Environmental Emergencies Part 1 Wilderness Emergencies

Environmental Emergencies Part 1 Wilderness Emergencies
Emergency Medicine Clerkship Series Author: Todd A. Parker, M.D. Co-author: Tom Bottoni, M.D.

Vacation! You get that much needed time off
Your significant other wants to go to St. Tropez But you really want to climb Mt. McKinley (Denali) Highest peak in North America-20,320 ft! She decides to give it a try, and you’re off! 4 days into the climb, you are at camp 4000 ft from the summit, and she complains of a headache and is confused…..

High Altitude Sickness
Definitions: - Moderate altitude ft - High Altitude - Extreme High Altitude >18000 Can occur at altitudes greater than 5000 ft Although most occur above 11,500 feet Influenced by: - Rate of ascent - Final altitude - Sleeping altitude - Duration at altitude

Who is at risk? Hard to predict who will get it! Higher risk
Younger > Older Males > Females Except during water retaining phase of cycle (premenses) Persons with previous high altitude illness Can occur in previously unaffected Those with previous illness can be unaffected Persons who overexert themselves Physical fitness not necessarily protective Smoking, Alcohol, Sedatives

Physiology Hypoxia due to ↓ in barometric pressure
Hypoxemia due to ↓ PO2 of inspired air Impact on cell variable Ability to acclimatize/compensate Pre-existing medical conditions

Acclimatization Ventilation – increases almost immediately
Cardiovascular Increased Cardiac Output (CO) Increased pulmonary perfusion Improves V/Q mismatches Increase in cerebral blood flow Hematologic Relative increase in Hg due to diureses Erythropoietin – stimulates bone marrow Effect takes weeks

Types of illness Altitude-exacerbated conditions
NOT the focus of this talk, but be aware! Congenital Heart Disease Pulmonary Hypertension Coronary Heart Disease CHF Sickle Cell Disease / Trait Obstructive Sleep Apnea Pregnancy Radial Keratotomy (Corrective Eye Surgery)

High Altitude Illnesses
Acute Mountain Sickness High Altitude Cerebral Edema High Altitude Pulmonary Edema

Acute Mountain Sickness
Defined as headache and one or more of: - Anorexia - Fatigue/weakness - Nausea/Vomiting - Difficulty Sleeping - Dizziness - Lightheadedness Develop 6-10 hours after ascent May be <1 hr Usually Self Limiting

AMS - Treatment Rarely need to descend – slow / halt ascent
Analgesics/antiemetics prn Consider acetazolamide ( mg BID) Speeds acclimatization Descend if sx do not improve Dexamethasone 4mg PO/IM if unable to descend Graded ascent is best preventive measure (600m/day)

High Altitude Cerebral Edema (HACE)
AMS – Sx progress to global cerebellar dysfunction Ataxia or altered mental status Vertigo, Diplopia, rarely seizures Usually > ft (have occurred as low as 9K) Begin 12 hrs or greater after onset of AMS Sx usually global Isolated focal sx – concern for CVA/TIA

HACE - Treatment Immediate descent definitive tx
Supplemental O2 (highest flow or sats >90%) Dexamethasone 8mg PO/IM then 4mg Q6h If cannot descend, hyperbaric therapy (more later)

High Altitude Pulmonary Edema (HAPE)
Non-cardiogenic pulmonary edema Accounts for most high altitude deaths Occurs 1-3 days after arrival at altitude Rarely occurs after 4 days – consider alternative dx 1-2% of high altitude climbers 15% of those with rapid ascent

HAPE Pathophysiology Hypoxia leads to pulmonary artery HTN
Increased pulmonary vascular resistance However, occurs in everyone – not just HAPE Pulmonary capillary pressure increases Leads to overperfusion  Capillary leakage Fluid as well as proteins leak out  Exudative fluid With descent, pressure decreases Capillaries “reseal”, leakage stops  Recovery Inflammatory mediators likely not primary process, but secondary to leaked proteins

