Environmental Emergencies Paramedic

Transcript

Environmental Conditions Objectives       Define “environmental emergency” and list the major types. Identify risk factors most predisposing to environmental emergencies. Identify environmental factors that may cause illness or exacerbate a preexisting illness and those that may complicate treatment or transport decisions. Describe the mechanism of normal body temperature regulation and identify normal, critically high and critically low body temperatures. Describe several methods of temperature monitoring. Identify mechanisms by which the body loses and retains heat. Objectives  Discuss the pathophysiology, high risk groups, signs and symptoms, and field treatment of the following:    Heat cramps Heat exhaustion Heat stroke (classic and exertional)   Define fever and discuss its pathophysiologic mechanism. Identify the fundamental thermoregulatory difference between fever and heatstroke and discuss how one may differentiate between the two. Discuss the pathophysiology, high risk groups, signs/symptoms, field treatment and prevention of the following:   Frostbite   Superficial Deep Hypothermia Mild Severe Objectives       Discuss the importance of attempting resuscitation in a pulse less hypothermic patient. List factors that contribute to drowning. Differentiate between and describe the pathophysiology, signs/symptoms and field treatment of drowning and neardrowning. Differentiate between the effects of salt vs. fresh water on the lungs and circulatory system in drowning. Discuss the incidence of “wet” vs. “dry” drowning and the differences in their management. Describe the effects of cold water on drowning patients. Objectives   Define self-contained underwater breathing apparatus. Describe the pathophysiology, signs/symptoms and field treatment for the following diving emergencies:  Decompression illness b. Air embolism   Describe the function of the Divers Alert Network (DAN) and how its members may aid in the management of diving related illnesses. Describe the specific function and benefit of hyperbaric oxygen therapy for the management of diving accidents. Scenario You respond to an athletic field at 3:00 p.m. for a “person down.” It is hot and humid. You know that the college football team started practice this week. Your patient is an unconscious 21-year-old, 230 pound male. His skin is wet and very hot. Vital sign assessment reveals: BP 82/64 mm Hg; HR 136/min; R 28/min. As you administer oxygen, he has a grand mal seizure. Discussion     What factors point to a heatrelated emergency on this call? What other emergencies should you rule out? Describe additional assessments that should be done Outline your priorities of care based on your current information Environmental emergency  Medical condition caused or exacerbated by weather, terrain, atmospheric pressure, or other local factors  A medical emergency resulting from physical exposure to the environmental elements – water, heat, humidity, cold, altitude, wind Thermoregulation  Regulatory center - Hypothalamus Peripheral thermoreceptors Central thermoreceptors   Thermoregulation  Body temperature increased or decreased by:  Regulation of heat production  Thermogenesis Thermolysis  Regulation of heat loss  Normal body temperature is 37 degrees Centigrade or 98.6 F, though it may range from 96.5-99.5o (Recent studies show that 98.2o is more average) Your body temp fluctuates daily – sleep vs exercise, etc. Extremely elevated body temperatures can cause multisystem damage and physiological collapse: (>105.8oF or 41oC) Body temperatures below 90oF (32C) cause decreased LOC, poor judgment, the cessation of shivering, and uncoordination. Body temperatures below 82.4oF (28C) usually result in unconsciousness and possible vfib. Regulating Heat Production  Muscular    Baseline muscular activity Exertion Shivering Processing of food and nutrients     Metabolic  Carbohydrates (sugars and starches) Fats Proteins  Glycogen Role of hormones in basal metabolic rate  Endocrine  Regulating Heat Loss     Radiation Heat waves rise off of our skin (head) This starts to be ineffective above 88 degrees. Most body heat is lost through the skin Conduction Heat loss by direct contact with colder object- snow, ice Convection Heat loss by moving air (wind chill, ceiling fans) Evaporation Any fluid absorbs heat from surrounding objects and air. We lose heat by sweating, being wet or in wet clothes, and from respirations. This is why animals pant! Sweating is only effective if humidity is low enough for the water to evaporate! Evaporative rate decreases if humidity is above 75%. At levels approaching 90%, evaporation essentially ceases. Hyperthermia Compensation  Hyperthermia compensation  Increased heat loss Vasodilation of skin vessels  Sweating   Decreased heat production Decreased muscle tone and voluntary activity  Decreased hormone secretion  Decreased appetite  Hypothermic Compensation  Decreased heat loss Peripheral vasoconstriction  Reduction of surface area