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Environmental 1JONATHON DEIBEL, MDCENTRAL MICHIGAN UNIVERSITY

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DisclosureNo disclosures

Outline• Bites and Envenomation

• Dysbarism

• Altitude Sickness

• Lightning

• Plants

Bites and Envenomation

Reptile BitesCrotalidae

◦ Pit vipers◦ Rattlesnake, cottonmouth, copperhead

Elapidae◦ Coral snakes

Gila Monsters

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Crotalidae25% are dry bites

Venom effect• Cell injury: Swelling, tissue necrosis

• Coagulation: Increased PT and INR

• Decreased platelet and fibrinogen

• Systemic: Capillary leak and myocardial depression

CrotalidaeDry Bites• Should be observed for 8-12 hours

• If no signs of envenomation develop they can be discharged

CrotalidaeManagement• Immobilize in field

• No tourniquets

• No incision or suction

• Antivenin• Polyvalent crotalidae immune Fab (CroFab)

• Tetanus immunization

CrotalidaeIndications for Antivenin• Progression of local injury

• Swelling, pain and ecchymosis

• Evidence of coagulopathy

• Increased PT and INR

• Decreased plt and fibrinogen

• Systemic effects• Hypotension, persistent n/v, fasciculation or paresthesia

CrotalidaeAntivenin• CroFab • 4-6 vials IV

• Goal of therapy is to neutralize the venom

• End point of therapy

• Arrest the progressive symptoms and coagulopathy

• If initial dose fails to reach the end point give 4-6 more vials

• Once control is established give 2 vials q6h X 3 doses

• Treatment of the coagulopathy and elevated compartment pressures is more antivenin

Coral SnakesRed on yellow, kill a fellow, red on black, venom lack

Symptoms• Neurotoxic – Paralysis, tremor, seizures, bulbar palsies

• No local edema

• Can be delayed up to 12 hours

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Coral snakesTreatment• Administer antivenin early – EVEN WITHOUT SYMPTOMS

• Antivenin is only available for the Eastern Coral snake

• Local wound care

Gila Monsters• Desert southwest

• Typically local pain and swelling

• Typically need local wound care

• Inspect wound for retained teeth

Venomous Insects

Brown Recluse

• Woodpiles, attics and closets

• Classically a painless bite

Brown recluseLocal Reaction• Aching pain 2-8 hrs

• Bulls eye lesion

• Necrosis develops in 3-4 days

• Irregular margins with necrotic center

• TX: No antivenin, Local wound care, Update tetanus, consider Dapsone

Systemic reaction• Uncommon, seen more in kids

• 24 hr post bite• N/V, fever, chills, arthalagia

• Anemia with hemolysis

• DIC-> AKI/ARF

• Tx: hydration, alkalinize urine, maybe IV steroids

Other spiders causing necrotic lesions• Golden orb weaver

• Running spider

• Wolf spider

• Black jumping spider

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Black widowClinical presentation• Systemic within 30 min

• Muscle cramping – RIGID ABDOMEN

• N/V

• HTN, Tachycardia

• Facial muscle spasm

Black widowTX• Local Wound care

• Tetanus prophylaxis

• Monitor 4 hr if spider identified

• Benzos for muscle spasm

• Antivenin• Old, young and sick only

ScorpionsClinical presentation• Immediate burning sensation without evidence of injury

• Pain/paresthesia remote from site

• Cardiac dysrhythmias

• CN or skeletal motor dysfunction

ScorpionsTX• Local wound care

• Tetanus prophylaxis

• Antivenin for severe

HymenopteraHoneybees, yellow jackets, wasps, hornets, fire ants

Sting reactions• Local

• Systemic

• Acute severe systemic

• Systemic toxicosis

HymenopteraLocal Reaction• Pain, pruritus, erythema and localized urticaria

• May persist 24 hr+ and appear cellulitic

Tx

• Remove stinger

• Ice, Elevate

• Tetanus prophylaxis

• Antihistamine

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HymenopteraSystemic reaction• Generalized urticaria