HAPE Treatment Descent! Supplemental O2 B-agonists:
Decreases pulmonary artery pressure up to 50% B-agonists: Increase fluid clearance from alveolar spaces No role for dexamethasone Limited role for acetazolamide (may dyspnea)

HAPE Treatment - Nifedipine
Controversial Reduces pulmonary artery pressure Does NOT improve oxygenation Use only if Descent impossible Supplemental O2 unavailable Downside: Lowers systemic BP also CPP = MAP – ICP If risk for/concomitant HACE, lower MAP lowers CPP

Hyperbaric therapy Greatest benefit in HACE HAPE – likely beneficial
Use highest PSI available HAPE – likely beneficial Cost – benefit vs. Supplemental O2 generally precludes AMS – little additional benefit

HAI - Summary Medications: Stop ascent – attempt acclimatization
Supplemental O2 immediately if available If no improvement or worsening, descend Medications: Acetazolamide – best for acclimatization Little benefit in acute tx (no use in HAPE) Dexamethasone AMS and HACE No role in HAPE B-agonists useful in HAPE Nifedipine – likely beneficial in HAPE Use with extreme caution if concomitant concern for HACE

Recovery! With rest and oxygen, your significant other has recovered at base camp Now armed with more knowledge Begin ascent again You’re at camp 4000 ft from the summit again, and a storm hits – you’re stuck! That night, she says that she can’t feel her fingers…

Frostbite!

Frostbite Skin blood flow ↓ when skin temp < 140 C (57.20 F)
“Hunting Response” – alternating cycles of vasodilation and vasoconstriction at < 100 C (500 F) Vasodilation brings cooled blood to core As core body temp drops, cycles end and blood flow completely cut to extremities Tissue freezes – ice crystals form when temp 00 C Creates osmotic gradient pulling fluid from intracellular spaces Intracellular NaCl rises, proteins denature, membranes fail Reperfusion injuries – hours to days

Frostbite Classification
10: Non-sensate white area/surrounding erythema 20: Vesicles with surrounding erythema 30: Hemorrhagic blisters with eschar formation 40: Necrotic tissue, involves muscle/tendon/bone Reclassification – Superficial (First/Second) and Deep (Third/Fourth) Classified according to treatment/outcome vice tissue involved

Frostbite Treatment Thawing stage Consider delay if:
Adequate analgesia not available Delayed evacuation (i.e. ambulation required) Remove wet/constrictive clothing Rapid rewarming Use C water for minutes with motion Avoid hot untested tap water - risk of thermal burns! Avoid massaging and dry heat Parenteral analgesics

Frostbite Treatment Post-Thawing Treatment Debride CLEAR blisters
Apply aloe skin cream (Dermaide) Do NOT debride hemorrhagic blisters Elevate affected parts Tetanus prophylaxis Scheduled ibuprofen / prn narcotics Pen G 600,000 units q6h Daily Hydrotherapy at 400 C for mins No Smoking!

Foiled! She recovers from her mild frostbite
Since your flight home isn’t for 10 days, you propose another summit attempt, and get this look…

Plan B On second thought, you propose camping in beautiful Denali National Park to view the Northern Lights… You fall asleep, under the lights, after sharing a couple bottles of wine together You wake up a few hours later and you notice she is shivering violently and you have a hard time waking her…

Accidental Hypothermia
Definition: Core Temp < 350 C (950 F) Mild: 320 C – 350 C (89.60 F – 950 F) Moderate: 280 C – 320 C (82.40 F F) Severe: <280 C (82.40 F)

Mild Hypothermia 320 C – 350 C (89.60 F – 950 F) Signs / Symptoms:
Shivering Tachypnea / Tachycardia / Hypertension Ataxia / Dysarthria Loss of fine motor coordination Confusion / lethargy

Moderate Hypothermia 280 C – 320 C (82.40 F - 89.60 F)
Signs / Symptoms: Shivering Stops Bradycardia Osborn (J) waves on EKG Altered Mental Status Slowed Reflexes Cold Diuresis Pupil Dilation

