Ohio ACEP Board Review: Environmental Emergencies II

Environmental Emergencies II

Nicholas E. Kman, MD FACEP

Associate Professor

The Ohio State University

Department of Emergency Medicine

Objectives

Learner will review the following topics: Snake Envenomations Spider Bites Marine Envenomations Drowning Dysbarism

Dive MedicineHigh Altitude Illness

Snake Envenomations

Snake Envenomations

Snake Bites

9,000 snakebites annually in U.S. with 2,000 treated as envenomations

Est. 2.5 million venomous snakebites occur internationally, with 125,000 deaths annually.

About 12 deaths/year in U.S. 60% rattlesnakes Important to know distribution of venomous snakes

in your area

Lavonas et al. BMC Emergency Medicine 2011, 11:2

Snake Bites

Statistics

Crotalinae – 99% of venomous snakebites in U.S.

65% - rattlesnakes

25% - copperheads

10% - cottonmouths

Snake Bites

 Species of Snakes Viperidae ‑ rattlesnakes, cottonmouth, copperhead

(pit‑vipers) Elapidae ‑ coral snake only member in U.S.; others

include cobra and sea snakes

Rattlesnakes CopperheadCottonmouth Pit Viper

Coral Snake (Elapidae)

Only 1/100 bites in U.S. annually

Distinct red band bordered by yellow stripes

Neurotoxic component to their potent venom

Short fixed fangs making it difficult to envenomate humans

Coral Snake (Elapidae)

Effects may be delayed up to 12 hrs Mild envenomation:

localized swelling only

Severe envenomation: Any systemic symptoms Nausea, vomiting, headache,

mental status, neurologic Respiratory distress

Coral Snake (Elapidae)

Initial appearance may be innocuous Early evacuation to prepare for antivenom

administration Evacuate ALL patients with elapidae bites,

regardless of symptoms

N Engl J Med, Vol. 347, No. 5·August 1, 2002

Signs and Symptoms

Check for signs of envenomation:

1 or more fang marks, pain, edema, erythema, or ecchymosis. Bullae may appear.

Systemic effects: AMS, tachycardia, tachypnea, resp distress, hypotension, coagulopathy, renal failure, hemolysis.

Snake Bites

Grades of Envenomation Grade 0

Fang marks No envenomation

Grade I "Mild" envenomation Fang marks Pain and edema at site Local ecchymosis Blistering Necrosis Minimal to no spread of edema proximal to site

Torpy, Janet M (04/18/2012). "Snakebite". JAMA : the journal of the American Medical Association (0098-7484), 307 (15), p. 1657.

Moderate

56% of bites Severe pain Spreading edema beyond

site of bite Systemic signs – nausea,

vomiting, paresthesias, muscle fasciculations, mild hypotension

Photo by N. Kman

Severe

• Marked swelling of extremity that occurs rapidly• Subcutaneous ecchymosis• Systemic symptoms – coagulopathy,

hypotension, altered mental status

Lavonas et al. BMC Emergency Medicine 2011, 11:2

SNAKE BITES

Management Maintain vital signs (ABC’s) Reduce venom effects Prevent complicated sequelae Minimize tissue damage

SNAKE BITES

Immediate First Aid Get away from the snake Stay calm Immobilize the bitten extremity at a

position of heart Apply a constricting band (Coral

Snake) TRANSPORT TO MEDICAL

FACILITY

http://www.howitworksdaily.com/environment/how-to-survive-a-snakebite/

SNAKE BITES

Treatments to Avoid in (Pit Viper) Snakebite Cutting and/or suctioning of wound Ice NSAIDs Prophylactic antibiotics or fasciotomy Routine use of blood products Shock therapy (electricity) Steroids (except for allergic phenomena) Tourniquets

Lavonas et al. BMC Emergency Medicine 2011, 11:2

SNAKE BITES

ED Management Notify Regional Poison Center ABC’s At least 1 IV line, draw labs while starting If no signs of envenomation, observe 8 hours for

further progression Measure circumference of limb, mark leading

edge every 15-30 minutes If signs of envenomation, antivenin admin.