• Flushing and vasodilation

• Cramps with vomiting and diarrhea

HymenopteraAcute severe systemic (anaphylaxis)• IgE mediated

• Occurs rapidly within 10-20 minutes

• Usually seen with 1-2 stings

• Hypotension, arrhythmias, laryngeal edema, bronchospasm and stridor

HymenopteraABC

Epinephrine 1:1000 IM• 0.3 – 0.5 ml in adults

• 0.01 ml/kg in peds

IV Fluid

H1/H2 antagonists

Steroids

Fire AntsClinical Presentation• Papule at sting site that develops into a sterile pustule in 24 hours

• Anaphylactic reaction possible

TX• Antihistamine

• Topical steroid

Marine envenomations

A 32-year old man vacationing in Florida presents 12 hours after eating sea food and rice. He is complaining of N/V, a sensation that cold objects feel warm, and paresthesias. What is the most likely cause of these symptoms?

A. Bacillus cereus

B. Ciguatera

C. Clostridium perfringens

D. Scombroid

E. Vibrio parahaemolyticus

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ScombroidDark meat fish (Mahi mahi, dolphin, tuna, mackerel)

Heat stable toxin

◦ Histamine

Improper refrigeration

Metallic, bitter or peppery taste is described

Scombroid• Abrupt onset in 20 – 30 minutes of ingestion

• Flushing, headache and diarrhea

• Symptoms usually resolve in under 6 hours

• Treat with H1 and H2 antagonists

Looks like an allergic reaction but isn’t

Ciguatera• Coral reef fish (red snapper, grouper, sea bass)

• Dinoflagellate accumulates up the food chain

• Bigger, older fish

• Tasteless, odorless, heat and acid stable toxin that is very resistant to everything that we might do to preserve or prepare the fish

CiguateraClinical Presenation• N/V

• Neuromuscular – May persist for months, worse with ETOH• Reversal of hot and cold sensation

• Myalgis, paresthesia

• Sensation of loose teeth

Treatment• Supportive

• Mannitol for neuro symptoms

TetrodotoxinPuffer fish

Acts on NA channels

Clinical presenation

• Generalized urticaria

• Flushing and vasodilation

• Cramps with vomiting and diarrhea

• Lip/tongue paresthesias

• Ascending paralysis

• Hypotension, bradycardia, conduction blocks

• Seizure, coma, death

TetrodotoxinTreatment• 50% mortality

• No antidote

• Supportive• Early airway management

• Gastric decontamination

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Marine envenomationsVenomous fish• Sting rays, scorpion fish and sea urchins

Nematocysts• Jelly fish, corals and sea anemones

Venomous FishClinical Presentation

• Mainly local symptoms

Treatment

• Remove spines/stingers

• Immerse in hot water (Heat labile poison)

• Irrigate

• Tetanus prophylaxis

• Consider antibiotics

NematocystsPhysical contact -> nematocyst discharge -> mainly local symptoms

Treatment ◦ Scrape off nematocysts

◦ Hot water immersion

◦ Td, pain control

Antivenin exists for the Box Jellyfish

Invasive gastroenteritis from eating raw oysters is most appropriately treated with what?

A. Ampicillin

B. Diphenhydramine

C. Doxycycline

D. Loperamide

E. Supportive therapy

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Dysbarism

Boyle’s LawVolume of a gas varies inversely with the pressure (PV = K)

Accounts for the “squeeze” syndromes on descent and the barotrauma syndromes of ascent• The squeeze syndromes: cannot equalize pressures

• The barotrauma syndromes: failure to exhale on ascent

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Henry’s LawAmount of gas dissolved in a liquid is directly proportional to the partial pressure of the gas in contact with the liquid

Nitrogen comes out of solution and forms bubbles in blood and body tissues

DysbarismDescent (squeeze syndromes)

