Environmental Emergencies

(submersion, body temp extremes, thermal injuries)

Submersion

Drowning: asphyxiation caused by submersionin a liquid that causes interruption of the body’soxygen absorptionNear-drowning: a term formerly used to describevictim’s survival at least 24 hours after submersion• salt versus fresh water is no longer emphasized as degree

of pulmonary insult is determined by quantity aspirated• Epidemiology: 8000 deaths per year in the United States

– 20% to 25% are children

Pathophysiology

• Wet drowning: Aspiration of water into airways and lungs (85%)– 1 to 3 cc of aspirated water will lead to destruction of

surfactant, alveolar instability, noncardiogenic pulmonary edema, and impaired gas exchange

• Dry drowning: Severe parasympathetically mediated laryngospasm (15%)

• Both types result in common pathway of hypoxia which leads to acidosis, cardiac arrest, and brain death

Risk factors

1. Drug and alcohol intoxication2. Cardiac arrest3. Hypoglycemia4. Seizure5. Suicidal or homicidal behavior6. Child abuse

Symptoms and signs

• Hypoxia: Key factors predicting outcome are duration and severity of hypoxia

• Vomiting: – 66% of victims who receive rescue breaths vomit – 86% of victims who require chest compressions and

ventilations vomit• Mental status changes, tachycardia, cardiac

dysrhythmias, tachypnea, wheezing, pulmonary edema, cyanosis, apnea

• Diving injuries:– Potential head or cervical spine injury must be considered

Studies

• Arterial blood gas (ABG)– Hypoxemia may be out of proportion to patient’s

clinical presentation• Electrolyte panel• Chest x-ray (CXR)

Managment• Routine stabilization of cervical spine unnecessary unless

– History of diving– Use of water slide– Signs of injury– Signs of alcohol intoxication

• Rescue breathing– No need to clear airway of aspirated water as it does not obstruct the

trachea• Heimlich maneuver/abdominal thrusts unnecessary• Airway management

– Endotracheal intubation as necessary– Noninvasive ventilatory support as necessary– Serial ABGs traditionally used to guide need for ventilatory support

Extremes of Body Temperature

• Thermoregulation: ability to maintain normal body temperature physiologic levels despite external environmental temperature

Mechanism of action• Heat conservation

– Shivering, vasoconstriction, and piloerection• Cooling

– Radiation (60%)• Transfer of heat via electromagnetic waves from body to cooler air • Greatest source of heat loss

• Evaporation (30%)– Heat loss by perspiration, breathing, saliva– Acetylcholine regulates sweat glands and is impaired by anticholinergic drugs

• Convection (8%)– Transfer of heat from body to fluid, surrounding air or water vapor– Wind or “wind chill” is an example

• Conduction (2%)– Direct transfer of heat via physical contact

Hypothermia

• Normal: 97.7°F to 98.6°F (36.5°C to 37°C)• Mild: 93.2°F to 96.8°F (34°C to 36°C)• Moderate: 86°F to 93.2°F (30°C to 34°C)• Severe: <86°F (<30°C)

Etiology

• Environmental exposure• Toxicologic—mnemonic COOLS– Carbon monoxide, oral hypoglycemics, opioids,

liquors, sedatives (eg, benzodiazepines)– Alcohol intoxication may lead to impaired decision

making and prolonged environmental exposure• Systemic– Sepsis, hypothyroid, hypoadrenalism,

malnutrition, central nervous system (CNS) injury

Symptoms and signs• Mild hypothermia 93.2°F to 96.8°F (34°C to 36°C)

– Shivering• Moderate hypothermia 86°F to 93.2°F (30°C to 34°C)

– Confusion– poor judgment– Paradoxical undressing

• Prolonged vasoconstriction becomes overwhelmed and vasodilates, causing the skin to feel “hot”

– Tachycardia and tachypnea– Dilated pupils– “Shivering” reflex no longer present at 86°F (30°C)– Cold diuresis

• Severe hypothermia <86°F (<30°C)– Bradycardia and slow atrial fibrillation– <82°F (<28°C)—patient may appear dead (unresponsive, fixed pupils, apneic) – Asystole and ventricular fibrillation common

Complications

a. Pancreatitisb. Acute tubular necrosisc. Rhabdomyolysisd. Disseminated intravascular coagulopathy

(DIC)e. Acute respiratory distress syndrome

Diagnosis• Temperature

– Rectal probe for continuous temperature monitoring– Warm patients to normal or near normal body temperature before declaring them dead

• Laboratory tests– ABG

• Elevated pH• PCO2 decreased

– Complete blood count (CBC)• Hematocrit levels rise 2% for every 1°C drop in temperature• False hemoconcentration such that a normal hematocrit could represent severe anemia

– Coagulation profile prolonged– Evidence of DIC (low fibrinogen, elevated split products, abnormal coagulation profile)– Creatinine kinase may be elevated with rhabdomyolysis– Amylase or lipase may be elevated with pancreatitis

• ECG: Osborn waves (Figure 7–1)– Size of the wave correlates with degree of hypothermia– Usually resolves with rewarming– No prognostic value