Snake Bite Antivenin

Polyvalent Crotalinae antivenin

Available in U.S. since 1947

Mainstay of medical management

Horse serum derived

Dosing varies according to severity

Production discontinued in 2002

SNAKE BITES

Ovine (Sheep Derived) Fab Antivenin (CroFab) Mix 4-6 vials in 250ml of NS Additional 4-6 vials until control achieved Scheduled 2-vial doses at 6, 12, and 18 hr Initial dose given slowly for first 10 min Rest of dose over 1 hr

SNAKE BITES

Other Management Cleanse wound thoroughly Tetanus prophylaxis General supportive care Opioid Analgesics

SNAKE BITES

Complications Compartment syndrome – surgery is rarely indicated; if

worried, do pressure monitoring Serum sickness (type III hypersensitivity) – up to 3

weeks after antivenin; fever, chills, arthralgias, diffuse rash

Rx-steroids and antihistamines

Quiz

A 23 year old male was playing with a copperhead when he was surprisingly bit. He had premedicated with about “eleventeen” beers. He is complaining of severe pain, spreading edema, and has mild hypotension. What is the best treatment?

A. Lecture on the dangers of mixing snakes and alcohol

B. 4 Vials of CroFab Antivenin C. 2 Vials of Horse Serum Derived Antivenin D. Applying oral suction to the bite site

Quiz

A 23 year old male was playing with a copperhead when he was surprisingly bit. He had premedicated with about “eleventeen” beers. He is complaining of severe pain, spreading edema, and has mild hypotension. What is the best treatment?

A. Lecture on the dangers of mixing snakes and alcohol

B. 4 Vials of CroFab Antivenin C. 2 Vials of Horse Serum Derived Antivenin D. Applying oral suction to the bite site

Spider Envenomations

Ohio’s Biting Spiders

2 main groups of spiders; the recluse spiders and the widow spiders.

The black widow, Latrodectus mactans, and the northern widow, Latrodectus variolus.

Widow Spiders

• Black Widow – Latrodectus mactans• Widespread, esp. SE/SW• Garages, barns, outhouses, foliage• Alpha-latrotoxin: causes increased release of

multiple neurotransmitters

Black Widow

• Initial bite may be no more than a prick• Within 30 min – systemic symptoms• Muscle cramping – local to large groups such as

abdomen, back, chest, thighs• Nausea, vomiting

Black Widow

May mimic an acute abdomen Hypertension, tachycardia Latrodectus facies – spasm of

facial muscles, edematous eyelids

Priapism, weakness, diaphoresis, fasciculations may all occur in severe envenomation

Treatment

Ice to bite site Pain medication Benzodiazepines for muscle spasm Calcium gluconate no longer recommended Tetanus prophylaxis Antivenin – for severe symptoms not relieved by

above measures, esp. hypertension; pregnancy

Brown Recluse

• Loxosceles reclusa• Coast to coast• Attics, closets,

woodpiles, storage sheds• Violin-shaped marking• Cytotoxic• Necrotic arachnidism• Local and systemic

effects

Cutaneous Loxoscelism

Initially a sharp stinging sensation, some report no awareness of being bitten

Over 2-8 hrs aching and itching develop Bulls-eye lesion: erythema surrounds vesicle

circumscribed by a ring or halo of pallor Necrosis may develop within 3-4 days, becoming

ulcerated

Brown Recluse Venom

Cytotoxic enyzmes cause destruction of local cell membranes:

Alkaline phosphatase

5-ribonucleotide phosphohydrolase

Esterase

Hyaluronidase

SPHINGOMYELINASE D

Brown Recluse

Treatment

Immobilization, ice, elevation Tetanus prophylaxis Antihistamines Dapsone? Skin grafting once area has demarcated Antivenin - research

Systemic Loxoscelism

Rarely correlates with the severity of the skin lesion

Children most at risk Fever, chills, myalgias, arthralgias, morbilliform

rash DIC, seizures, renal failure, hemolysis Steroids may decrease amount of hemolysis Alkalinize urine

Quiz

A 19 year old male is reaching into a tackle box when he feels a prick. He thought he poked himself with a fishing lure, but becomes nauseated and presents complaining of severe abdominal pain. On exam, his abdomen is rigid and tender. What is the next best treatment?