Severe Hypothermia <280 C (82.40 F) Signs / Symptoms:
Unresponsive / Coma Hypotensive V Fib / Asystole Acidemia Loss of reflexes

Lab Tests (if able) BMP – pay attention to electrolytes (esp K+)
CBC – Hct increases 2% for each 10 C drop Trauma – normal Hct may mean blood loss ABG – interpret as is (blood rewarmed in lab) Coags: May be normal - blood is rewarmed Do not necessarily reflect physiology in patient Other labs as indicated if another underlying cause o hypothermia suspected EtOH/UDS Cardiac Enzymes, etc

Hypothermia Treatment
Large Bore IV(s) – Bolus with warm fluids Intubate if indicated Immediate Actions – ACLS! Check Vital Signs and ECG Check seconds for pulse – difficult to detect Rectal thermometer – must be low temp capable Standard thermometers only to C (940 F) If no pulse, begin CPR Controversial in severe hypothermia, however likely beneficial

Most dysrhythmias convert on rewarming A. Fib/Flutter Sinus bradycardia Transient ventricular dysrhythmias V. Fib / V. Tach – defibrillate at 1-2J/kg One shock only May be ineffective at temps < 300 C If fails, reattempt after each degree rise

Intravenous drugs May be ineffective below 300 C Give at longer intervals above 300 C Amiodarone drug of choice for V. Fib Avoid procainamide – may worsen If EtOH – Replete glucose and thiamine Hypoglycemia and Wernicke’s may help precipitate hypothermia

Rewarming Cornerstone of treatment – REWARM!
Rapid rewarming to 30 degrees Minimize risk of dysrhythmias Once above 30 deg, can slow rewarming rate Cardiovascular status is most important

Passive Rewarming Ideal method: Slow, physiologic
Must have intact thermoregulation Shivering intact Caution in underlying diseases Likely only effective in mild hypothermia Methods: Remove from environment Remove wet clothes Blankets

Active External Rewarming
Use for moderate hypothermia Monitor closely! Rapid peripheral vasodilation May return cooled blood to core Likely not clinically significant Consider rewarming trunk alone Warm water immersion – ensure monitoring Heating blankets Forced air (BAIR Hugger) Radiant heat

Active Core Rewarming ALL Patients Warmed IV Fluids
Warmed humidified Oxygen Small heat gain – mostly prevents further heat loss

Active Core Rewarming Severe hypothermia/cardiac instability
Lavage with warm fluids - Nasogastric/rectal Pleural (via thoracostomy) Bladder (via Foley) Peritoneal (via DPL catheter) Mediastinal Lavage via open thoracotomy If available Cardiopulmonary Bypass Hemodialysis Set up difficult, but most effective!

That’s it! Although she recovers uneventfully, she’s had it with this cold weather vacation! You’re on the next flight for Hawaii That afternoon, after landing, she decides to unwind by going for a run 2 hours later she hasn’t returned, you drive out to find her and she’s sitting on the side of road…

Heat Emergencies Predominant forms of heat loss Causes:
Radiation (65%): loss via electromagnetic waves Only occurs if temperature differential (stops at 950 F) Evaporation (30%): transfer of heat via sweat and saliva evaporation Minimal if humidity > 80% Causes: Increased internal heat production Increased external heat exposure Impaired heat dispersion

Increased Internal Heat
Physical Activity Exercise Seizures Combative behavior Pharmacological agents Amphetamines, cocaine, LSD, PCP Endogenous Fever NOT the same as environmental hyperthermia Should not be exogenously cooled

Increased External Heat
High Ambient Temps Minimizes radiation heat loss High Humidity Minimizes evaporative heat loss Direct exposure to sunlight

Impaired Heat Dispersion
CV disease Impaired circulation Impaired compensation Obesity Adipose - decreased vascularity Insulates the body Skin alterations Clothing Medications Anticholinergics Cardiovascular drugs Diuretics Sympathomimetics Phenothiazines Alcohol/Drugs Extremes of Age Dehydration

