Summer Hazards: Part 2

Educational Objectives

The goal of this program is to improve the management of bites and stings from certain arthropods (tarantulas, scorpi­ons, and bees), treatment and prevention of heat exhaustion and heat stroke, and evaluation and treatment of the pa­tient recovered from water after near drowning. After hearing and assimilating this program, the clinician will be better able to:

1.   Select the appropriate treatment for tarantula bites and scorpion and bee stings.

2.   Describe the causes and characteristics of heat exhaustion, classic heat stroke (CHS), and exertional heat stroke (EHS), and their recommended course of treatment.

3.   Discuss the methods of rapid cooling and pharmacologic adjuncts that have been used in the management of classic and exertional heat stroke.

4.   Explain the  effects of fresh water vs salt water aspiration.

5.   Accurately assess and effectively treat the patient who is brought in after near drowning.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning com­mittee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the faculty and the planning committee reported nothing to disclose.

Acknowledgements

Dr. Erickson was recorded at the 22nd Annual National Conference on Wilderness Medicine, held August 6-10, 2008, in Big Sky, MT, and jointly sponsored by the American College of Emergency Physicians (ACEP), the ACEP State Chapter of California, Inc, and Wilderness and Travel Medicine. Drs. Lucas and Booth spoke at Clinical Decision Making in Emergency Medicine, held June 26-28, 2008, in Ponte Vedra Beach, FL, and jointly sponsored by Mount Sinai Medical Center, the University of Florida, Jacksonville, the Mayo Clinic College of Medicine, the George Washington University, the Brigham and Women’s Hospital, the Foundation for Education and Research in Neuro­logic Emergencies, Best Practices, Inc, and Emergency Medicine Practice. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

Arthropod Bites and Stings: Part 2

Timothy B. Erickson, MD, Professor and Assistant Head, Department of Emergency Medicine, and Director, Clinical Toxicology, University of Illinois College of Medicine, Chicago

Tarantulas: burrowing spiders; have poor eyesight; may spit urticaria-producing hairs if too close; bite only if pro­voked;  treatment for bites  —  tetanus prophylaxis; analgesics; antibiotics (only for secondary infections); antihista­mines; topical steroids

Spiders with necrotizing bites: running or sac; brown recluse; wolf; hobo; orb weaver

Scorpion stings:  most stings minor; clinical signs include hypertension, hyperactivity, and hyperesthesia (do tap test); symptoms more severe in children, and include dysphagia, dyspnea, bladder and bowel incontinence, and dis­conjugate roving eye movements (nystagmus; “tell-tale sign”); treatment  —  benzodiazepines; narcotics (controver­sial but work well); antivenin (no longer manufactured; very scarce supply)

Bee stings: cause »33% of all reported envenomations in United States and 50 to 150 annual deaths; honey bees  —  not aggressive; only females sting; die after losing stinger; vespids  —   hornets, wasps, yellow jackets; aggressive, can sting multiple times without provocation; African killer bees  —  very aggressive; sting in swarms; management  —  ice; antihistamines; remove stinger manually; greatest concern is anaphylactic reaction (treat with epinephrine); immunotherapy

Heat Emergencies

Raymond Lucas, MD, Assistant Professor and Residency Director, Department of Emergency Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC

Introductory remarks: basic heat emergencies are heat exhaustion and classic or exertional heat stroke (CHS or EHS); during urban heat wave, can expect to see »20 cases of HS per population of 100,000; untreated CHS can have fairly high mortality (if treated, mortality »14%); EHS third leading cause of death among high school ath­letes who die from sports-related activity

Heat exhaustion: syndrome of being overheated with constellation of symptoms; patient may or may not be hyper­thermic (classically, temperature elevation modest but not extreme); exertional hyponatremia  —  related syndrome; check electrolytes, especially sodium; typically seen in people in road races; related to dilutional hyponatremia, usually from overhydration; more common in women and less acclimated, slower athletes; treatment of heat exhaustion  —  symptomatic; self-limited illness; remove clothing to cool patient down; rehydrate to euvolemia; check electrolytes, especially sodium, to rule out exertional hyponatremia; control nausea and vomiting with anti­emetics if needed; patient can often be treated in field or emergency department (ED) and released