A. Exploratory Laporatomy B. Calcium Gluconate C. Dapsone D. Analgesics and Benzos for muscle spasm and pain

Quiz

A 19 year old male is reaching into a tackle box when he feels a prick. He thought he poked himself with a fishing lure, but becomes nauseated and presents complaining of severe abdominal pain. On exam, his abdomen is rigid and tender. What is the next best treatment?

A. Exploratory Laporatomy

B. Calcium Gluconate

C. Dapsone

D. Analgesics and Benzos for muscle spasm and pain

Marine Envenomations

Jellyfish

Coelenterates (Portuguese man-of-war, true jellyfish, hydroid corals, sea anemones, corals)

Coastal areas of U.S. About 10,000 envenomations each summer off the

east coast of Australia Nematocysts are stinging cells on outer tentacle Box jellyfish causes most fatal envenomations

Jellyfish

Toxin contains complex mixture of proteins and polypeptides

Most common presentation is painful papular-urticarial eruption

Lesions can last for minutes to hours, and rash may progress to urticaria, hemorrhage, ulceration

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Jellyfish

Systemic reactions can develop – weakness, headache, vomiting, muscle spasm, fever, pallor, respiratory distress, paresthesias

Seabather’s eruption – intensely pruritic maculopapular eruption on skin that has been covered by swimwear – larvae of thimble jellyfish; develops within 24 hrs of exposure and lasts 3-5 days

http://www.sdtn.com/dive_resources/technical_articles/sea-bathers-eruption-and-seaweed-dermatitis-whats-difference#.U-5b8fldV8E

Treatment

ABCs

Inactivate nematocysts

Remove

Jellyfish Treatment

Rinse with saltwater Remove tentacles with protected hand Pour acetic acid (vinegar) on it to inactivate the

nematocysts Until pain ceases Use isopropyl alcohol if vinegar not available

Scrape off nematocysts May then use ice to decrease pain Evacuate patients with continued symptoms or

suspected box jellyfish envenomation

Removal

Wear gloves for protection Apply shaving cream, baking soda paste Shave with razor or other sharp edge Tetanus prophylaxis Antihistamines Watch for infection

http://www.prweb.com/releases/2011/10/prweb8913589.htm

Echinoderms

• Sea urchins, starfish, sea cucumbers• Venoms usually contained in spines• Local effects most common • Systemic effects do occur• Deaths are extremely rare

Echinoderms

Remove visible spines Immersion in hot water for 30-90 minutes Local or regional anesthesia if hot water alone is not

adequate X-ray or ultrasound to look for retained fragments –

surgery may be needed Tetanus prophylaxis Watch for infection

Quiz

A patient presents to your emergency department after being stung by a jellyfish. At the scene life guard treated with wound with urine, shaving cream, vinegar, sea water, and taco sauce. What is the next best treatment?

A. Local wound care and tetanus prophylaxis B. More urine C. Vinegar mixed with shaving cream D. Cold Tap Water

Quiz

A patient presents to your emergency department after being stung by a jellyfish. At the scene life guard treated with wound with urine, shaving cream, vinegar, sea water, and taco sauce. What is the next best treatment?

A. Local wound care and tetanus prophylaxis B. More urine C. Vinegar mixed with shaving cream D. Cold Tap Water

Drowning

The Eve Method

August 1946 copy of Popular Science

Szpilman D, Bierens J, Handley A, Orlowski J. Drowning. N Engl J Med. 2012;366(22):2102-10.

Terminology

Drowning: Process resulting in respiratory impairment from submersion / immersion in liquid medium. Victim may live or die during or after process. The outcomes are classified as death, morbidity, and no morbidity.

The Drowning Process: A continuum that begins when the victim’s airway lies below the surface of liquid, usually water, preventing the victim from breathing air.

