer + Parse + Obiain cervical pine and chest xays. + Exhaustion + insert gat tube + Coma + Cosxisting iess (eM or inury ‘Ongoing Monitoring (€9,. conical spine iniy) + Monitor ABCs, vita signs, evel of + Gore temperatire aight elevated or below consciousness. rormel depending on water temperature arc) + MontorO, saturation, care rythm. length of submersion ‘Monitor temperature and maintan oxmothermia, + Monitor for signs of acute respiratory faire ACs, Airway, behing, circulation; BVM, bag-alve-mank; IV inravenos; MT myocardial infarction Erne) 1834 Section 12 Nursing Care in Specialized Settings through teeth, fangs, stingers, spines, or tentacles have local or systemic effects. Death associated with animal bites is due to blood loss, allergic reactions, or lethal toxins. Injuries caused by Insects, spiders, ticks. snakes. animals (e.g., dogs. cats, rodents), ‘and humans are described here Hymenopteran Stings ‘The Hymenoptera family includes bees, yellow jackets, hornets, wasps, and fire ants. Stings can cause mild discomfort ot life- threatening anaphylaxis (see Chapters 14 and 67), Venom may be cytotoxic, hemolytic, allergenic, or vasoactive. Symptoms may begin immediately or be delayed up to 48 hours. Reactions are more severe with multiple stings. Most hymenopterans sting re: peatedly, However, the domestic honey bee stings only once, usu: ally leaving a barbed stinger with an attached venom sac in the skin so that release of venom continues. ATticanized honey bees (killer bees) which look and sting like domestic bees have mi ‘grated into North America, If threatened, these bees aggressively swarm and repeatedly sting their victims (e.g, humans, animals). ‘These attacks can be fatal I'stung, the stinger should be removed with a scraping motion with a fingernail, knife, or needle. Tweezers squeeze the stinger ‘and may cause more venom release. However, the fastest method ‘of removing the stinger is ultimately the best, so if weezers are available, they can be used. “Manifestations vary from stinging, burning, swelling, and itching to edema, headache, fever, syncope, malaise, nausea, vomiting, wheezing, bronchospasm, laryngeal edema, and hypotension. Treat. ‘ment depends on the severity of the reaction. Mild reactions are treated with elevation, cool compresses, antipruritic lotions, and oral antihistamines, Rings, watches, and restrictive clothing are removed More severe reactions require intramuscular or IV antihistamines (eg, diphenhydramine (Benadryl)), subcutaneous epinephrine, and corticosteroids (e-g., dexamethasone [Decadron]). Allergic reactions and anaphylaxis are discussed in Chapter 14. Spider Bites (Arachnid) Although there are 20,000 species of venomous spiders in the ‘world, only 50 species cause illnes. Two venomous spiders found in the United States are the black widow spider and the brown re- clase spider2* Their venom can eause a localized reaction or sys- temie anaphylaxis. Tarantulas appear more dangerous than they actually are because thei bite causes only localized stinging and pain, Other types of spiders telease Venom when they bite and may cause allergi reactions in some individuals, but they are not con- sidered poisonous. Black Widow Spiders. Black widow spiders are the most feared of al spiders. The female's venom is especially poisonous to people. Both the female and male are black in color (Fig. 69-6). The female rarely leaves the web, biting defensively if disturbed Black widow spiders are found among fallen branches, among firewood, and under objects of many kinds, including furniture, outhouse seas, and trash, ‘The black widow spider venom is neurotoxic. When bitten, the patient will feel a pinprickclike sensation and a tiny, ed bite mark will appear. Approximately 15 to 60 minutes late, the patient will report severe pain that will increase over the next 12 t0 48 hours Systemic symptoms will develop 30 minutes alter envenomation (the imoducton of poisonous venoms into the body by a bite ora sting). These can include nausea, vomiting, abdominal eramping hypertension, dyspnea, paresthesias. and tachycardia, Symptoms FIG. 69-6 Female tack widow spider The fully gronn female is about 1.2 am (05 in) ong and «jet Back, war hourglass shaped red mack onthe Underside ofthe abdomen. Te feral’ sing potions to humans Males are ‘only about half slong and usuaby have four pas of ed dos along the sides the abdomen, Males ae rarely Seen and when they metre, they lose ther poi sonous abit usually peak 2 t0 3 hours after onset; however, muscle spasms and jon can recur for 12 to 24 hours. Chest and abdominal ‘abdominal rigidity, whereas bites on the upper body lead to chest, back, and shoulder rigidity. A black widow spider