ManagementRewarming methods• All patients

– Remove wet and cold garments– Cover with warm blanket– Cardiac monitoring– Handle gently as hypothermic

heart is irritable and prone to unstable dysrhythmias

Rewarming techniques• Passive rewarming

– Cover with blanket• Active external rewarming

– Forced hot air, warming blanket– Rewarm trunk

• Active internal rewarming– Warm IV fluids to 115°F (45°C)– Warm humidified oxygen– Peritoneal lavage– Bladder lavage

• Extracorporeal rewarming– Cardiopulmonary bypass

ManagementStable patients• Mild hypothermia 93.2°F to

96.8°F (34°C to 36°C)– Passive rewarming– Active external rewarming

• Moderate hypothermia 86°F to 93.2°F(30°C to 34°C)– Passive rewarming– Active external rewarming

• Severe hypothermia 86°F (<30°C)– Passive and active external

rewarming– Active internal rewarming until

core temperature >95°F (35°C)

Unstable patients• Start CPR• Defibrillate ventricular

tachycardia and fibrillatioN• Intubation with warm humidified

oxygen• Warm IV fluids• Mild or moderate hypothermia

– As per ACLS protocol• Severe hypothermia

– Withhold IV medications– Active internal rewarming

ACLS

• The cornerstone of ACLS in the severely hypothermic patient is active rewarming

• Hypothermic bradycardia is not caused by increased vagal tone but rather slowing of automaticity, and unlikely to respond to atropine

• Medications ineffective until patient is 82°F (>28°C) and may accumulate to toxic levels if given indiscriminately

• Current 2005 ACLS recommendations for defibrillation– 86°F to 88°F (30°C to 32°C): defibrillate once, then resume CPR and

rewarming– No additional attempts to defibrillate should be made until the

patient is >86°F to 88° F (30°C to 32°C)

HyperthermiaEpidemiology: The elderly, very young, or chronically ill are most vulnerable to hyperthermia

– Exertional heat stroke is the second leading cause of sports-related mortality (secondly only to spinal cord injuries)

Etiology• Loss of radiation

– Radiation account for 60% of heat loss– Radiation of heat becomes less efficient with increasing ambient temperature– Ceases when ambient temperature > body temperature

• Inefficient evaporation– Normally accounts for 30% of heat loss– Less efficient with increasing ambient humidity– Ceases when humidity approaches 100%– Lack of acclimatization (individual not used to hot climate) results in inefficient perspiration until days 7 to 10– Impaired sweating

• Anticholinergics• Skin disorders—scleroderma, psoriasis, burns• Autonomic disorders—diabetes

– Toxicologic• Sympathomimetics (amphetamine, cocaine)• Neuroleptic malignant syndrome, serotonin syndrome, malignant hyperthermia• Anticholinergics• Salicylate poisoning

• Systemic conditions– Hyperthyroid, infection, pheochromocytoma

Symptoms and signs:Continuum of illness ranging from heat cramps and heat exhaustion to heat

stroke• Heat cramps

– Etiology: inadequate intake of fluids and electrolytes– Symptoms and signs: muscle cramping usually affecting the calves and abdomen

• Heat exhaustion– Nonspecific weakness, headache, nausea and vomiting caused by dehydration– Temperature <106°F (41°C) or normal

• Heat stroke– Temperature >106°F (41°C)– Organ damage (Table 7–1)– Mental status change (irritability to coma)

• Presence of CNS dysfunction differentiates head exhaustion from heat stroke

– Anhidrosis (not universal)

Complications

• Rhabdomyolysis• Compartment syndrome• Liver failure• Seizure• Dysrhythmias• Pulmonary edema and acute respiratory distress

syndrome (ARDS)• Acute renal failure• DIC

Diagnosis• Laboratory testing

– CBC, CPK, glucose, BUN/creatinine, and LFTs– Hypoglycemia is a common occurrence– Abnormal liver function tests almost universal with heat stroke

• CXR to rule out pulmonary edema• Head CT and lumbar puncture may be required to differentiate encephalitis/meningitis from heat strokeManagement• Hydration, but excessive fluids should be avoided to avoid pulmonary edema• Rapid cooling

– Temperature 106°F (>41°C) requires immediate management– Cool to a target of 102°F (39°C) within 10 to 20 minutes

• Mechanical cooling– Remove clothing– Cool mist and fan (augments heat transfer via convection, radiation, and evaporation)– Ice water immersion advocated by some

• Pharmacologic– Antipyretics (NSAIDs and acetaminophen) have no role in environmental heatstroke

• Acetaminophen may be harmful with fulminant liver failure– Benzodiazepines to manage agitation and shivering

Clinical effects of heat stroke• Systemic inflammatory response Inflammatory mediators (ie, leukotrienes) released,

triggering inflammatory cascade• Cardiac Nonspecific electrocardiographic changes

– Myocardial enzyme elevations possible• Neurologic Mental status alteration

– Outcome related to time with elevated temperature– Permanent cerebellar injury may result

• Renal Acute renal failure in 10%– Injury is secondary to myoglobinuria, direct injury to tubules, and volume depletion