Heat stroke: defined as elevated core body temperature ³40ºC accompanied by central nervous system (CNS) dys­function, eg, delirium, bizarre behavior, hallucinations, seizures; CHS  — typically seen in urban areas during heat wave; due to prolonged environmental exposure to heat; most often seen in elderly and very young; more common in patients with psychiatric or cardiovascular illness; develops over days; patients tend to have lower core tempera­tures than those with EHS; often confused with other conditions, eg, sepsis; EHS  —  rapid onset; usually related to heavy physical exertion in area with high ambient temperature and humidity; vomiting and diarrhea common; end organ effects more rapid and dramatic than in CHS, especially, acute renal failure, rhabdomyolysis, and dissemi­nated intravascular coagulation (DIC); treatment  —  same for CHS and EHS; management of airway, breathing, and circulation (ABCs);  monitoring of core temperature; rehydration to euvolemia; monitoring for effects, eg, multior­gan failure, rhabdomyolysis; DIC; rapid cooling most important component of treatment; target to get core temper­ature <40ºC within 30 to 60 min; indicators of bad outcome evidence of end organ damage upon presentation to ED, eg, hypotension, need for intubation, coagulopathy; length of time at elevated temperature more significant than actual temperature, hence importance of rapid cooling

Pathophysiology of HS: starts with  heat stress; patient has thermoregulatory response (volume depletion, markedly increased cardiac output [CO], and splanchnic vasoconstriction); acute-phase inflammatory response  — heat expo­sure causes tissues to release cytokines (eg, interleukin 1 and 6 ([IL-1; IL-6]) into blood stream; this produces in­creased vascular permeability in gut, leading to release of endotoxin from gut flora; endotoxin triggers inflammatory cascade and microvascular injury, leading to activation of clotting cascade and DIC; brain  —decreased cerebral perfusion from hypotension may lead to cerebral edema and microvascular flooding (cause of CNS effects seen in HS);  heat shock response  —  body  produces heat shock proteins in response to subclinical ex­posure to heat; these bind to enzymes in cells and prevent cell proteins from becoming denatured during subsequent exposures to heat; in future, may be used for prophylaxis of HS

Optimum cooling method: options for cooling  —  evaporation, ice packs to groin, axillae, and trunk; cold water im­mersion, cooling blankets (or other cooling devices), and dry fanning; unclear which technique best; however, re­ported cooling rates faster with ice water immersion (vs evaporative techniques); American College of Sports Medicine (ACSM; 2007) Level A recommendation for immersion therapy for EHS; American Association of Fam­ily Physicians Level B recommendation for evaporative methods (pertains mostly to CHS); caveat  —although im­mersion techniques may be faster, clearly difficult (may be impractical in severely ill patients)

Pharmacologic adjuncts: dantrolene  —  studies by Channa et al (1990) and Bouchama et al (1991) suggest that dan­trolene not effective in treatment of HS and does not provide any clinical benefit; activated protein C (APC)  —  recent animal study by Chen et al (2006) found APC (drotrecogin alfa [Xigris]) effective in treatment of HS (asso­ciated with longer survival and improvements in biomarkers of inflammation, DIC, and end organ failure); cur­rently no good human studies; other options  —  hyperbaric oxygen; estrogen; human umbilical cord cells; steroids; none of these have proven effective; take-home point  —  no pharmacologic adjunct clearly effective in treatment of HS

Risk factors for CHS: meta-analysis of »6 case series (>1000 heat-related deaths during heat waves) found risk greater among patients confined to bed, unable to leave home or to care for self, or with underlying psychiatric, car­diovascular, or pulmonary illness; living on upper floors of multistory building also risk factor; patients at less risk for HS are those with access to home air conditioning, able to visit cool environments, or with increased social con­tact

Strategies for prevention of CHS: use of home health workers and social service organizations to prevent heat-re­lated illness (Memphis model); cooling shelters and apartment building lobbies; fans by themselves not helpful; deaths tend to occur on days 2 to 4 of heat wave

Preventing EHS: ACSM recommendations  —  dehydration reduces endurance, decreases time to exhaustion, and in­creases heat storage; 10 to 14 days of exercising in heat provides acclimatization and reduces risk for EHS; practice and competition should be modified, based on temperature, humidity, and intensity of exercise; ACSM guidelines for prevention of dehydration  —  eat normal meals during »24 hr before exercise; consume »500 mL of fluid during »2 hr before; during exercise, attempt to replace fluid lost; if exercising continuously for >1 hr, must add carbohy­drate supplementation and should consider adding sodium supplementation; studies have shown that when fluid flavored, cool, and has some sodium content, people more likely to drink it and stay well hydrated; pearls for sports medicine  —once body weight reduced by 3% to 5% from dehydration (eg, at start of football practice in August), normal thermoregulatory response impaired and risk for EHS increased