bit is not prominent and can be easly missed, Patents not aware of the bit can be misdiagnosed, because symptoms mimic a perforated ulcer, appendicitis, pancreatitis, or other abdominal emergency ‘Treatment includes cooling the area to slow the acto neurotoxin, IV access should be established and oxygen adminis tered as needed, The wound shouldbe cleaned and tetanus a laxis given as appropriate. Muscle spasns are treated with cle gluconate, diazepam (Valium), or methocarbamol (Robaxin), Se- Xere pain may requite opioid analgesia. Although antivenin is, rarely used, it can be used for severe reactions, young children, or adulls with hypertension or cardiac disease Brown Recluse Spiders. Brown recluse spiders are usually found in dark areas such as garages, cosets, and boxes. The spider, common in the southeaster, south-central, and southwestem United States. is a light brown color with a characteristic dark brown fiddle shape that extends from the eyes down the back. The venom is cytotoxic, so local tissue effects can be dramatic. Ini- tially, the bite is insignificant, with a local reaction (ez. itching, erythema) beginning in 6 to 12 hours. A painful, bluish-purple purpura develops in a ring around the bite and eventually may progress to a necrotic uleerating wound by 7 to 14 days, though it ‘may take as long as 6 months. The wound can extend deep into tissue and may persist for weeks. Occasionally, systemic manifes tations of envenomation occur and ean include fever, chills, join pain, malaise, nausea, and vomiting.® ‘Treatment depends on severity of the reaction. Treatment is necessary when there is bleb or bulla formation, intense pain, and signs of rapidly progressive ischemia and necrosis. Initial inte ventions include cleansing the bite with mild antiseptic soap. providing cool compresses, and elevating the affected extremity Analgesia, tetanus prophylaxis, antihistamines, corticosteroids, and antibiotics for prevention of secondary infection may also some patients. Hyperbaric oxygen therapy may also be const ered to enhance tissue healing. Dapsone (Avlosulfon), a poly morphonuclear leukocyte inhibitor, has been used for patients with deep crater wounds, bat efficacy has not been validated. Pa of the o— eh. t FIG. 69-7 Tick removal A, Use tvcezrs to rasp the tick close tothe skin B, With 6 steady moti, pull he t's body any fom the sin. Oo not be ried 4 the teks mouthparts feman in the skin. Once the mouthparts ae ved om the ret ofthe tc, can no longer vans ease. tients with systemic manifestations are hospitalized and moni toted for hemolysis, disseminated intravascular coagulation, and acute renal failure” Tick Bites Ticks are found throughout the United States, but they are most common inthe northwestern, Rocky Mountain, and the northeastern regions. Emergencies associated with tick bites include Lyme dis: Rocky Mountain spotted fever, and tick paralysis. Disease is ed by an infected tick or by the release of neurotoxin. Ticks re se a neurotoxic venom as long as the tick head is attached tothe body. Therefore removal ofthe attached tick is essential for effective tweatment. Forceps or tweezers may be used to safely remove the tick by grasping atthe point of entry and pulling upward ina steady ‘motion (Fig. 69-7). After the tick is removed, the skin should be leaned with soap and water. Do not use a hot match, petroleum jelly, nal polish, or other products to remove the tick.§* Lyme disease is the most common arthropod-bome disease in the United States. Symptoms appear within 2 10 30 days of a bite from the Lxodid (hard) tick and result from exposure to the spiro- chete Borrelia burgdorferi that is found on the tick. The initial stage ofthis disease is characterized by nonspecific flu-like symp- toms (e.g. headache, stiff neck, fatigue) and a characteristic bull's eye rash—an expanding circular area of redness of 5 em diameter ‘or more. Symptoms will disappear in 2 weeks if not treated, Mono: articular arthritis, meningitis, and neuropathies occur days or ‘weeks after the initial symptoms. Chronic arthritis and myocarditis, characterize the later stage of the disease, which can develop sev cral months to 2 years after the initial skin lesion, Treatment in- cludes doxyeycline (Vibramycin) and cefuroxime. (Lyme disease is discussed in Chapter 65.) Rocky Mountain spotied fever is caused by Ricketsia rickemsi, ‘bacteria that is spread to humans by the /xodid tick. I has an cubation period of 2 to 14 days, and a pink. macular rash appears ‘on the palms. wrists, soles, feet, and ankles within 10 days of ex- sure, Other symptoms include fever, chills, malaise, myalgias, @ each, Dingncis is often cfc inthe eal sage, and fhout treatment it