• Skeletal muscle Rhabdomyolysis– Elevated CPK– Hyperkalemia when myocytes destroyed– Hypocalcemia

• Gastrointestinal Vomiting– Diarrhea

• Coagulation Direct injury to clotting factors– Disseminated intravascular coagulation (DIC)– Acute liver injury, often

Thermal Injuries

• Frostbite: Tissue injury due to prolonged exposure to below freezing temperatures (<32°F, 0°C)

• Frost nip: mild, reversible superficial cold injury without tissue destruction or crystal formation

• Trench foot: prolonged wet, cold but nonfreezing exposure causing reversible neurovascular injury

• Chilblain (pernio): skin injury consisting of painful edema, erythema, and plaques caused by repeated dry, cold but nonfreezing exposure

Pathophysiology

• Vasoconstriction leads to decreased delivery of warm blood to extremities and formation of ice crystals in tissue

• Leads to sludging at capillary level and microvascular thrombosis

• Reperfusion injury occurs when frozen tissue thaws

Frostbite: Symptoms and signsNumbness followed by anesthesia is suggestive of frostbite• First-degree frostbite

– Definition injury is confined to the epidermis (conified epithelial cells)– Symptoms and signs: erythema and edema

• Second-degree frostbite– Definition: injury to epidermis and dermis (middle layer containing capillaries, nerve

endings, hair follicles)– Symptoms and signs: hard edema and clear blisters

• Third-degree (full thickness) frostbite– Definition: injury through and involving the hypodermis (connective tissue and adipose

connecting dermis to underlying structures)– Symptoms and signs: hemorrhagic bullae, pale grey extremity

• Severe pain with rewarming

• Fourth-degree frostbite– Definition: injury through to and involving the skin, muscles, tendons, bones– Painless during rewarming

Management• Rewarming

– Thawing in warm water 104°F to 108°F (40°C to 42°C)– Do not use dry heat such as a hair dryer– Do not rewarm if risk of refreezing exists as subsequent injuries worsen prognosis– Thawing requires 20 to 40 minutes for superficial injuries and up to 1 to 2 hours for deep

injuries (third- and Fourth-degree frostbite)– Inadequate thawing often due to early stoppage because of inadequate analgesia– Endpoint of thawing is a warm and soft extremity

• Wound care– Unroof clear blisters rich in injurious thromboxane– Do not unroof hemorrhagic blisters– Topical aloe vera over all affected areas– Update tetanus status– Antibiotics if infection or penetrating wound

• Consultation with surgery since tissue requires 6 to 8 weeks to determine need for amputation

Thermal BurnDegree Thickness Exam

1st Epidermis Erythema, tenderness, painSunburnNo blisters

2nd Epidermis/Dermis Very painful unless deep second-degree burnSuperficial partial thickness : Skin is red and blanches with pressure Deep partial thickness: Blisters, which usually ruptureif not promptly cared for

3rd All skin Layers Pale, leathery appearance Insensate secondary to destruction of nerveendings and blood supply

4th Skin, fascia, muscle, tendon, bone

Correlated to the severity and the extent of involvement of underlying subcutaneous tissue

Diagnosis

• Carbon monoxide levels for all patients involved in a fire• Cyanide toxicity should be suspected in industrial Fires– Sources of cyanide include insecticides, internal combustion

engines, tobacco smoke, plastics made from acrylonitrite• Estimation of body surface area (BSA) involved– Rule of nines (Figure 7–2)

• Pediatric version: patient’s palmar surface is 1% of BSA• Note that the head is the highest percentage in pediatric patients

Rule of Nines

Fluid management• Parkland formula: 4 mL/kg × % total BSA burned (in pediatrics give 3

mL/kg)– 50% given in the first 8 hours and remainder over 16 hours– Ringer lactate is preferred IV fluid

• Maintain urine output at a minimum of 1 mL/kg/hTransfer to burn center if • >10% BSA of partial thickness degree burns Third-degree burn

(guidelines do not specify BSA)• Second- or third-degree burns of hands, feet, genitalia, perineum, or

over joints • Electrical, chemical, or inhalation injury• Significant comorbid conditions

ManagementWound management• Blisters should be left intact (controversial)• Apply silver sulfadiazine or triple antibiotic ointments to burned areas• Deep burns require sterile management• Silver sulfadiazine should not be used on cartilaginous areas (eg, nose, ears) because of dark silver staining• Open wounds should be covered with sterile saline-soaked gauze as there is an increased risk of infection• Update tetanus status• Consider escharotomy for circumferential and full-thickness burns• Circumferential full thickness burns may cause vascular insufficiency in limbs and digits• Circumferential full thickness burns involving the chest may cause respiratory compromise• Consider securing airway if inhalation injury suspected• Suspect inhalation injury if:

– Sore throat and dyspnea– Stridor with airway edema– Soot or burns to the nasopharynx– Singed facial or nasal hair– Carbonaceous sputum

• Patient’s airway can unexpectedly and suddenly obstruct secondary to edema • Strongly consider prophylactic intubation as it is difficult to predict which patients will deteriorate• Consider fiberoptic laryngoscopy in patients with low suspicion for significant inhalation injury