Toxicology 2: Environmental
CCRMC Emergency Medicine
General Coverage
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1. Envenomation: Snakes/Spiders/Aquatic
2. Plants n’ ‘Shrooms
3. Exposure: Hot & Cold
4. Diving, Altitude and Near Drowning
5. Burns: Thermal and Electrical
Two things are infinite,
the universe and human stupidity.
I’m not so sure about the universe.
Einstein
PLAYING WITH NATURE
(most of which have warning signs not to)
• Hymenoptera/BEES-WASPS
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Most Common Allergic rxn:Vespidae(hornet/yellow-jacket)
LOCAL=local pain+erythema+edema+pruritus
TOXIC= LOCAL+N/V/D BUT no urticaria/bronchospasm
ANAPHYLACTIC= pruritis/urticaria+
airway edema/bronchospasm
Short interval between sting and onset
Be ready for a rough/rapid fight
– No correlation of reaction and number of stings
– DELAYED RXNS: 10-14 d after, serum-sickness-like signs: fever,
malaise, HA, urticaria, polyarthritis
PLAYING WITH NATURE
Treatment of Hymenoptera
• Remove stinger and cleanse wound
• Minor local: Oral anithistamines, analgesics, DC.
• More severe: 1:1000 Epi IM 0.3-0.5mL adult
0.01mL/kg(max 0.3mL) in a child
• May require second injection in 10-15 minutes
• IV H1/H2 blockers, and IV steroids
• Hypotension: aggressive IVF, Dopamine +/- Epi gtt
• Bronchospasm: Albuterol
• Moderate sx = monitor 6+ hours, D/C w/steroids+Epipen
• Severe rxns=Admit
• All get referred to allergist
PLAYING WITH NATURE
Arachnida: SPIDERS/SCABIES/MITES/CHIGGERS/SCORPIONS
Brown Recluse
Black Widow
Scorpion
Loxosceles bites are
NOT seen in California
PLAYING WITH NATURE
Arachnida: SPIDERS/SCABIES/MITES/CHIGGERS/SCORPIONS
• BLACK WIDOW SPIDER
– Bite initially painful, within 1 hr, may experience erythema
(often target shaped), swelling, diffuse mm cramps- esp of
lg. mm groups (the abd. pain here can mimic peritonitis).
– Severe pain wax/wane for 3 d, but mm weakness/pain can
last for wks to months
– Serious complications: HTN, Resp. failure, shock, coma
– TREATMENT: Local wound care and supportive care.
Analgesics and benzos for pain and cramping (? Benefit of
IV calcium gluconate)
• IF SEVERE!!!, antivenin available from horse serum, (so serum
sickness is serious side effect…) if pt tolerates standard cutaneous
test dose, usual IV dose is 1-2 vials over 30 minutes
PLAYING WITH NATURE
Arachnida: SPIDERS/SCABIES/MITES/CHIGGERS/SCORPIONS
• SCABIES
– Burrows, web spaces. Direct contact. Permethrin.
• CHIGGERS
– Itching Papule Nodule. Outdoor exposure. Antithistamines
PO. Severe: topical or oral steroids. Permethrin. (Has been
assoc. fever, erythema multiforme)
• FLEAS
– Zig zag lines esp on legs/waist. Hemorrhagic puncta surrounded
by red/itchy patches. Main concern=2o infxn. Antihistamines PO,
starch baths at bedtime. Severe: topical steroids.
• LICE
– Mites and eggs. Red spots papules/wheals. Permethrin (body
lice). Personal articles sterilized in hot water. Hair infestation
requires Rid/Lice-X applied and reapplication in 10 days.
PLAYING WITH NATURE
Arachnida: SPIDERS/SCABIES/MITES/CHIGGERS/SCORPIONS
• SCORPIONS
– Of all in North America, only bark scorpion (C.
exilicauda) capable of producing systemic toxicity
– Immed. burning/stinging, no local injury visible.
– Systemic effects infreq. and seen at extremes of age.
Tachycardia, XS secretions, roving eye mvmts,
opisthotonos, & fasiculations.
• TREATMENT
– Local wound care. Supportive. Reassurance. Local ice.
Pain with absence of toxic sx: briefly observe before
DC with analgesics… Mm spasm and fasiculations
respond promptly to Benzos.