Acclimatization Increases ability to provide peripheral blood flow, protect kidneys, and increase sweating Improved physical condition = improved cardiac response to vasodilation Increased efficiency at shunting blood from non-critical areas Increased activation of renin-angiotensin-aldosterone system Enables increased sodium retention Expansion of plasma volume Sweat glands increase sweat production

Heat Emergencies Minor heat illnesses Heat Exhaustion Heat Stroke
Head Edema Heat Rash Heat Syncope Heat Cramps Heat Exhaustion Heat Stroke

Heat Edema Cutaneous vasodilation and orthostatic pooling
Resolves spontaneously If treatment instituted Removal from heat Elevation of legs with support hose Do not use diuretics Dehydration more risky May cause electrolyte disturbances

Heat Rash Pruritic maculopapular rash
Stratum corneum blocks sweat ducts Ducts rupture Localized inflammation Pruritic Avoidance Light, loose fitting clothes Minimize sweating Treatment: Antihistamines and avoidance

Heat Syncope Secondary to Treatment Peripheral vasodilation
Decreased vasomotor tone Volume Depletion Treatment Remove from heat source Oral or IV fluids Rest

Heat Cramps Usually secondary to electrolyte disturbances from sweating Dehydration or water-only rehydration Hyponatremia Hyperkalemia Treatment Remove from heat Oral hydration with electrolyte containing fluids IV fluids

Heat Exhaustion Signs and Symptoms: Non-specific!
Temp usually elevated but < 410 C Fatigue/weakness/dizziness /syncope Nausea/vomiting Headaches Myalgias and muscle cramps Tachycardia Piloerection Profuse sweating usually present

Heat Exhaustion - Treatment
Remove from heat and minimize activity Cool with fans/ice packs to neck, groin, axillae Oral rehydration w/electrolyte containing fluids IV Fluids if not alert or nausea/vomiting Replace fluids over several hours Monitor vital signs Urine output Orthostatics

Heat Stroke Signs and Symptoms
Elevated Temp – usually > 410 C (1060 F) Hyperdynamic cardiac parameters Tachycardia/Tachypnea Increased systolic / increased pulse pressure CNS Dysfunction - Seizure - Delirium - Cerebellar dysfunction - Coma - Hallucinations - Pupil dysfunction Oliguria Anhydrosis – often present but not required!

Heat Stroke - Treatment
Initial resuscitation ABC’s, IV access, cardiac/pulse ox monitoring Rectal thermometer for continuous monitoring Intubation if indicated Begin IV fluid boluses (Normal saline or LR) Place foley and NG Tube Rapid Cooling is key

Cooling Techniques Goal is 38-390 C to avoid overshoot
Evaporative cooling preferred Remove clothing, spray with lukewarm water Use large fans to blow air across skin Immersion – rapid cooling in ice water Difficult to monitor patient May cause shivering Very uncomfortable if awake Internal cooling (lavages – i.e. bladder, gastric) Effective, but probably unnecessary CP bypass – likely not worth risks

Adjunct Therapies Antipyretics – NO ROLE! Benzodiazepines
May interfere with endogenous thermoregulation Benzodiazepines Help reduce agitation / shivering / seizures EtOH / Drug withdrawal Avoid large volumes of IV fluid May lead to pulmonary edema (even healthy pts) Except in rhabdomyolysis Renal failure Hemodialysis if unresponsive to fluids / acid-base correction

Fortunately… She just has a mild case of heat exhaustion. You get her water and into your air conditioned vehicle Back at the hotel, after she’s rested for a couple hours, she decides to go for a swim in the ocean You tell her you’ll meet her out there in a minute You lose track of time watching a great ER rerun, and 30 minutes later you arrive to find several lifeguards carrying her in Apparently a rip tide pulled her under, and it took the lifeguards several minutes to pull her out…

Submersion Injuries Drowning – Death within 24 hours of submersion
Near Drowning – survival after submersion injury Third leading cause of accidental death Freshwater > Saltwater EtOH/Drugs commonly involved Most victims children/ adolescents

