Environmental emergencies ii kman 8 15 final

Environmental Emergencies II
Nicholas E. Kman, MD FACEP
Associate Professor
The Ohio State University
Department of Emergency Medicine

Objectives
Learner will review the following
Emergencies:
Snake Envenomations
Spider Bites
Marine Envenomations
Drowning
Dysbarism
Dive Medicine
High Altitude Illness

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 Bite 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

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
File:Coral snake close-up.jpg - Wikimedia Commons

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

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

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

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 or wrap (Coral
Snake)
TRANSPORT TO MEDICAL FACILITY
http://www.howitworksdaily.com/environment/how-to-survive-a-snakebite/

Snake Bites: Treatments to Avoid
Tx 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

Snake Bite 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 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 Bite General Wound Care
Cleanse wound thoroughly
Tetanus prophylaxis
General supportive care
Opioid Analgesics

Snake Bite 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

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
File:Black widow spider 9854 lores.jpg -
Wikimedia Commons

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
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
https://en.wikipedia.org/wiki/Sicariidae#/medi
a/File:Brown_recluse_spider,_Loxosceles_reclus
a.jpg

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

Treatment
Immobilization, ice, elevation
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

The Deep Blue Sea
https://www.flickr.com/photos/7thstreettheatre/15250533391

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

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

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
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
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

LLSA: 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%
Wikipedia

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 = K Every 33 ft of descent increases the pressure by 1 atm.

Boyle’s Bubbles
Boyle’s law states: pressure of gas
is inversely related to volume.
As pressure increases with descent,
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 – amount of 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
DCS II
Dive must be long
enough to saturate
tissues
Onset is latent (often
2-6 hrs)
Spinal cord and brain
Cerebral AGE
May occur after any
type of dive
Onset is immediate
(<10-120 min)
Only 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
http://phil.cdc.gov/phil/details.asp

High Altitude Illness
Rate of ascent:
Altitude reached:
Sleeping altitude:
Individual physiology:

High Altitude Illness
Rate of ascent: Graded ascent is safest 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
Medications

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)
Starts within hours and can last for days
AMS is present if at altitude and, in addition to
headache, at least one of following is present:
Dizziness or lightheadedness
Fatigue or weakness
Nausea/vomiting/anorexia
Insomnia

AMS
Hypoxia=The hypoxic-ventilatory response
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

Other Treatments
Ginko Biloba (120mg PO BID starting 5 days prior
to ascent)-modest evidence
Prophylaxis against HAPE
Nifedipine 20mg PO q8 for patients with
recurrent HAPE
Salmeterol-effective in reducing risk of HAPE in
those with recurrent episodes

Golden Rules of AMS
#0: It’s ok to get AMS. It’s not ok to die of it.
#1: Any illness is AMS, until proven otherwise
#2: Never ascend with AMS symptoms.
#3: If you are getting worse, go down at once.
#4. Never leave someone with AMS alone.

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

High altitude retinal hemorrhage: generally
occurs at > 17,000 ft.
UV Keratitis: delayed onset of symptoms
(hours).

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.

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

Acute Mountain
Sickness (AMS)
Anorexia
Nausea
Vomiting
Insomnia
Dizziness
Lassitude
Fatigue
Lightheaded
High Altitude
Cerebral Edema (HACE)
Headache
Disorientation
Loss of coordination
Memory loss
Psychotic behavior
Coma
High Altitude
Pulmonary Edema (HAPE
Chest tightness
Persistent cough
Frothy sputum
Feeling of impending suffocation
During sleep

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

Environmental emergencies ii kman 8 15 final

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