can be fatal. Antibiotic therapy with doxyc cline (Vibramycin) is the treatment of choice Tick paralysis accurs 5 to 7 day’ afler exposure to & neurotoxin Introduced by a wood tick or dog tick. Classie symptoms are Mac- 1835 Emergency and Disaster Nursing Pit viper [venomous snake) ® ‘Wiangle-shaped hood Anal plete Single row of subeaudl plotes Rotle(ratlesnake) FIG. 69-8 Pipe (2 ype of venomous snake), FIG, 69-9 western cara snake 1 venom rom this sake is newton cid ascending paralysis, which develops over I to 2 days, Without tick removal, the patient dies as respiratory muscles become para lyzed, Tick removal leads to return of muscle movement, usually within 48 to 72 hours Snakebites Only 375 of the 3000 species of snakes in the world are poisonous, Poisonous snakes indigenous to the United States are members of the Crotalidae and Elapidae family. Crotalidae, or pit vipers, in clude rattlesnakes, copperheads, and water moccasins (Fig. 69:8) Coral snakes belong 10 the Elapidae family. Coral snakes do not exhibit the triangular head of pit vipers but are recognized by their bright colors. Coral snakes always have a blunt black snout and ‘ed, yellow, and black rings that completely encircle the body (Fig. {69.9), Coral snakes are poisonous non-pit vipers. ‘Venom from the pit viper is hemolytic, whereas coral snake venom is neurotoxie. Envenomation occurs in approximately 75% © 80% of all snakebites. If swelling does not occur within 30 minutes after the bite, envenomation is unlikely. Local reaction is characterized by one or two fang matks associated with pain, bruising, and edema within 36 hours of injury, petechiae, ecehy- ‘mosis, and erythema. Loss of function and necrosis ofthe affected Jimb may occur 16 to 36 hours after the bite. Systemic reactions Include nausea and vomiting, dizziness, tachycardia, muscle fas ciculations, gastrointestinal (Gl) bleeding, and respiratory prob: lems. The patient may experience a metallic or rubber taste. Neu rologic symptoms such as constricted pupils, drowsiness, weakness, fasciculations, muscle weakness, and seizures oceur with neuro: problems associated with systemic toxic venom, fore ond 1836 Nursing Care in Specialized Settings Pee mes TABLE 69-11 paresthesia listo moderate ‘no eystemic reactons Moderate: Fang marks, progressive sweling beyond bite, mid systemic reaction fe... nausea, ving, parethesias, hypotension) Envenomation Signs and Symptoms ~ Number of Vials of Antivenint one Fang mar, no toca swell, Femorhage No aver, tetanus propa, observation -Mid: Fang marks, local sweting of hands or feet, pain, Init dose: 4-6 vias (3000-4500 ma) intused over: infusion ‘shoud be initiated slowiy for he frst 10 min to detect any allergic reactions; final control of symptoms isnot achieved, ‘dose may be repeated once Actiona agian 2 vals ever 6h for 18 hr "Polya! Crouse avon one Fab (COPD For Ctl exsenomation (eg atesnaks,coppetheas) ‘envenomation include severe hemorrhage, renal failure, and hypo. volemic shock. Treatment focuses on preventing the spread of venom. Rings, watches, and restrictive clothing should be removed, and then the affected limb should be immobilized at the level of the heart. lee and touriquets are not recommended. Incision of the wound is controversial. If done within 3 minutes of injury with the appropri ate device (e.g., Sawyer extractor), 5% to 30% of the venom may ‘be removed. Caffeine, alcohol, and smoking increase the spread of venom and should be avoided. ED management includes vascular access with a large-bore (14. to 16-gauge) catheter and administration of crystalloids to maintain blood pressure. Diagnostic tests include complete blood ‘count, urinalysis, coagulation studies, blood urea nitrogen, creati- nine, creatine kinase, and electrolytes. Other measures include as: sessment of extremity swelling, usually through documentation of circumference every 30 to 60 minutes, Pain should be treated with acetaminophen (Tylenol). Aspirin and nonsteroidal antinflamma tory drugs should be avoided because they may exacerbate bleed: ing: opioids may cause respiratory depression, Tetanus prophy’ laxis should be administered as needed (see Table 69-6). Secondary infection caused by microorganisms in the snake's mouth or other contaminants may require antibiotic therapy. Debridement or fas ciotomy (see Chapter 25) is necessary in some patients, Antivenin (polyvalent Crotalidae antivenin ovine Fab (CroFab)) therapy is used in mild to moderate reactions; the amount of antivenin re ‘quired depends on the timing, type, and severity of envenomation (Table 69-11), Incomplete dosage is the most common cause of treatment failure. Animal and Human Bites Every year over 2 million animal bites