Submersion Injuries Sequence:
Breath holding Panic Swallowing water / emesis Breathing water “Dry drowning” – laryngospasm/glottic closure Final common pathway - hypoxemia

Pulmonary Injuries Fresh Water Salt Water
Inactivates surfactant Atalectasis and loss of pulmonary compliance Salt Water Osmotic gradient pulls fluid into alveoli Intrapulmonary shunting / VQ mismatch If survive initial aspiration – ARDS or pneumonia

Signs/Symptoms 4 categories Asymptomatic Symptomatic
Altered mental status / anxiety Hypothermia/Tachycardia/Bradycardia Any dyspnea, no matter how slight Cardiopulmonary Arrest Obviously Dead Normothermic Asystole No neurologic response

Submersion – Labs/Studies
ABG essential CBC, BMP, Lactate, Coags Follow creatinine – renal failure delayed EtOH / UDS Chest X-ray CT Spine / Head CT if at risk for injury C-Collar until cleared by mechanism or studies

Submersion Treatment Pre-hospital Unless certain, assume spinal injury
C-Collar and backboard Maintain precautions when moving Rescue breathing and supplemental O2 CPR – start on almost all patients In water chest compressions generally worthless Begin rewarming

Submersion Treatment -ED
Unless obviously dead, assume survivability Especially children Intubate if unable to oxygenate/ventilate PEEP - Improves ventilation and volume Shifts fluid into capillaries Consider BIPAP if awake If intubated, perform bronchoscopy ACLS algorithms if indicated Rewarm patient (as per hypothermia protocols)

Complications ARDS Pneumonia Disposition/Treatment Supportive care
Direct water aspiration Aspiration of gastric contents Contaminants / organisms in water Bacteria and fungi common, esp warmer waters Disposition/Treatment Most need admission, ICU if warranted Prophylactic antibx / antifungals not necessary, unless sx Extended spectrum PCN / B-lactamase + aminoglycoside If asymptomatic and no injuries, observe and discharge

Turns out she’s OK You decide that you’ll go back in the water, together, but this time with scuba tanks to check out a nearby reef After enjoying a beautiful dive, you begin your ascent to the surface Suddenly, a large jellyfish stings her, she panics and races for the surface You remember your dive tables, and ascend as rapidly as you can, safely At the surface, she seems to be doing OK but is complaining of severe leg pain (where she was stung) as well as itchy skin and right shoulder pain….

Diving Injuries / Dysbarism
Sea level – ambient air pressure = 1 atm Ascending - ambient pressure halves at ft Diving – ambient pressure increases by 1 atm every 33 feet! Boyle’s Law – pressure/volume inversely proportional As pressure increases, volume decreases (diving) Vice versa (ascending) Henry’s Law – gas enters liquid in proportion to partial pressure As descend, partial pressure increases – gases more soluble During ascent, gases come out of solution Oxygen metabolized, nitrogen does not Coalesces into bubbles if ascent too quick

Types of Injuries Barotrauma of descent Barotrauma of ascent
Direct barotrauma Arterial gas emboli (AGE) / Dysbaric air embolism (DAE) Indirect effects of ascent Nitrogen Narcosis Decompression Sickness

Descent Barotrauma (“Squeeze”)
Ear Squeeze External (Barotitis Externa) Air trapped in ext canal compresses TM bulges out Trauma to TM and surrounding external canal Middle (Barotitis Media) – most common! Cannot equalize air in middle ear TM bulges inward – may rupture May cause trauma to ossicles/ round window Inner (Barotitis interna) Trauma to round window Air enters inner ear Classic triad – tinnitus, hearing loss, vertigo Also nausea/vomiting, ataxia, nystagmus

Descent Barotrauma (“Squeeze”)
Sinus Squeeze Air trapped in sinuses Causes pain / hemorrhage into sinuses  epistaxis Treatment of ear and sinus squeeze Decongestants (oral and nasal spray) Antibiotics if TM rupture Analgesia Avoidance of diving Mask Squeeze Must equalize pressure behind mask during descent Can cause localized petechiae /conjunctival hemorrhage