by body position (or clothing)  Piloerection (not effective in humans)  Hypothermic Compensation  Increased heat production     Shivering Increased voluntary activity Increased hormone secretion Increased appetite External Environmental Factors May contribute to a medical emergency      Climate Season Weather Atmospheric pressure Terrain Predisposing Factors       History of exposure Poor planning, preparation, education Conditioning, health, nutritional status, other illnesses or associated trauma Age Use of alcohol, drugs, and prescription medications Poverty Environmental Factors Heat Cold Wind Humidity Water Altitude Possible remote location and delay in identifying problem (lost person) and accessing EMS Difficulty in accessing or extricating patient (identifying lack of contact with elderly who lives alone in a common urban scenario) Hyperthermia  Thermoregulatory mechanisms overwhelmed by:  Environmental  conditions Heat stress  Excessive exercise in moderate to extreme environmental conditions  Failure  of thermoregulatory mechanisms Older adults or ill or debilitated patients  Either may result in heat illness Heat Cramps  Brief, intermittent, often severe muscular cramps occuring in muscles fatigued by heavy work or exercise. Caused primarily by a rapid change in extracellular fluid osmolarity resulting from sodium and water loss. Heat Cramps 1-3 L of water per hour may be lost through Sweating. Each liter contains between 30 and 50 mEq of sodium chloride. Muscle cramping is caused by the water and sodium loss. Signs & Symptoms    Alert, hot, sweaty skin, localized muscle cramps in extremities, occasionally in abdomen. Vital signs normal with tachycardia, BODY TEMP NORMAL; skin cool or slightly warm Field treatment: remove from hot environment, replace the sodium and water (sodium especially), IV NaCl HEAT EXHAUSTION Usually caused by exercising or exertion in hot ambient temperature, more severe water and salt deficiency occurs. This electrolyte imbalances causes vasomotor regulatory disturbances and inadequate cerebral and peripheral perfusion.  More severe form of heat illness  Heat Exhaustion Temperature elevation (<103° F [39° C])     Mental status changes Nausea, headache Sweating Management   Remove from heat Oral or IV fluids Signs & Symptoms   Minor aberrations in mental status, such as irritability, confusion, poor judgment, headache, or light-headedness. Skin pale with excessive sweating, slight or no temperature increase (<103 degrees) Tachycardia, BP normal or slightly decreased, increased respiratory rate Field treatment includes removing the patient from the hot environment, oxygen, IV HEAT STROKE Syndrome occurring when the thermoregulatory mechanisms that normally cool the body fail completely. This results in a body temperature of usually > 105.8o. Damage occurs to the hypothalamus itself as a result of prolonged exposure to heat. Heat Stroke  Thermoregulatory mechanisms fail    Body temperature >105.8° F [41° C]) Multisystem tissue damage Physiological collapse   Medical emergency Two types   Classic heat stroke Exertional heat stroke Classic Heat Stroke   High temperatures and humidity Risk factors  Age  Infants, elderly Diabetes, heart disease, alcoholism Psychotropics, diuretics, antihypertensives  Chronic illness   Medications  Exertional Heat Stroke  Young, healthy patients Athletes, military recruits Vigorous exercise in high heat Inadequate hydration No acclimation     Signs & Symptoms    Dizzyness, headache, bizarre or unusual behavior, seizures, coma. Vital signs include a normal or decreased BP, tachycardia with a bounding pulse, tachypnea. Skin is usually hot, red, and dry, but may be wet or have wet clothing if exertional heatstroke. Temp is highly elevated! Heat Stroke—Assessment       Confusion, coma, seizures Skin flushing Dry skin (25% sweat) Tachycardia, hypotension Pulmonary edema Other systems affected Heat Stroke—  Move toManagement cool location     Maintain airway, oxygen, ventilation Active cooling Fan wet skin Ice Paks   IV fluid: 500 mL over 15 min  For hypotension Medications as prescribed   Sedation, seizure control ECG - FEVER  Increased body temperature kills many microorganisms and has adverse effects of the growth and replication of others Body temperature decreases serum levels of iron, zinc, and copper, all of which are needed for bacterial replication Body temperature causes lysosomal breakdown and autodestruction of cells, thus preventing viral replication in infected cells   FEVER    ↑ body temperature (heat) increases lymphocytic transformation and motility of polymorphonuclear neutrophils, thus facilitating the immune response ↑ body temperature enhances phagocytosis ↑ body temperature may augment the production of antiviral interferon Hypothermia   Hypothermia Marked decrease in the body’s core temperature. (or systemic cooling) Frostbite Localized hypothermia (or freezing) of the body’s tissues; more common in lower extremities than upper, also seen in nose, ears, cheeks CBT less