Drowned: refers to a person who dies from drowning

Drowning

Second only to MVA as most common cause of accidental death in US

Risk factors: male sex age <14 years alcohol use/risky behavior Low income/Poor education rural residency aquatic exposure lack of supervision.

Drowning Pathophysiology

Most important abnormality of drowning is a profound HYPOXEMIA resulting from asphyxia.

Sequence of cardiac rhythm deterioration is usually tachycardia followed by bradycardia, pulseless electrical activity, then asystole.

Drowning Treatment

Immediate and adequate resuscitation is most important factor influencing survival.

For unconscious: in-water resuscitation may increase favorable outcome by 3 times.

Drowning persons with only respiratory arrest usually respond after rescue breaths. If no response, assume cardiac arrest & start CPR.

Full neurologic recovery is not predicted if victim has been submerged >60 min in icy water or >20 min in cool water.

Predictors of Outcome

Early BLS and ACLS improve outcomes (ABC’s) Duration of submersion and risk of death/severe

neurologic impairment after hospital discharge 0–5 min — 10% 6–10 min — 56% 11–25 min — 88% >25 min — nearly 100%

http://ondrowning.blogspot.com/2013/01/lifeguard-fatigue-and-cpr.html

Diving Medicine

Dysbarism

All the pathologic changes caused by altered environmental pressure

Altitude-related event Underwater diving accident Blast injury that produces an overpressure effect

Types

Barotrauma – dysbarism from trapped gases Decompression sickness – dysbarism from

evolved gases Nitrogen narcosis – dysbarism from abnormal

gas concentration (“Rapture of the Deep”)

Pressure is doubled, volume is halved.

PV = KEvery 33 ft of descent increases the pressure by 1 atm.

Boyle’s Bubbles

Boyle’s law states: pressure of gas is inversely related to its volume.

As pressure increases with descent, the volume of gas bubble decreases, as pressure decreases with ascent, the volume of gas bubble increases.

Air-containing spaces act according to Boyle’s law. Lungs, middle ear, sinuses and gastrointestinal tract.

Middle Ear Squeeze

Barotitis media-Most common diving-related barotrauma

Equalization of pressure via eustachian tube is unsuccessful

Too rapid descent or infection/inflammation

TM is pulled inward & can rupture Fullness in ears, severe pain,

tinnitus

Middle Ear Squeeze

PE – erythema or retraction of TM, blood behind TM or rupture, bloody nasal discharge

Reverse ear squeeze occurs on ascent Treatment – prevention: clear ears during dive If TM not ruptured – pseudoephedrine and

oxymetazoline nasal spray If TM ruptured – antibiotic for 7-10 days Suspend diving activities

Other Barotrauma

Barotitis externa Alternobaric vertigo Barosinusitis Barodontalgia Face mask squeeze

Pulmonary Over-Pressurization

A too-rapid ascent Lung emptying is incomplete Lung volume expands rapidly Pneumothorax, pneumomediastinum, SQ

emphysema, rupture into pulmonary vein causing air embolism

Simple pneumothorax may progress to tension on further ascent

Arterial Gas Embolism (AGE)

Results from air bubbles entering pulmonary venous circulation from ruptured alveoli

Usually develops right after diver surfaces Sudden LOC on surfacing should be considered

an air embolus until proven otherwise Cardiac – ischemia, dysrhythmias, cardiac arrest Neurologic – LOC, confusion, stroke-like sx

AGE

Vann, RD.; Butler, FK.; Mitchell, SJ.; Moon, RE. “Decompression illness.” The Lancet, v. 377 issue 9760, 2011, p. 153-64.

