Ohio ACEP Board Review: Environmental Emergencies II
-
Upload
nicholas-kman-md-facep -
Category
Health & Medicine
-
view
1.213 -
download
1
description
Transcript of 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
45
46
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?