than 93.2° F [34° C] Hypothermia— Pathophysiology        Vasoconstriction Sympathetic discharge Shivering, tachycardia Shivering stops: Rapid cooling Respiration, pulse, BP decrease ECG changes Respiratory and cardiac arrest Hypothermia  Progression of signs and symptoms  Mild  Core temperature 93.2°-96.8° F (34°-36° C) Core temperature 86°-93° F (30°-34° C) Core temperature below 86° F (30° C)  Moderate   Severe  Hypothermia—Risk Factors  Outdoor enthusiasts     Older adults, young children Medical/psychiatric illness Trauma Medications   Alcohol, antidepressants Antipyretics, phenothiazines Hypothermia— Management  High index of suspicion     High index of suspicion Evacuate to warmth Remove cold, wet clothes Cover with warm blankets Rapid transport  Hypothermia— Management Passive rewarming  Move to warm environment and remove wet clothes Radiant heat Forced hot air Warm IVF Warmed oxygen Lavage Cardiopulmonary bypass  Active external rewarming     Active internal rewarming    Mild Hypothermia— Treatment  Passive rewarming  Passive rewarming Warm drinks  With sugar    External hot packs No alcoholic beverages Warm, heated oxygen Moderate Hypothermia— Treatment    Can’t shiver or perform tasks Passive rewarming first Keep patient at rest External rewarming  Cover warm packs to prevent burns  Transport for evaluation Severe Hypothermia  Support airway, ventilation and circulation Passive and external rewarming Oxygen If ventricular fibrillation - start CPR and shock once Rapid transport     Considerations in Hypothermia     Assess for vital signs for 30-45 sec If presence of pulse questionable - start CPR Intubate Sinus bradycardia may be protective  Pacing usually not indicated If T>30C increase time between doses  Withhold IV drugs until T>30C  Frostbite     Localized injury Freezing of body tissues Pathophysiology Predisposing factors Frostbite— Classification/Symptoms  Superficial frostbite (frostnip)  Minimal tissue loss  Deep frostbite  Significant tissue loss even with appropriate therapy Superficial Frostbite  Some freezing of epidermal tissue Initial redness followed by blanching Diminished sensation   Deep Frostbite       Freezing of epidermal and subcutaneous layers White appearance Hard (frozen) to palpation Loss of sensation pale, cold, yellow, blue numb decreased movement Field Management          Remove patient from cold environment Support the patient’s vital functions (be wary about systemic hypothermia) Rewarm in tepid (105o) H2O; no contact with container No rewarming if a possibility of refreezing No walking on frozen extremities No coffee, alcohol, nicotine No rubbing Remove wet and/or tight clothing Wrap affected extremities in dry, sterile dressings; then immobilize Frostbite Edema and blister formation 24 hrs after frostbite injury in area covered by tightly fitted boot Frostbite Gangrenous necrosis 6 wks after frostbite injury Pulseless Hypothermic Patient.    Hypothermic patients who appear dead may still be successfully resuscitated. The lowest recorded temperature that an adult patient has survived in accidental hypothermia is 61oF. Children especially have a better chance of survival, some believe due to the mammalian dive reflex. Drowning    Fifth-leading cause of unintentional death 85% male, ⅔ don’t know how to swim Drowning    Process that results in primary respiratory impairment Caused by submersion/immersion in liquid Liquid/air interface at airway prevents breathing Factors Contributing To Drowning        ETOH, drugs Trauma Inability to swim Stupidity, overconfidence Exhaustion Muscle cramps Fear, panic Salt vs Fresh water SALTWATER Hypertonic to body fluids; draws water to it. Plasma and fluid move into the alveoli, resulting in pulmonary edema, poor ventilations of alveoli, hypoxia. Salt vs. Fresh Water FRESHWATER Hypotonic to body fluids; moves out of alveoli into circulation. Blood volume can increase, causing RBCs to rupture (hemolysis), and electrolyte abnormalities. Surfactant is “washed out” or diluted, causing atelectasis, then hypoxia in the alveoli. Submersion Incident Pathophysiology  Wet vs. dry drowning     Fluid in posterior oropharynx stimulates laryngospasm Aspiration occurs after muscular relaxation Suffocation occurs with or without aspiration Aspiration presents as airway obstruction  Fresh versus saltwater considerations  No difference in prehospital treatment Progression of a Drowning Incident Drowning vs. Neardrowning Drowning Asphyxia after submersion (death <24 hours) Near-drowning Submersion accident where the patient survives for at least 24 Drowning  Hypothermic considerations     Common concomitant syndrome May be organ protective in cold water submersion Treat hypoxia first Treat all submersion patients for hypothermia Factors that Affect Clinical Outcome  Water temperature Length of submersion Cleanliness of water Age of patient     Submersion Incident— Management ABCs Trauma considerations   Spinal precautions if MOI suggests injury Adult respiratory distress syndrome (ARDS) or renal