Ascent Barotrauma Reverse process of squeeze Occurs from gas expansion
Normally gas escapes into atmosphere If escape blocked, barotrauma

Ascent Barotrauma (cont)
Ears and sinuses – usually not affected If air got in on descent, can get out Barodontalgia (“Tooth Squeeze”) Descent - compressed air gets in fillings/decay Ascent – expands Cannot escape  Pain GI Barotrauma (Aerogastralgia) - air trapped in GI tract Swallowing air (improper valsalva) Drinking carbonated beverages or heavy meal prior Generally self-limiting pain/discomfort – rupture rare If pneumoperitoneum, also consider GU source (esp females)

Pulmonary Barotrauma Most severe barotrauma of ascent
Air normally breathed out equalizes pressure If air not breathed out, expands Ruptures into surrounding tissue Pneumomediastinum and SubQ emphysema common Usually self-limiting Pneumothorax and Arterial Gas Embolism Require intervention Pneumothorax – needle decompression / thoracostomy

Arterial Gas Embolism Rupture of alveolar air into pulmonary veins
Air embolism  left heart  systemic circulation Symptoms of thromboembolic disease CVA type symptoms or myocardial infarction Any sudden, severe symptoms of thromboembolism on ascent should be treated as AGE Immediate recompression/hyperbaric treatment Resuscitate per ACLS Position right lateral decubitis or supine Do not place head down – cerebral edema

Nitrogen Narcosis Nitrogen – increased solubility at increased partial pressures (remember Henry?) Intoxication effect at high partial pressure Most feel effect by feet Impaired >200 ft, unconscious >300ft Effects reverse with ascent Can precipitate other errors Impairs recollection of dive / ascent – impairs history

Decompression Sickness (DCS)
Dissolved nitrogen forms bubbles if ascent too rapid Direct effect of bubbles Indirect effect of inflammatory response to bubbles Causes activation of clotting/inflammatory cascades Net effect Decreased tissue perfusion Ischemic injury

Type 1 DCS “Niggles” – mild pains, begin to resolve ~ 10 mins
Pruritis (“Skin Bends”) Skin rash Lymphatic involvement Peripheral edema Pain (“The bends”) Aching pain Usually in joint, tendon, occasionally muscle Shoulder most commonly affected

Type 2 DCS Pain uncommon (30%) Neurologic system
Nitrogen very soluble in fat – myelin sheath Spinal cord most commonly affected (esp lower) Bladder dysfunction Pulmonary DCS (The “Chokes”) Venous nitrogen emboli Chest pain, cough, dyspnea, pulmonary edema Can progress to hemoptysis

Physical Exam In addition to vital organs, pay close attention to
Sclera / retina Tympanic membranes Thorough neurologic exam Urinary retention Differentiating AGE from DCS Length of dive (must be longer dive to develop DCS) Time of onset (AGE rapid / DCS delayed) AGE – only CNS effects are on the brain

DCS Treatment Prehospital Extricate from water / immobilize if trauma
Supplemental O2 May result in resolution of mild DCS ASA for anti-platelet activity Consider in-water recompression only if in remote location CPR if indicated Needle decompression of tension ptx Avoid trendelenburg

DCS Treatment ED care All of the prehospital measures apply
100% O2 – intubate if warranted Aggressive fluid resuscitation Goal UOP is 1-2ml/kg/hr Treat nausea and headaches Arrange transfer to HBO facility Consider even if improvement in symptoms Relapses / worsening occur Ensure air transport can maintain pressurization!

She recovers (again) Supplemental oxygen and about 30 minutes of rest, and she’s feeling better But what about that jellyfish sting?