Drowning: Managing the Near-Death Experience

Ashley E. Booth, MD, Assistant Professor of Emergency Medicine, Assistant Program Director, and Director of Governmental Affairs, University of Florida College of Medicine, Jacksonville

Definitions: drowning  —  death from inadequate intake of O₂ within »24 hr of submersion; near drowning  —  survival >24 hr after submersion, regardless of injury or eventual outcome; dry drowning  —  10% to 15% of cases; sub­merged patient develops laryngospasm, which prevents aspiration of water into airway; end result same as in wet drowning; wet drowning  —patient aspirates water; this leads to hypoxia, hypercapnia, acidosis, and death; second­ary drowning (postimmersion syndrome)  —  death due to respiratory distress or failure that develops »72 hr after initial event; 2% to 15% of near-drowning cases

Drowning: accounts for 4000 to 8000 deaths annually in United States; fourth leading cause of death in adults and third leading cause in children overall (leading cause of accidental deaths in children <1 yr of age); 2 peaks in age distribution of drowning/near drowning victims (children <4 yr of age; adolescents and young adults 15-25 yr of age); risk factors  —  age; location; sex (incidence much higher in males); ethnicity (blacks and American Indians at higher risk); ability to swim; seizure disorders or other underlying medical conditions; drugs and alcohol

Effects of fresh water vs salt water aspiration: fresh water  —destroys surfactant, leading to alveolar collapse, intra­pulmonary shunting and hypoxemia; most fresh water victims drown in swimming pools, thus are more likely to develop pneumonitis (secondary to chlorine) than people who drown in salt water; salt water  —results in fluid-filled alveoli, which also leads to intrapulmonary shunting and hypoxemia; exposure to pathogenic bacteria (vic­tims may be at higher risk for infection); salt water drowning victims tend to be more hypothermic than fresh water victims

Prehospital care: if head and neck injuries suspected, use backboard to protect patient’s cervical spine; administer O₂ as early as possible; always check blood glucose early on (hypothermia causes hypoglycemia); avoid Heimlich maneuver and lung drainage; transport all patients removed from water after near drowning (can have no signs and symptoms initially and still develop secondary drowning)

ED assessment: clinical presentation  variable, and management differs depending on how patient presents; focus on ABCs (O₂ vs intubation, plus or minus C-spine protection); initiate Advanced Cardiac Life Support (ACLS) proto­col, paying close attention to acidosis

Patient history and physical examination: history  —  incident; duration of submersion; water temperature; associ­ated trauma; drug and/or alcohol involvement; loss of consciousness (LOC); prehospital cardiopulmonary resusci­tation (CPR; for how long); medical history; examination  — assess for related injuries

Laboratory tests: vary depending on clinical presentation; most patients require minimum of chest x-ray, complete blood cell count, brain natriuretic peptide assay, electrocardiography, and urinalysis; may need arterial blood gas and C-spine imaging; consider prothrombin time and partial thromboplastin time, liver function tests, and creatine kinase if patient severely symptomatic

Treatment of asymptomatic patient: recent studies suggest that with secondary drowning, signs and symptoms de­velop within first 8 to 12 hr; current protocol to admit patient, put him or her on O₂ and on monitor, and observe; most patients who remain asymptomatic after 8 to 12 hr can be discharged safely

Treatment of symptomatic patient: indications for intubation  —apnea; unstable airway; risk for aspiration; neuro­logic deterioration; difficulty with oxygenation or ventilation; pulmonary complications  —  pulmonary edema (PE); most symptomatic patients present with mild-to-severe PE; usually clears in first »24 hr with positive-pressure ven­tilation or airway O₂; prevent development of acute respiratory distress syndrome

Methods of ventilation: 100% O₂ delivered via nonrebreather mask (if symptoms mild); continuous positive airway pressure (CPAP; if patient spontaneously breathing with mild hypoxia); positive end-expiratory pressure (PEEP; if symptoms more severe; decreases intrapulmonary shunting; reduces ventilation-perfusion [V/Q] mismatch; in­creases functional residual capacity; may prevent secondary drowning; disadvantage that PEEP may worsen neuro­logic status, as it increases intracranial pressure [ICP]); persistent hypoxia despite ventilation may be result of aspirated foreign material; aggressive suctioning or bronchoscopy indicated; consider extracorporeal membrane oxygenation in patients unresponsive to 100% O₂ and PEEP