failure often occurs postresuscitation Symptoms may not appear for 24 hrs  Post resuscitation complications    Transport all submersion patients Diving Emergencies   Incidence Medical emergencies caused by:  Mechanical effects of pressure  Barotrauma   Air embolism Breathing of compressed air   Decompression sickness Nitrogen narcosis Mechanical Effects of Pressure  Basic properties of gases   Increased pressure dissolves gases into blood Oxygen metabolizes; nitrogen dissolves Boyle’s Law   When pressure is doubled, volume of gas is halved PV = K    P = Pressure V = Volume K = Constant Trapped gases expand as pressure decreases Dalton’s Law   Pressure from each gas in a mixture of gases is the same as it would be if that gas alone occupied the same volume Pt - PO2 + PN2 + Px     Pt = Total pressure PO2 = Partial pressure of oxygen PN2 = Partial pressure of nitrogen Px = Partial pressure of remaining gases Henry’s Law   At constant pressure, solubility of gas in liquid is proportionate to partial pressure of gas %X = Px/Pt x 100    %X = Amount of gas dissolved in liquid Px = Partial pressure of gas Pt = Total atmospheric pressure Barotrauma of Descent ”Squeeze”       Pain Sensation of fullness HA, disorientation Vertigo Nausea Bleeding from nose or ears Pre-hospital care  Supportive    Reverse squeeze Breath holding during ascent POPS     Barotrauma of Ascent Alveolar rupture Pneumomediastinum Subcutaneous emphysema Air embolism  Administer oxygen Transport for possible hyperbaric care  Air Embolism  Complication of pulmonary barotrauma      Expanding air disrupts tissues Air forced into circulatory system Air passes through left side of heart Lodges in small arterioles Blocks distal circulation Air Embolism       Paralysis or sensory change Aphasia Confusion Blindness Convulsions Loss of consciousness Signs & Symptoms History of a recent dive Change in LOC CVAICP MI       Maintain ABCs Remove wet clothing and keep warm Oxygen, IV, EKG Initially- place on left side trendelenberg position After 30-60 minutes, place supine to prevent the worsening of cerebral edema Transport to hospital with hyperbaric chamber Air Embolism—Care Decompression Sickness    Bends, dysbarism, caisson disease, and diver's paralysis Multisystem disorder Nitrogen in compressed air converts from solution to gas  Forms bubbles in tissues and blood Decompression Sickness       Dyspnea Itch Rash Joint pain Crepitus Fatigue      Vertigo Paresthesias Paralysis Seizures Unconsciousness Decompression Sickness  Symptoms 12-36 hrs after dive Pre-hospital care     Support vital functions High-concentration oxygen Fluid resuscitation Rapid transport for recompression Nitrogen Narcosis “Rapture of the deep” Nitrogen dissolved in blood High atmospheric pressure Impaired judgment Slowed motor response Euphoria Potential memory loss Nitrogen Narcosis  Supportive care Assess for injuries Transport   High-Altitude Illness  >8000 ft above sea level    Reduced atmospheric pressure Hypobaric hypoxia Associated with: Mountain climbing  Aircraft or glider flight  Hot-air balloons  Low-pressure or vacuum chambers  High-Altitude Illness— Prevention      Gradual ascent Limit exertion Decrease sleeping at altitude High CHO diet Medications  Controversial Acute Mountain Sickness (AMS)  Rapid ascent of unacclimatized person to high altitudes     4-6 hrs after reaching high altitude Maximal within 24-48 hrs Abates on 3rd or 4th day Gradual acclimatization Acute Mountain Sickness (AMS)          Headache Nausea, vomiting Dizziness, irritability Dyspnea on exertion Tachycardia or bradycardia Ataxia Altered vomiting postural hypotension Acute Mountain Sickness (AMS)  Pre-hospital   Oxygen Descent  Hospital    Diuretics Steroids Hyperbaric therapy High-Altitude Pulmonary Edema (HAPE)  Increased pulmonary artery pressure develops in response to hypoxia  Leukotrienes released  Increase pulmonary arteriolar permeability    Leakage of fluid into extravascular spaces 24-72 hrs after reaching high altitudes Often preceded by exercise HAPE Signs & Symptoms           Hyperpnea Crackles, rhonchi Tachycardia Hyperpnea (deep, rapid breathing) Cyanosis Immediate descent to a lower altitude Shortness of breath, cough Weakness, lethargy Crackles, rhonchi Decreased LOC as hypoxia sets in High-Altitude Cerebral Edema (HACE)  Severe acute high-altitude illness    Global cerebral signs with AMS Related to increased intracranial pressure  From cerebral edema and swelling  Distinctions between AMS and HACE are blurred Mild AMS to unconsciousness with HACE occurs within 12 hrs  1-3 days of exposure to high altitudes  Same as AMS, headache to decreased LOC  Hallucinations, stupor, coma, death HACE  Urgent management to prevent   Coma Death   Airway, ventilation, circulation support Descent to lower altitude Conclusion Many emergencies result from exposure to environmental elements. The paramedic must be able to recognize and manage these conditions by understanding their causative factors and underlying pathophysiology. Questions?