Arterial Gas Embolism (AGE)

Recompression in hyperbaric chamber Transport supine, not in Trendelenburg 100% oxygen, intubate if necessary IVF Aspirin for antiplatelet activity if not bleeding Transport in plane pressurized to sea level or

helicopter no higher than 1000 ft. above sea level

Decompression Sickness (DCS)

Henry’s Law – the amount of a gas that will dissolve in a liquid is proportional to partial pressure of gas over the liquid

Nitrogen equilibrates through the alveoli into the blood, but is 5 times more soluble in fat

The longer and deeper the dive, the more nitrogen gas will be accumulated in the body

Decompression Sickness

During a slow ascent, pressure decreases, nitrogen in the tissues is released into blood and alveoli

If ascent is too quick, gas comes out of solution and forms gas bubbles in the blood or tissue

Type I – extravascular gas bubbles Type II – intravascular nitrogen gas emboli

Type I DCS

“The Bends” – periarticular joint pain is most common symptom of DCS

Shoulders and elbows most often affected Dull, deep ache, mild at first and becomes more

intense Palpable tenderness Vague area of numbness around the affected joint

Type I DCS

Cutaneous – pruritus, cutis marmorata, hyperemia, orange peel

Lymphedema Fatigue, especially if severe

Vann, RD.; Butler, FK.; Mitchell, SJ.; Moon, RE. “Decompression illness.” The Lancet, v. 377 issue 9760, 2011, p. 153-64.

Type II DCS

Pulmonary system (The Chokes) Nervous system (The Staggers) Decompression shock

Cerebral AGE vs. DCS II

Cerebral AGE May occur after any type

of dive Onset is immediate (<10-

120 min) Only brain

DCS II Dive must be long

enough to saturate tissues

Onset is latent (often 2-6 hrs)

Spinal cord and brain

Pulmonary DCS

“The Chokes” May begin immediately after dive but often takes up

to 12 hours to develop Triad – shortness of breath, cough, and substernal

chest pain or chest tightness Cyanosis, tachypnea, and tachycardia

Neurologic DCS

Spinal cord is the most common site affected Lower thoracic and lumbar regions Low back pain, “heaviness” in legs, paresthesias,

possible bladder or anal sphincter dysfunction Brain – variety of symptoms and difficult to

distinguish from AGE Scotomata, headache, confusion, dysphasia

Decompression Shock

Vasomotor decompression sickness Rapid shift of fluid from intravascular to extravascular

spaces (unknown reason) Rare but often lethal Weakness, sweating, hypotension, tachycardia, pallor Despite fluids, hypotension may not respond until

recompression

DCS Diagnostics

History is most important Lab used to rule out other conditions and/or obtain

baseline measurements CXR ECG CT MRI Testing should not delay transfer to HBO

DCS Treatment

ABCs Transport supine, not Trendelenburg 100% oxygen IVF Recompression therapy Divers Alert Network (DAN): 919-684-8111 75-85% have good results when recognition and

treatment are prompt

Quiz

You are on a plane from Key West to Cleveland when the passenger next to you starts to arch his back and bend his knees. He then starts to rapidly breath and call for the flight attendant. She asks, “is there a doctor on the plane?” What do you do?

A. Lecture the passenger on diving too close to a flight B. Start high flow O2, keep the patient supine, and get

the patient to a hyperbaric chamber upon landing C. Intubate and hyperventilate

Quiz

You are on a plane from Key West to Cleveland when the passenger next to you starts to arch his back and bend his knees. He then starts to rapidly breath and call for the flight attendant. She asks, “is there a doctor on the plane?” What do you do?

A. Lecture the passenger on diving too close to a flight B. Start high flow O2, keep the patient supine, and

get the patient to a hyperbaric chamber upon landing C. Intubate and hyperventilate

High Altitude Medicine

High Altitude Illness

Rate of ascent

Altitude reached

Sleeping altitude

Individual physiology

High Altitude Illness

Rate of ascent: Graded ascent is safest method to facilitate acclimatization and prevent sickness.

Altitude reached: AMS usually seen at altitudes in > 2000 meters (6560 ft) and caused by hypobaric hypoxia.

Sleeping altitude: Increases >600 meters in sleeping altitude should be avoided.

Individual physiology: Age, gender, and fitness level do NOT play a role in susceptibility to altitude illness.