Marine Envenomations ~1200 species of venomous or poisonous marine animals worldwide Few cause major medical issues Broad array of species Various neurotoxic and proteolytic venoms Used for paralyzing / killing prey Humans are often accidental victims or hosts

Marine Envenomations Invertebrates Coelenterates Mollusks Echinoderms
Anemones and Jellyfish Mollusks Octopus/Squid Cone Snails Echinoderms Sea Urchins Poriferae Fire Sponge Vertebrates Stingrays Scorpion fish Catfish Sea snakes (Hydrophidae)

Jellyfish / Man O’ War

Fire Coral

Sea Urchins Blue Ringed Octopus

Scorpion Fish Stingrays

Marine Envenomation -Treatment
Cornerstones – ABC’s First! Detoxify venom – rinse with normal saline Freshwater may activate venom Pain and symptom relief – narcotics, antihistamines Local wound care FB removal Deactivation and removal of attached nematocysts 5% acetic acid / isopropanol (further deactivate) Apply baking soda slurry or shaving cream Allow nematocysts to coalesce and scrape off May remove with adhesive tape Marine wounds prone to infection Aeromonas, Vibrio, Pseudomonas, Erysipelothrix spp Prophylactic antibiotics for serious wounds

She’s had it with the ocean!
You make one last attempt to salvage your vacation, and let her pick the spot She wants as far away from the ocean as possible Off to the Grand Canyon!

First night of camping Your significant screams, and you wake up to see this guy in tent!

Land Envenomations Meanwhile, her hand begins to swell
rapidly and goes numb as the wound site oozes blood, and she starts to get nauseated and dizzy…

Snake Envenomations Poisonous or Not?
Exception: Coral Snakes (Elapidae)

Epidemiology 14 Families of snakes 3 main poisonous snake families
Viperidae Vipers and Pit Vipers Rattlesnakes Elapidae Cobras and Mambas Coral Snakes Hydrophidae – Sea snakes Colubridae – Asps and Mole Vipers ~4000 snake bites annually reported in USA <20 deaths / year

Poisonous snakes Rattle Snakes Coral Snakes Copperhead Snakes

Components of Poisonous Venom
Fibrinogenases, phospolipases Platelet aggregation inhibitors Enzymes with hemorrhagic activity Numerous other uncharacterized proteinases Neurotoxins (for coral snake venom)

Crotalid Envenomations
None (dry bites) - ~15-20% Mild - local swelling and pain No systemic features Moderate – progression of swelling Local tissue destruction Hematologic abnormalities Systemic sx Severe – marked swelling Bullae and tissue necrosis Shock Coagulopathy

Crotalid Envenomations – Initial Management
Immobilize injured part at or below heart level Provide local wound care Cleansing Debridement Prophylactic ABX Tetanus Lab eval CBC, CMP, CPK Coags and DIC panel Observe for 24h or admit, for sx of progression Consider antivenin early, for mod / severe envenomations

Role of Antivenins Neutralizes circulating venom toxins when given early (<6H) Can mitigate local tissue destruction Slows/prevents coagulopathy and systemic sx Active against: US rattlesnakes Copperheads, and cottonmouths Some sea snakes Separate antivenin for coral snakes No dose adjustment for children Dose is based on venom load, not subject weight! Call local poison control center

Crotalid Antivenin Indications for Antivenin Rapid progression of sxs
Significant coagulopathy Profound thrombocytopenia Hemodynamic compromise Neuromuscular toxicity Contraindications for Antivenin Hypersensitivity to horse or sheep serum Hypersensitivity to papain or papaya Poorly controlled atopy Concurrent beta blocker use May worsen anaphylaxis

Complications of Envenomations
Immediate (<24H) Local tissue necrosis Systemic shock Coagulopathy Rhabdomyolysis Compartment Syndrome Neurotoxicity Delayed (24-96H) Renal Failure Compartment syndrome Antivenin Rebounds Serum Sickness

Desert Scorpion – in attack posture!
Scorpions Numerous venomous species worldwide Several species native to US southwest Only Centruroides bark scorpions have a poisonous venom Centruroides spp are indigenous to AZ and CA Natural Light UV Light Desert Scorpion – in attack posture!