At depth• Nitrogen narcosis

• Oxygen toxicity

Ascent• Barotrauma

• Decompression sickness (DCS)

Middle Ear Squeeze• Ear squeeze

• Pain from pressure on the TM

• Unable to equalize pressure

• Treatment: decongestants, open the Eustachian tube

Other Barotraumas• Barotitis externa

• Barotitis interna

• Barosinusitis

• Alternobaric vertigo

• Barodontalgia

• Face-mask squeeze

Nitrogen Narcosis• Occurs at depth from breathing compressed air

• Euphoria, confusion, disorientation, poor judgment and diminished motor control

• Controlled ascent to decrease the amount of dissolved nitrogen in the brain

Oxygen Toxicity• Occurs at depth from breathing compressed air

• Increased depth = increased partial pressure

• O2 is toxic to CNS at high partial pressures

• Nausea, muscle twitching, visual changes, irritability and seizures

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Pulmonary Barotrauma• Rapid uncontrolled ascent

• Expansion of unvented lung gases on ascent, must exhale on ascent

• Pneumothorax, pneumomediastinum, pneumopericardium and pneumoperitineum

Pulmonary Barotrauma• Arterial gas embolism (high morbidity and mortality)

• Alveolar gas enters the systemic circulation

• Air emboli in coronary (ACS-like) and more commonly the cerebral arteries (stroke-like)

• Presents within 10 minutes of surfacing

• Altered mental status, seizures are common

Decompression Sickness• Occurs on ascent

• Ascending too quickly causes nitrogen bubbles to form in blood and tissues

• Dive length and depth are major factors

• Obesity is also a factor as nitrogen is lipid soluble

Decompression sicknessTwo types• Type I

• Extravascular air bubbles

• skin and musculoskeletal “bends“

• Type II• Intravascular air bubbles

• CNS and pulmonary – More severe

Treatment is recompression

Type I DCS – “The Bends”• Musculoskeletal, skin and lymphatics

• Periarticular pain (elbow, shoulder and knee)

• Pruritus, erythema, skin marbling (cutis marmorata) from venous stasis

Type II DCS• Pulmonary “The Chokes”• Triad• SOB, Cough, Chest Pain

• Cyanosis

•Neuro “The Stagers”• Spinal cord most common

• Pain, paresthesia, incontinence

• HA, confusion, seizures

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RecompressionDefinitive treatment for DCS and AGE

Watch for:• Delayed symptom onset

• More subtle symptoms may develop after treatment

• Minor symptoms may progress

• Treatment is useful up to 14 days after symptom onset

Recompression Risks with flight• Commercial aircraft are pressurized to 5,000 - 8,000 ft

• This will worsen all DCS symptoms

• Symptoms may develop in divers w/o prior symptoms

• No flying for 3 – 7 days after treatment of Type I DCS and one month for Type II DCS

High Altitude IIIness

Which of the following is least likely to contribute to high altitude illness?

A. Altitude of residence B. Fitness levelC. History of high-altitude illnessD. Physical exertion

High Altitude IllnessFactors• Rate of ascent

• Altitude reached

• Sleep altitude

• Individual physiology

High Altitude IllnessRisk Factors• Prior history

• Living at < 900 meters

• Exertion at altitude

• Conditions with increased pulmonary vascular resistance:• Intracardiac/intrapulmonary shunts

• Pulmonary hypertension

• Mitral stenosis

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High Altitude IllnessSyndromes• Acute Mountain Sickness (AMS)

• High Altitude Cerebral Edema (HACE)

• High Altitude Pulmonary Edema (HAPE)

High Altitude IllnessPhysics• With ascent barometric pressure decreases• Decreased partial pressure of oxygen