Risk Factors

History of high altitude illness Residence at altitude below 900 m Exertion Preexisting cardiopulmonary conditions Age < 50 years Physical fitness is not protective

High Altitude Medicine

Acute Mountain Sickness (AMS)

High Altitude Cerebral Edema (HACE)

High Altitude Pulmonary Edema (HAPE)

Acute Mountain Sickness

History is key (total elevation gain and rate of gain) AMS is present if one is at altitude and, if in addition

to headache, at least one of the following symptoms is present: Dizziness or lightheadedness Fatigue or weakness Nausea/vomiting/anorexia Insomnia

AMS

Hypoxia Neurohumeral and hemodynamic responses Overperfusion of microvascular beds Elevated hydrostatic capillary pressure Capillary leakage Consequent edema

AMS

Avoid further ascent until symptoms have resolved Descend if no improvement in 24 hours or worsening

symptoms Non-narcotic pain relievers for headache Supplementary oxygen Acetazolamide, dexamethasone Gamow bag

Acetazolamide

For both treatment and prevention of AMS Mechanism of action: increase urinary excretion of

sodium, potassium and bicarbonate resulting in a hyperchloremic metabolic acidosis, which stimulates ventilation, improving arterial oxygen saturation

Decreases periodic breathing and improves sleeping

Acetazolamide

Speeds up acclimatization 250 mg po bid for treatment 125-250 mg po bid starting 24 hr before ascent and

the first 2 days at high altitude

Dexamethasone

For treatment or prevention of AMS Does NOT speed up acclimatization May improve integrity of blood-brain barrier, thereby

reducing edema 4 mg po every 6 hrs for treatment 4 mg po every 12 hrs for prevention

http://www.jyi.org/issue/on-the-mountains-high-altitude-sickness-in-nepal/

High Altitude Cerebral Edema (HACE)

HACE: progression of AMS to life-threatening end-organ damage.

Defined as severe AMS symptoms with additional obvious neurologic dysfunction: Ataxia Altered level of consciousness Severe lassitude

HACE almost never occurs without antecedent AMS symptoms as a harbinger.

The progression of AMS to coma typically occurs over 1 – 3 days.

HACE

Progression of AMS Ataxia is the single most useful sign Diffuse neurologic dysfunction Altered mental status, nausea, vomiting, seizures,

decreased LOC, coma and finally death Once coma present – 60% mortality rate Cause of death – brain herniation

http://www.altitudemedicine.org/index.php/altitude-medicine/learn-about-altitude-sickness/what-is-hace

HACE Treatment

Descend Descend ! Descend !! Oxygen Dexamethasone 8 mg load followed by 4 mg every 6

hrs Gamow bag if descent not possible

HAPE

Accounts for most deaths from high altitude illness Non-cardiogenic pulmonary edema Commonly strikes the second night at a new altitude Rarely occurs after more than four days

HAPE

Early diagnosis is crucial to recovery Decreased exercise performance Dry cough initially Tachycardia and tachypnea at rest Dyspnea at rest Rales typically originate in right axilla and become

bilateral as illness progresses Cerebral signs and symptoms are common

HAPE

Patient admitted with progressive respiratory distress 24 hours after arriving at town at 2700 meters above sea level.

http://radiopaedia.org/images/1564322

HAPE

Pulmonary hypertension due to hypoxic pulmonary vasoconstriction

Elevated capillary pressure Stress failure of pulmonary capillaries as a result of

high microvascular pressure is the presumed final process leading to extravasation of plasma and cells

Impaired clearance of fluid from alveolar space probably has a role

HAPE Treatment

Descent is treatment of choice Exertion may worsen the illness Oxygen Gamow bag if unable to descend Nifedipine 10 mg po initially, then 20-30 mg extended

release every 12 hrs – decreases pulmonary artery pressure

Inhaled beta-agonists

http://www.jyi.org/issue/on-the-mountains-high-altitude-sickness-in-nepal/

Quiz

You decide to climb to the top of Mt. Everest. While nearing the top, your partner begins to have a seizure and becomes unresponsive. What is the best treatment for him?

A. Prednisone taper B. Acetazolamide IV C. High Flow Oxygen D. Descent

Quiz

You decide to climb to the top of Mt. Everest. While nearing the top, your partner begins to have a seizure and becomes unresponsive. What is the best treatment for him?

A. Prednisone taper B. Acetazolamide IV C. High Flow Oxygen D. Descent

Questions?