Pulmonary complications: treat bronchospasm with b-agonists; neither steroids nor antibiotics shown to improve survival and not recommended for prophylaxis

Cardiovascular complications: monitor heart rate, rhythm, blood pressure, capillary refill, and urinary output; in more severe patients, consider monitoring central venous pressure and pulmonary artery wedge pressure; give ade­quate fluid resuscitation (start vasopressors early if needed); monitor volume status; be aggressive in treating meta­bolic acidosis; avoid dysrhythmias; aggressively treat hypothermia (contributes to arrhythmias; sinus bradycardia and atrial fibrillation most common); monitor for ischemia

Neurologic assessment: neurologic status of primary importance in determining prognosis; always assess and docu­ment level of consciousness when patient presents; cerebral resuscitation  —  goal to keep intracranial pressure (ICP) <20 mm Hg and central perfusion pressure >50 mm Hg; how well patient does depends primarily on rapid stabilization and correction of hypoxia and acidosis; be aggressive in treating agitation and seizures; treat elevated ICP (raising head of bed 30° helpful); avoid aggressive hyperventilation; unproven therapies for cerebral resuscitation  —  induced hypothermia; therapeutic dehydration; barbiturate coma; paralysis; calcium channel block­ers; O₂ radical scavengers

Hypothermia management: remove wet clothes;  warm patient (eg, with warm intravenous fluids; internal rewarm­ing techniques); however, if patient has sustained prolonged hypoxia or asphyxia, consider maintaining core body temperature near »30ºC (leaving patient slightly cold shown to be neuro-protective)

Prognostic variables: at scene  —  length of submersion; water temperature; whether CPR required (poor prognosis); resuscitation time >25 min (poor prognosis); in ED  —  if CPR still required; pH <7.0; whether mechanical ventila­tion and high amounts of PEEP required; level of consciousness

Suggested Reading

Al-Aska AK et al: Simplified cooling bed for heatstroke. Lancet 1:381, 1987; Armstrong LE et al: Whole-body cooling of hyper­thermic runners: comparison of two field therapies. Am J Emerg Med 14:355, 1996; Belyea DA et al: The red eye revisited: ophthal­mia nodosa due to tarantula hairs. South Med J 91:565, 1998; Biswal N et al: Outcome of scorpion sting envenomation after a protocol guided therapy. Indian J Pediatr 73:577, 2006; Bonnor R et al: Rhabdomyolysis associated with near-drowning. Am J Med Sci 318:201, 1999; Bouchama A et al: Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 19:176, 1991; Brenner RA: Prevention of drowning in infants, children, and adolescents. Pediatrics 112:440, 2003; Brueckmann M et al: Beyond sepsis: activated protein C and heat stroke. Crit Care Med 34:2020, 2006; Causey AL et al: Predicting discharge in uncom­plicated near-drowning. Am J Emerg Med 18:9, 2000; Chen CM et al: Activated protein C therapy in a rat heat stroke model. Crit Care Med 34:1960, 2006; Howe AS, Boden BP: Heat-related illness in athletes. Am J Sports Med 35:1384, 2007; Jardine DS: Heat illness and heat stroke. Pediatr Rev 28:249, 2007; Jones RG et al: A novel Fab-based antivenom for the treatment of mass bee at­tacks. Am J Trop Med Hyg 61:361, 1999; McDermott BP et al: Acute whole-body cooling for exercise-induced hyperthermia: a sys­tematic review. J Athl Train 44:84, 2009; Meyer RJ et al: Childhood drowning. Pediatr Rev 27:163, 2006; Mitchell A: Africanized killer bees: a case study. Crit Care Nurse 26:23, 2006; ; Ranu Alpay N et al: Unusual presentations of scorpion envenomation. Hum Exp Toxicol 27:81, 2008; Rumbak MJ: The etiology of pulmonary edema in fresh water near-drowning. Am J Emerg Med 14:176, 1996; Spicer ST et al: Acute renal impairment after immersion and near-drowning. J Am Soc Nephrol 10:382, 1999; Tasic V: Ne­phrotic syndrome in a child after a bee sting. Pediatr Nephrol 15:245, 2000; Weiner JS, Khogali M: A physiological body-cooling unit for treatment of heat stroke. Lancet 1:507, 1980.