are reported in the United States.) Children are at greatest risk. The most significant prob- lems associated with animal bites are infection and mechanical destruction of the skin, muscle, tendons, blood vessels, and bon ‘The bite may cause a simple laceration or be associated with crush injury, puncture wound, or tearing or avulsion of tissue. The sever- ity of injury depends on animal size, vietim size, and anatomic lo- cation of the bite. Animal bites from dogs and cats are most com- ‘mon, with wild or domestic rodents (e.g., squirrels, hamsters) following dogs and cats as the third most frequent offenders in re ported animal bites.” Dog bites usually occur on the extremities; however, facial bites are common in small children, Most victims own the dogs that bite them, Dog bites may involve significant tissue damage with fatal ties reported, usually in children. Skull fractures with intracranial injury and death may occur in children less than 2 years old. Dis- Figuring wounds of the face should be evaluated by a plastic surgeon. ‘Cat bites cause deep puncture wounds that can involve tendons and joint capsules and result in a greater incidence of infection (30% to 50%). Septic arthritis, osteomyelitis, and tenosynovitis, have been reported in cat bites. The most common causative or zanisms of infections from cat und dog bites are from the Pastew rella species (eg, P.canis), This organism is found in the mouths ff most healthy cats and dogs." Human bites also cause puncture wounds or lacerations and carry a high risk of infection from oral bacterial flora, most com monly Staphylococcus aureus and streptococci, and hepatitis vi- rus." Hands, fingers, ears, nose, vagina, and penis are the most common sites of human bites and are frequently a result of vio- lence or sexual activity. Boxer’s fracture (fracture of the fourth or fifth metacarpal) is often associated with an open wound when e knuckles strike teeth. The human jaw has great crushing ab causing laceration, puncture, crush injury, soft tissue tearing, even amputation, More than 40 potential pathogens found in the ‘human mouth aceount for an infection rate of approximately 50% in cases where vietims did not seek medical intervention within 24 hours of injury. Collaborative Care. Initial treatment for animal and hu- man bites includes cleaning with copious irrigation, debride- ment, tetanus prophylaxis, and analgesies as needed. Prophylac- tie antibiotics are used for animal and human bites at risk for infection, such as wounds over joints, those greater than 6 0 12 hours old, puncture wounds, and bites of the hand or foot. In dividuals at greatest risk of infection are infants, older adults, immunosuppressed patients, aleoholics, diabetics, and people taking corticosteroids Puncture wounds ate left open, whereas lacerations are loosely sutured. Wounds over joints are splinted, However, initial closure is reserved only for facial wounds. The patient is admitted for IV antibiotic therapy when an infection is present. There creased incidence of cellulitis, osteomyelitis, and septic arthritis in these patients. Animal and human bites must be reported to the police in many states. ‘Consideration of rabies prophylaxis is an essential component in ‘management of animal bites. A neurotoxic virus found in the saliva cof some mammals causes rabies. If untreated, the condition is fatal in humans. Rabies exposure should be considered if an animal a tack was not provoked, involved a wild animal, or involved ad te animal not immunized agin abies, Rabies propyl “oo "ways given when the animal eannot be found or & carnivorous W ‘animal causes the bite. An initial injection of rabies immune globu- lin (RIG [BayRab)) to provide passive immunity starts the prophy~ Emergency and Disaster Nursing 1837 ‘Acids and alkalis + Acios toiet bowel cleaner antrust compounds + Akal: eran cleaners, cish- ‘washing detergents, ammonia + Aspien and asprin-containing ragicatone Bleaches Carton monoxide Cyanide Ethylene alycol Nonsteroidal antintlammatory rugs ‘Teyolic antidepressants (eg, amitripiyine (levi) ‘Alcohol, barbiturates, benzodiazepines, cocaine, hallucinogens, stimulants saphoresis, nausea and vomiting ‘Phase 2: 24-28 h: right oper quadrant pan, decreaced urine output, mined nausea, Ute rise ‘Phase 3: 72-96 hr: nausea and vomiting, ‘malaise jaundice, hypoglycemia, enlarged iver, possible coagulopathies, including DIC Phase 4:7-8 days after ingestion: recover, resoluon of symploms, LFTs return to normal Excess salvation, dysphagia, epigastric pain, ne ‘mont; burns of mouth, esophagus, and Tachyonea. tachycardia, hyperthermia, seizures pu- monary edema, occult biesdinghemornage, metaboie acidosis Irtation