• Decrease alveolar and blood pO2 = HYPOXIA

Pathophysiology• Hypoxia-> overperfusion of microvascular beds-> capillary leak-> interstitial

edema with increased sympathetic activity

High Altitude Illness• Fitness level is not predictive/protective

• Age > 50 is protective

• Women < HAPE

• kids = adults

High Altitude IllnessAcute Mountain Sickness (AMS)• Clinical Constellation

• Headache

• Recent arrival at > 2500m

• N/V, insomnia, dizziness, lassitude

• Typically appear with in 6 hrs

High Altitude IllnessHigh Altitude Cerebral Edema (HACE)

• Continuation of AMS

• Increased intracranial pressure

• Clinical constellation

• Ataxia, AMS, N/V, seizures

• PE

• Papilledema, retinal hemorrhage, CN palsies, AMS

High Altitude IllnessAMS/HACE treatment• Supplemental O2 and descent

• Descent of 500-1000m

• Simulated descent in HBO chamber (Gamow bag)

• Acetazolamide

• Dexamethasone

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High Altitude IllnessAcetazolamide • Bicarbonate diuresis-> metabolic acidosis w/ compensatory respiratory

alkalosis-> increase respiratory drive -> decreased hypoxia

• Effectively decreases periodic breathing associated with sleep

• Decreases CSF production

• Decreases cerebral vasodilatation

• Sulfa derivative

High Altitude IllnessHigh Altitude Pulmonary Edema (HAPE)• Most common cause of death

• ½ have AMS and 14% have HACE

• Tends to develop 2nd night after ascent

High Altitude IllnessHigh Altitude Pulmonary Edema (HAPE)• Symptoms

• cough, fever, tachycardia, tachypnea

• Hemoptysis is a late finding

• PE• rales

• CXR: patchy infiltrates RML and RLL

• ABG: hypoxia (PaO2 of 30-40 mmHg) and respiratory alkalosis

• TX• Descend

• O2, Positive pressure (CPAP or BiPAP)

• Inhaled beta-agonist

• Nifedipine

High Altitude IllnessPrevention• Acclimatize with gradual ascent

• Acetazolamide 125-250 mg bid the day before ascent

• Dexamethasone

Lightning

LightningStrike types• Direct (most serious)

• Ground current

Flashover – current passes over the skin rather than through the body, thus deep injury is rare

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Lightning• Asystole due to massive direct current injury

• Respiratory arrest due paralysis of medullary respiratory centers

• Heart restarts but respiratory arrest persists which leads to hypoxia induced ventricular fibrillation

• CPR/Ventillatory support

Lightning• Ruptured TM’s are fairly common

• Feathering (fern-like burns)

• Discrete entrance and exit wounds

• Flaccid motor paralysis

• Fetal demise is common (50%)

Lightning

Delayed complications• Cataracts

• Cognitive defects

• Motor defects

Seen months to years later

Toxic Plants

Allergic Contact Dermatitis• Poison Ivy, Oak and Sumac

• Type IV delayed hypersensitivity reaction• T lymphocytes become sensitized to the antigen

• Does not involve antibodies or the complement system

• Urushiol is the antigen

• Vesicle fluid does not contain any antigen

Allergic Contact DermatitisExposure types• Direct

• Indirect: pets, clothes and airborne

Lesions appear 6 hr - 3 days after exposure and last up to 3 weeks

Linear vesicles = contact dermatitis

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Allergic Contact DermatitisTreatment• Remove Urushiol

• Topical• Calamine

• Corticosteroids

• Systemic• Antihistamines

• Oral or IM steroids for severe cases

Poison Ivy

Poison OakPoison Sumac

MushroomsAmanita• 95% of fatalities

• Amatoxin binds to hepatocytes and inhibits the formation of messenger RNA

• Clinical progression• Phase I: N/V/D onset (6-10 hr)

• Phase II: Symptoms subside, LFTs continue rising

• Phase III: Toxic hepatitis, renal failure, seizure, death (1-6 days)

• Treatment• Activated charcoal

• Supportive

Mushrooms

Symptoms that develop within 2 hours of ingestion suggest a benign ingestion, while symptoms that are delayed for 6 - 24 hours are consistent with a toxic ingestion

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