PLAYING WITH NATURE
Snakes: Crotalidae (Pit Vipers) & Elapidae
Pygmy Rattlesnake
Water Moccasin
Copper Head
Coral Snake
PLAYING WITH NATURE
RattleSNAKES
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Only venomous North American= Pit viper (Crotalidae =eg., rattlesnake, copperhead, water
moccasin,& massasauga) and Coral (Elapidae)
• Crotalid venom= local tissue injury, systemic vascular
damage, hemolysis, fibrinolysis, neuromuscular dysfxn.
• Cardinal manifestations: 1+ fang marks, localized pain, and
progressive edema extending from bite.
• 3 criteria of severity:
– 1. Degree of local injury (swelling/pain/bruising)
– 2. Degree of systemic involvement (HoTN, tachycardia, nausea
paresthesia)
– 3. Evolving coagulopathy (thrombocytopenia, INR,
hypofibrinogenemia, AMS, HoTN, Resp. distress)
– *ANY +, confirms envenomation. ABSENCE of all after 8-12
hours RULES OUT venom injection
PLAYING WITH NATURE
RattleSNAKES
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Keep pt. calm, limit movement, extremity below level of heart
Cleanse wound & provide dT.
IV, Monitor, BLOODWORK: CBC, Coags, UA, Type & Screen
NO ice packs, tourniquets, incision, electric shocks, steroids, abx
Q 30”, mark advancing edema, and measure limb circumference at several
sites above wound
ANY PT with progressive swelling, systemic effects or coagulopathy
SHOULD IMMEDIATELY RECEIVE CROFAB ANTIVENIN
Be prepared to treat severe allergic reactions
Warn patients about delayed serum sickness & recurrent coagulopathy
ADMIT ALL patients treated with antivenin
Watch for compartment syndrome - virtually always resolves with Crofab
alone - have Ortho see the patient
ALL pts must be observed for at least 8 hours
Pts with NO evidence of envenomation may be discharged
PLAYING WITH NATURE
Coral SNAKES
• Red on yellow, kill a fellow. Red on black, venom lack.
• Neurotoxic. No real local injury.
– Tremors, salivation, dysarthria, diplopia, bulbar paralysis
with ptosis, fixed and contracted pupils, dysphagia,
dyspnea, and seizures. (immed. Cause of death=resp.
paralysis)
• Signs and sx may be delayed up to 12 hrs. Admit and
observe for 24-48 hrs. Not easily reversed.
• Definitely bitten: 3 vials of anitvenin, b/c may not be
possible to reverse effects that have already developed
PLAYING WITH NATURE
RABIES
• Beware of bats:
• Usually no history of bite
• bat in room with child/sleeping/mentally
disabled/intoxicated person is indication for post
exposure prophylaxis
• otherwise seeing a bat is NOT an indication
• Raccoons, skunks, and foxes are all potential carriers
• Dogs and cats:
• Check owners vaccinations
• Was attack provoked?
PLAYING WITH NATURE
RABIES PROPHYLAXIS
• wash wound with copious amount of soap and water
and 70% ethanol or Betadine if available
– avoid closure
• contact County Rep. if bat, skunk, raccoon, stray
animal or rodent acting highly unusual
• standard prophylaxis consists of:
– IM rabies vaccine on days 0, 3, 7, 14 and 28
– one dose of 20 IU/kg of rabies immunoglobulin IM,
infiltrating as much into the wound as possible
• within 7 days of first dose of rabies vaccine
PLAYING WITH NATURE
MARINE FAUNA
• Coral cuts=MC underwater injury. Local stinging, redness, itchy may
progress to cellulitis with ulceration, tissue sloughing, lymphangitis and
reactive bursitis.
• Vibrio may cause cellulitis, myositis, and necrotizing fasciitis (V.
vulnificus=assoc w/sepsis in chronically ill esp. with liver failure and has
60% mortality)
• Aeromonas hydrophila can cause rapidly developing cellulitits or
necrotizing myositis
• Stingray envenomation=MC among vertebrates. Spine produces
puncture/laceration and may be retained in wound. Systemic effects:
weakness, N/V/D, syncope, sz, paralysis, HoTN, and dysrrythmias.