of ips, mouth, and eyes. superical nur to ‘esophagus; chemeal pneumonia and pulmonary era Dyspnea, nesdache, tachypnea, contusion, impaired judgment cyanosis, respiratory epression ‘Almond oder to breath, neadache, dizziness, nausea, confusion, hypertension. bradycardia folowed by hypotension ard tachycardia tachypnea folowod by bradypnea and respiratory ‘Sweet aromatic odor to breath, nausea and vom ing, sured speech, ataia,lthargy, respiratory depression Vomiting (often bloody), dlarhea (atten blood, {ever hypargyeema Isthargy, hypotension, Gastroenteritis, abdominal pain, drowsiness, nystagmus, hepatic and eral damage In low doses: anticholinergic eftects, agitation hypertension, tachycardia; in high doses: central ‘nervous systom depression, dysthythmias, Inypotension, respiratory depression See Cnapter 12 ison Manifestations: Treatment cause vomiting IV form avalabie on expermertal basis) Immediate dition water, mk), corticosteroids (or akal ‘bus nduced vomiting contraindicated Gastrc lavage, activated charcoal, une akalnizatio, hemodiays for severe acute ingestion, tation ‘and mechanical ventilation, supportive care Washing of exposed skin and eyes, ction wth water ‘and milk. gastric lavage, prevention of vomiting and aspicton Removal from source, administration of 19086 O; via ror-tebreather mass, BVM. or intubation ac ‘mechanical venation. consider nyperbare oxygen therapy “Amy ntrate (asa) IV soclum nitrate, NV sodium thiosulfate, supportive care Gastic lavage, activated charcoal, supportive care asin avage, chelation therapy (seleroxamne [Pesteral) GGastic lavage, actvated charcoal, supportive care Muldose activated charcoal, gastric lavage, serum ‘akanzation wih sodium bicarbonate, intubation and mechanical ventiation.suppertve care: never induce vomtng ‘Soe Chapter 12 AVM, Bag valve mask, DIC. diemaicd avascular Iaxis regimen. This is followed by a series of five injections of ho: ‘man diploid cell vaccine (HDCV [RabAvert}) on days 0, 3. 7. M4 and 28 t0 provide active immunity. Dosage is based on the patients ‘weight. (Rabies is discussed in Chapter 57.) POISONINGS Severity of the poisoning depends on type, concentration, and route of exposure, Toxins can affect every tissue of the body, $0 ‘symptoms can be seen in any bexly system. Specific management of absorption, enhancing implementation of toxin-specic interventions. The local poison control center is available 24 hours a day and should be consulted for the most current treatment protocols for specific poisons ‘Options for decreasing absorption of poisons include gastric la vag, dermal cleansis activated charcoal, ig. and eye strigation Gastric lavage involves oral in re ofa large-diameter (36- 10 42-French) gastric tube for installation of copious amounts of Tine, The head of the bed should be elevated or the patient placed ‘om the side to prevent aspiration, Patients with an altered level of ‘consciousness or diminished gag reflex must be intubated before lavage. Lav is contraindicated in patients who in {s, co-ingested sharp objects, or ingested nontoxic substances, sed caustic Seetion 12 Nursing Care in Specialized Settings Gastric lavage must be performed within 2 hours of ingestion of most poisons to be effective.” Problems associated with lavage include epistaxis, esophageal perforation, and aspiration The most effective intervention for management of poisonings is administration of activated charcoal orally or via a gastric tube ‘within 60 minutes of poison ingestion." Many toxins adhere to charcoal and are excreted through the GI tract rather than absorbed into the circulation. Activated charcoal does not absorb ethanol hydrocarbons, alkali, ion, boric acid, lithium, methanol. or cya nde, Adults receive 50 to 100g of charcoal. For some toxins (e, ‘Phenobarital) muliple-dose chareoal may be required." Con: sto charcoal administration include diminished bowel gestion of substance poorly absorbed by Charcoal can absorb and neutralize antidotes (e-., Neacetyleysteine [Mucomyst} for acetaminophen toxicity) and these should not be given immediately before, with, o shortly charcoal.» ‘Skin and ocular decontamination involves removal of toxins from eyes and skin using copious amounts of water or saline. With the exception of mustard gas, most toxins can be saely removed with water or saline. Water mixes with mustard gas and releases chlorine gas. AS a general rule, dry substances should be brushed from the skin and clothing before water is used. Powdered ime should not be removed with water: it should just be brushed off. Personal protective equipment (e.g, gloves. gowns, goggles. esp rators) should be wor for decontamination to prevent secondary exposure, Decontamination