Scorpion Venom Components
Numerous digestive enzymes Hyaluronidase Phospholipases Neurotoxins Stabilizes Na+ channels in open position Causes overfiring of N-M junction and autonomic nervous system

Clinical Presentations
Most encounters Local, immediate pain and inflammation Subsequent paresthesias Sx often resolve in several hours with local wound and sx care Other symptoms (children at much higher risk) Diplopia and nystagmus Muscle fasciculations, seizures, and paralysis Rarely, cardiovascular collapse and resp failure Even rarer, pancreatitis

Scorpion Sting Management
Local wound care & irrigation Tetanus prophylaxis Benzos for sedation/muscle spasm control Severe envenomation Support ABC’s and hemodynamics Consider antivenin in consult with Poison Center

Spider Bites 50,000 spp of spiders in USA
Most possess paired poison glands attached to jaw like fangs Few poisonous spiders capable of penetrating human skin Predominant Poisonous Spiders in USA Latrodectus (black widow) Loxosceles (brown recluse) Tarantulas (none in US are poisonous) Localized wound effects – systemic effects very rare If indigenous area, may not be just an abscess!

Poisonous Spiders Brown Recluse (Loxosceles)
Black Widow Spider (Latrodectus)

Spider Venom Components
Loxosceles Digestive enzymes Collagenases, proteases & phospholipases Sphingomyelinase D Cytotoxic & hemolytic agent Local tissue necrosis Latrodectus Digestive enzymes Alpha latrotoxin Binds to synaptic receptors Ca+ channel dysfunction Release of Ach with motor end plate stimulation

Black Widow – Clinical Presentation
Local puncture wound Central clearing and outer ring of erythema Painful within 30 min Painful muscle cramps Fasciculations follow in 3-4h Board like rigid abdomen Resembles an acute surgical abdomen Complications (rare) Diaphoresis, nausea/vomiting Severe HTN Cardiorespiratory collapse

BWS Bite - Management Local wound care Tetanus
6-8h observation – supportive interim care IV calcium and benzos to treat muscle cramping Narcotic pain control Consider Latrodectus antivenin

Latrodectus (Black Widow) Antivenin
Equine derived antivenin Small risk of anaphylaxis Indications Severe envenomations Elderly Cardiac pts not responding to supportive care Pregnant patients- prevent preterm labor

Loxosceles (Brown Recluse) Envenomations
Immediate painful burning sensation at site Hemorrhagic central vesicle/bulla with surrounding Gives way to a necrotic ulcer over next 48-72h Slow to heal (can last a >month) Rare complications Intravascular hemolysis DIC Secondary infections Difficult Dx – resembles many other disorders

Brown Recluse - Management
Local wound care Tetanus Dapsone – attenuation of necrotic ulcer formation Not clinically born out Hyperbaric Oxygen Goat derived antivenin, but not FDA approved for use Avoid surgery if possible Most heal without surgical intervention

Solenosis (Fire Ants) 5 native spp of Solenosis in USA
2 spp imported via Mobile, AL Have spread throughout gulf basin / west to AZ,/CA One nest can produce 200,000 ants! Swarm and attack en masse when provoked Cross reactivity of fire ant venom with Hymenoptera venoms Systemic sx in susceptible individuals

Fire Ant Venom Similar to Hymenoptera venoms of bees, wasps, hornets and yellow jackets Biogenic amines Ach, histamine, dopamine, serotonin) Proteases and alkaloids Hyaluronidase, phospholipase) Fire Ant Nest

Clinical Presentation
Numerous papules at site of bites Local urticaria, pruritus & angioedema Systemic anaphylaxis in susceptible persons

Fire Ant Bite Management
Local wound care Tetanus Removal of stingers & attached venom sacs Topical papain (meat tenderizer) to inactivate venom proteins H1 & H2 blockers, steroids, analgesics Tx of Anaphylaxis, airway management and hemodynamic support, where indicated.

It’s A Dangerous World Out There!
Now you’re better equipped to handle it Prevention is the most important step in treatment And your significant other? She leaves you to be with someone much safer Like a stuntman or explosives handling expert

Environmental Emergencies Part 1 Wilderness Emergencies

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