• Sea snakes=most abundant venomous reptiles. Contain neurotoxin and a
myotoxin (Myalgia, ophthalmoplegia, asc. Paralysis, resp. failure)
• Octopus bites, scorpionfish, & starfish spines can cause paresthesia,
paralysis, resp. failure. Most others are cutaneous manifestations or
lacs/crush/puncture wounds.
PLAYING WITH NATURE
MARINE FAUNA
• TREATMENT:
– ABCDE’s, correct hypothermia, irrigate wounds, debride if needed.
May get XR to R/O FB. Most should undergo delayed primary closure.
– Minor wounds/Healthy pts=NO PROPHYLACTIC ABX
– Extensive lacs/gross contamin/immunocomp= ABX. High risk pts get 1st
dose IV. Cover staph and strep. In ocean wounds cover vibrio (3rd gen
ceph, bactrim, doxy, quinilone, aminoglycoside)
– Cnidaria (jellyfish,etc): Rinse with saline, vinegar or isopropyl alcohol
inactivates the venom. Deactivated nematocyst removed with shaving
cream and razor.(corneal envenomation requires topical steroids)
– Generally anything with spicules/bristles get removed with tape.
– Spined vertebrates and Echinedermata (starfish/sea urchins, sea
cucumbers) should be immersed in hot water for 30-90 minutes,
remove spines… explore and debride if needed. Sea cucumbers may
get some relief with vinegar/rubbing alcohol.
– Sea snakes recommendations are similar to rattlesnakes.
HYPOTHERMIA:
CLINICAL PRESENTATION IS VARIABLE
• mild cases can mimic intoxication
– is there a To on the chart (rectal/esophageal if <36o)?
– NOTE: some standard thermometers don’t go below 94o
• weak correlation between symptoms and To
– pts with To of 25o still talking
• shivering usually stops at 32oC
• “paradoxical undressing” (don’t assume sexual assault)
• abdominal rigidity common (muscle spasm)
Rule out concomitant injuries/disease processes
HYPOTHERMIA
THE PARADOX
Iatrogenic hypothermia can be protective
(33-35o C for post cardiac arrest)
HOWEVER
Accidental hypothermia is not good, especially
for trauma pts => coagulopathy
OSBORNE J WAVES
OSBORNE WAVES
• Osborne wave (J wave) found <32o
– notching in downward deflection of QRS wave
– becomes more prominent as To deceases
– also found in myocardial ischemia, sepsis, SAH,
hypercalcemia, post VF
– does not predict prognosis
HYPOTHERMIA
OTHER ECG FINDINGS
• Progressively slowing bradycardia
• Prolonged PR interval, then widening of QRS
followed by prolongation of QT interval (can last for
days)
• Atrial fibrillation most common arrhythmia
– usually reverts to sinus with rewarming
• Any arrhythmia is possible
HYPOTHERMIA
COMMON LAB FINDINGS
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Electrolytes variable
– K >10.0 considered incompatible with survival;
however, exceptions have occurred
• Hyperglycemia
• no insulin until To normal
• Increased amylase, BUN, creatinine, LFS
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Prolonged INR and PTT: IGNORE
HYPOTHERMIA
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Hct. increases by 2% for every 1o C drop in temp.
Thrombocytopenia
Lactic acidosis
DO NOT CORRECT ABG FOR TEMP.
Also order Ca, Mg, ETOH, toxicology screen
TSH, cardiac markers and serum cortisol as indicated
HYPOTHERMIA
#1: SHOULD RESUSCITATION BE INITIATED?
• Mortality rate of ~50% if <32o in non-arrest patients
• BUT,
• Trauma patient => mortality approaches 100% if <32o C
probably 2o to thrombocytopenia and prolonged INR and PTT
• Miraculous “saves” have occurred
HYPOTHERMIA
• Although we are taught that a patient is “not dead
until they are warm and dead”
ACLS (2005) states:
“In the field resuscitation may be withheld if the
victim has obvious lethal injuries or if the body is
frozen so that nose and mouth are blocked by ice
and chest compression is impossible”.