procedures are usually done by those specially tained in hazardous material decontamination before the patient arrives atthe hospital and again, atthe hospital, if neces- sary. Decontamination takes priority over all interventions except basic life-support techniques Elimination of poisons is increased through administaion of cathantics, whole-bowel irigation, hemodialysis, hemoperfusion, urine alkalinization, chelating agents. and antidotes. Cathartcs. such as sorbitol, are given together with the first dose of activated charcoal 0 stimulate intestinal motility and increase elimination. Multiple doses of cathartics should be avoided because of poten- tilly fatal electrolyte abnormalities. Whole-bowi! ieigation is controversial and involves. administration of a nonabsorbable bowel evacu . GoLYTELY). The solution is ad- ministered every 4 10 6 hours until stools are clear. Ths process cam be effective for swallowed objects such as eocaine-filled bal- loons or eondoms, and heavy metals suchas lead and mercury ‘There isa high risk of electrolyte imbalance due to fluid and elec trolyte losses with this procedure." Hemosialysis and hemoperfusion are reserved for patients who develop severe acidosis from ingestion of toxic substances (ez. aspirin). Other interventions include alkalinization and chelation therapy. Sodium bicarbonate administration raises the pH (greater than 7.5), which is particularly effective for phenobarbital and salicylate poisoning. Vitamin C may be added to 1V fluids to en hance excretion of amphetamines and quinidine. Chelation therapy ‘may be considered for heavy metal poisoning (e.g. edetate cal cium disodium (Calcium EDTA] for lead poisoning). A limited ‘number of true antidotes are available, and many’ ofthese agents are themselves toxic.° Education for toxic emergencies focuses on how the poisoning ‘occurred. Patients who experience poisoning because ofa suicide attempt of related to substance abuse should be evaluated by a ‘mental health counselor and then referred for alcohol or drug de tonification or scheduled for follow-up with a mental health pr- traindicati sounds, ileus, and charcoal solution (¢ fessional. The Occupational Safety and Health Administration should isoning related to an occupational hay aluate all po VIOLENCE @ Violence is the acting out of the emotions of fear and/or anger 0 ‘cause harm fo someone oF something. It may be the result of or ganic disease (e-g., temporal lobe epilepsy). psychosis (e.. Schizophrenia), ot antisocial behavior (e.g., assault, homicide). ‘The patient cared for in the ED may be the vietim of violence or the perpetrator of violence. Violence can take place in a variety of settings, including the home, community, and workplace. EDs have been identified as high-risk areas for workplace violence." Measures to protect staf include the use of on-site security person- nel and police officers, metal detectors, surveillance cameras, and locked access doors. Research has shown that ED nurses believe ‘many of these measures are inadequate, making them vulnerable to violence at work. Comprehensive workplace violence preven tion plans should be implemented and evaluated in every ED.” Domestic violence is a patter of coercive behavior in a rela. tionship that involves fear, humiliation, intimidation, neglect, and or intentional physical, emotional, financial, or sexual injury (see Chapter 54 for information on is found in all professions, cultures, socioeconomic groups. age groups, and genders. Although men can be vietims of domesti vi lence, most victims are women, chikdren, and the elderly. It has bbcen reported that 1.5 million women and 834,000 men treated at EDs have been battered (assaulted) by spouses, significant others, or individuals known to them. As many as 20% of battered females are pregnant at the time of the assault." ED nurses are well situated to conduct domestic viol screening (e.g., Do you feel safe at home’ Are you being hurt anyone?), and routine screening for this risk factor is required Bartiers to conducting effective screening include limited privacy for screening, lack of time, and lack of knowledge about how to ‘obtain information regarding domestic violence. The development and implementation of specific policies, procedures, and staf edu cation programs can improve the domestic violence screening practices of ED staff." For any patient who is found to be a victim of abuse, appropriate interventions such as making referrals, pro: viding emotional support, and informing vietims about their op- tions (e., safe house, legal rights) should be initiated." See Re sources at the end of this chapter for additional information on domestic violence, AGENTS OF TERRORISM ‘The threat of terrorism is an ongoing concern Terrorism involves ‘overt actions such as the dispensing of disease pathogens (... bh terrorism) or other agents (e.g. chemical, radiologicinuclear, ex plosive devices) as weapons for the express purpose of causing harm. Prompt recognition and identification of potential health haz ards are essential in the preparedness of health care professionals. Table 69-13 summarizes general information regarding bio: logic agents of terrorism. The pathogens most likely to be used in 4 bioterrorist attack are anthrax, smallpox, botulism, plague, tu remia, and hemorrhagic fever. ‘Among the agents considered likely 10 be biologic weapog those hat ase ata, pag and tlre out be <@® fectively with commercially available antibioties if sufficient sl exual assault), Domestic violence plies were available and the organisms were not resistant. Smallpox cean be prevented or ameliorated by vaccination even when first given after exposure, Botulism can be treated with antitoxin, There TABLE 69-13 Clinical Chapter 69 Transmissibility Emergency and Disaster Nursin eed Treatment Gas “Anthrax Bacius antracis Inhalation Bacteral spores multiply nthe Toxins cause hemorhage and estructon of ung tissue High morality rate Cutaneous 195% of antivax infectons Least lethal orm ‘Spores enter skin through cuts or abrasions | Handling of contaminated animal skin products “Toxins destroy surounding tissue sstrointestinal Ingestion of contaminated, undercooked meat Intestinal lesions in leur or [cute inflammation of intestines Smallpox Varola major and minor viuses Unite States ended routine vaccination in 1971 Global eradication declare in 1080 Botulism Clostiaium botulinum ‘Spote-orming anaerobe Found in si Seven diferent toxins Lethal bacterial neurotoxin Can de within 24 nr Incubation period 1-2 days to 6 wie Abrupt onset Dyspnea Diaphoress Fever Coogh Chest pain Septicemia Shock Meningitis Respratory tature \Weened meciastium (seen on chest xray) Incubation period: up to 12 days ‘Small papule resembles an sect bite Advances o a depressed, black ulcer ‘Swollan lymph noes in achacent Esema Nausea, Vomiting Hematemesis Diariea ‘Abdominal pain Ascites Sepsis Incubation period: 717 days Suaiden onset of symptoms. Fever Headache Myalia Lesions that progress from macules to papules to pustular vesicles Malaise Back pain Incubation period: 12-36 he Abdominal cramps Darthea Nausea Yomting Cranial nerve palsies (noni, dysarthria dyschona, dysphagia) ‘Skeletal muscle paras Respratorytalure + No person-to-person spread + Found i nature ane ‘most commonly infects wid and domestic: hooted anmats + Spread through direct ‘contact with bacteria ‘and its spores + Spores are dormant ‘encapsulated bactora that become active when they enter a tving host + Hany contagious * Direct person-to-person spread + Transmited in air roplets + Transmit by handing contaminated matenaie + Spread through ai or food + No person-to-person spread + improperly canned foods + Contaminated wound Antibiotes prevent systamic rmantostations Ectve only # woated early Giprotoxacn (Cipro) s the treatment of choice Penciin Doxyeyetine Pstexoosure prophylaxis fr 30 days i vaccine avaiable) or {60 days it vaccine rot ‘avalabe) Vaceie has limite aval No known cure Cidotovir istic) under testing Isolation fr containment Vecine avaiable fr tose exposed Vaccinia immune globulin (VI) valatie Incuce vornting Enemas Antonin Mechanical vetiation No vaccine avaiable Toon can be inactivated by eating food eins to 212° F (100° Cora east 10min nts of terrorism and are eat e@ established treatment for viruses that cause hemorrhagic FChemicals may also be used as egorized according to their get organ or effect (Table 69-14), For example, sarin isa highly toxie nerve gas that can eause death ‘within minutes of exposure. Itenters the body through the eyes and skin and acts by paralyzing the respiratory muscles, Antidotes f nerve agent poisoning include atropine (AwoPen) and pralidoxime chloride (2-PAM chloride), Multiple doses may be nceded to re verse the effects of the nerve 1s notmally used in chemical manu ‘enough pe- Phosgene is a colorless facturing. If inhaled at h th concentrations for a Jon 1840 Section 12 Nursing Care in Specialized Settings Taste 69-15 |[EVen eee Clinical jifestations Pathogen and Description fague Yersia pestis + noubaton period: 2-8 days + Bactera found in rodents and Hemoptysss fleas + Cough Forms + High fever + Bubonic (most common) + hits + Preumonic| + Myagia + Septicamic (most deadly) + Headache + Respiratory faire Lyman nede sweling Tularemia Franeisaletlarensic + Incubation period: 3-10 days + "Bacteral infectious disease of + Sudden onset animais + Fever + Mortality rate about 35% + Swollen lymph nodes vithout treatment + Fatigue + Sor throat + Weight oss + Preumonia| + Pleural fusion * Urcerat sore fom tik bite Hemorthagic Fever + Caused by several veuses, including Marburg, Lassa, Junin, tnd Ebola + Ebola vies Fever Conjunctivitis Headache fe threatening Malaise of teaues and organs Verting Hypotension Organ faire 7 eke ak uk eed Transmissibility a ) + Direct person-to-person + Antibiotics only effective if spread administered immediately + Tranamitted through flea Drug of choice: streptomycin bites gentamicin + Ingeition of contams-—*‘Vaccine under development ated meat + Hospitaization + goltion fr containment + No person-to-person «+ Gentamicin treatmant of choice soread + Streptomycin, oxyeyctne. and + Aerosol or intradormal Ceprofloracin are alternatives route “+ Vaccine in development stage *+ Spread by rabbits and tks + Contaminated food, a, water + Carried by rodents and mosquitoes + Direct person-to-person spread by body fuids + Vins can be aerosolized ‘No intramuscular injections No antiplatelet drugs Isolation for containment Fibavrin (Virazole)efctve in + No known treatment available GF (cyciohexyimettvphosphonofluordate) VX (Oretry S-2-disopropylaminoety/} ‘methylphosphenothiolto) Nerve ~ Blood Pulmonary Blister/Vesicants ae) itycrogen cyanide Phosgene Iiropen end sur mustard Tabun thy NN-cimetyipnoephoramidoeyanidte) Cyanogen chonde Clore Lew an alate arsenic compounds Soman fonacoh! may phosphonate) Vi chide 2-chirouyioroarine) Phosgene oxime riod, it causes severe respiratory distress, pulmonary edema, and ‘death, Mustard gas is yellow to brown in color and has a garlic-ike ‘odor. The gas irritates the eyes and causes skin burns and blisters Protocols to treat casualties of chemical exposure are varied and relate to the specific agent.” Radiologic/nuelear agents represent another cat of terrorism. Radiologic dispersal devices (RDS), also known as “dirty bombs," consist ofa mix of explosives and radioactive mate rial (eg, pellets). When the deviee is detonated, the blast scatters radioactive dust, smoke, and other material into the surrounding ‘environment, resulting in radioactive contamination The main danger from an RRD results from the explosion, which can cause serious injuries to the casualties. The radioactive materials used in an RRD (c.g. uranium, fodine-131) do not usu: ally generate enough radiation to cause immediate serious illness, ‘except to those casualties who are in close proximity to the explo- ory of agents sion, However, the radioactive dust and smoke can spread) and ‘cause illness if inhaled. Since radiation cannot be seen, smelled, felt, or tasted, measures to limit contamination (e-g., covering the patient's nose and mouth) and decontamination (e.g., shower) should be initiated! Ionizing radiation, such as that from a nuclear bomb or damage {0 a nuclear reactor, represents a serious threat to the safety ofthe casualties and the environment, Exposure to ionizing radiation may or may not include skin contamination with radioactive mate- rial, F external radioactive contaminants are present, devontamina tion procedures must be initiated immediately, Acute radiation syndrome develops after a substantial exposure to jonizing @ tion and follows a predictable pattern (Table 69-15) Explosive devices (eg, TNT, dynamite) that are used as age ‘of terrorism result in one oF more of te following types of injuries: blast erush, oF penetrating. Blast injuries result from the super ene Whole Body Radiation from External Radiation or internal Absorption Phase of Sublethal Range Lethal Range Syndrome Feature 0-100 rad 100-200 rad «200-600 rad__—«600-800 rad «600-3000 rad >3000 rad Prodromal phase Nausea, vomiting ‘None 96-50% 50%-1009% 759%6-1009% 9096-1009% 100% Time of onast 36h 2a tan =the Mires Durston 26h <28 he 48 he =48 he NA Lymphocyte count Unatfacted Mirimaly decreased 1000 at 24 nv 500 at 24h Decreases within Decreases within ours ours CONS funtion No impairment No impairment Cogntive impairment Cognitive mparment api incapactation, often aera lucid period Yor 6-20 for 24h of upto soveal bows Latent phase ‘sence of >owk 718 98 0-7 days 02 days Nene (eubotnica) ‘meters ‘Acute radiation + Signs and symptoms None Moderate lkoperia Severe laukopena, purpura, hemormnage Diartea Convusios, sax, ‘ness or *mani- Preumonia Fover ‘roman thay a fest ness” Hair oos ater 200 rad Erctrohjte & hase lsturbance Time of onaat >2 wk 2ays-2 wk 19.daye Crtical pero Nene 4-6 wk—Mest potential for effective medical 2-14 days 1-48 he a inteventon g Organ systom None Homatopolee and respiratory (mucosa) Glract ons ‘ystems Mucosal systems g Hospitalization 3 o%

    You might also like