HYPOTHERMIA
ACLS (2005) also states:
“Once the patient is in the hospital, physicians should
use their clinical judgment to decide when
resuscitative efforts should cease in a victim of
hypothermic arrest”
One hypothermic person did survive neurologically intact
after 4 hrs and 10 minutes of CPR;
however, how many other patients suffered because
resources were tied up in a 4 hour resuscitation?
HYPOTHERMIA
Translation:
• you will be criticized for stopping CPR prematurely in
a hypothermic patient
• you will be criticized for prolonging a futile
resuscitation in a hypothermic patient
Some days you can’t win!
HYPOTHERMIA
KARLEE KOSLOFSKI Feb. 23, 1994
Lowest core To ever recorded for accidental hypothermia survivor
• 2 yr old locked outside at 2 AM in 22o weather in Rouleau, SK.
• found ~8AM
“Frozen like a block of ice”
• In PEA with core To = 14.16
• survived with left leg amputation
• lowest core To ever recorded for
accidental hypothermia survivor
HYPOTHERMIA
#2: HOW SHOULD CPR BE DONE?
• frequency of compressions/ventilations?
• should they be done at all?
• drugs ineffective <30o
– drugs should be administered at “less frequent”
intervals
• 1 shock <30o
– no further shocks until To>30o
HYPOTHERMIA
#3: HOW SHOULD PATIENT BE REWARMED?
Stop cooling (remove wet clothing, blankets etc)!
– passive external (warm blankets, esp. on head
and neck, etc)
• prevents further heat loss
– active external rewarming
– active core rewarming
Little evidence comparing one method with
another (slow better than fast unless unstable)
HYPOTHERMIA
ACTIVE EXTERNAL REWARMING
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Methods:
– Warm bath (40-44o C) ONLY if NO alternative
(interferes with monitor, CPR etc.)
– Hot water bottles to neck, axillae, thorax and
groin (avoid extremities)
– Bair Hugger
• Handle “gently” but do not delay indicated
procedures (e.g. IV, intubation)
• Rewarm at <1o C/hour
HYPOTHERMIA
ACTIVE INTERNAL REWARMING
• should be standard:
– heated O2 to 40-44o C
– heated IV solution to 40-44o C
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how much (cold diuresis)?
don’t microwave IV bags
use rewarming oven with overwrap on
can immerse in warm bath as long as overwrap on
– increases body To by <1o C/hour
HYPOTHERMIA
BECOME MORE AGGRESSIVE IF . . .
• hemodynamically unstable
• cardiac arrest
• DKA or other endocrine emergencies?
HYPOTHERMIA
HOW? – ACTIVE CORE REWARMING
• peritoneal dialysis
• extracorporeal warming
– hemodialysis, venovenous, AV rewarming
– CP bypass is the method of choice with warming
of 1-2o C every 3 – 5 min
• following are of questionable benefit (but easy):
– bladder irrigation
– stomach irrigation
– colonic irrigation
HYPOTHERMIA
REWARMING BY TUBE THORACOSTOMY IN HYPOTHERMIC
CARDIAC ARREST PATIENTS
• insert large bore tube (~36F) in 2-4 ICS MCL and 2nd
tube in 5-6 ICS mid-axillary line
– unilateral or bilateral
– has also been done through single chest tube
• 40-42o saline or tap water instilled passively into ant.
tube and allowed to drain passively from lateral tube
into container
– takes 30 to >100 L of fluid
• rewarming occurs at 3-5o C/hr
HYPOTHERMIA
MONITOR DURING REWARMING
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core temperature “after drop” (keep rewarming)
hypotension (IV fluids)
paralytic ileus (NG tube)
bladder atony (Foley catheter)
hypo/hyperglycemia (monitor glucose)
HYPOTHERMIA
OTHER ASSOCIATIONS
• rhabdomyolysis
• persistent hyperglycemia suggests DKA/hemorrhagic
pancreatitis
• bleeding diathesis
• cutaneous burns
AVOID
• CVP lines (theoretical?)
• TCP/transvenous pacing (theoretical?)
• vasopressors
“INDOOR” HYPOTHERMIA
• 2o to impaired thermoregulation
– often not related to ambient To
• usually elderly with co-morbidities
– stroke, CHF, sepsis, hypothyroid, medication
• mortality rate often >50%
Is there a temperature on the chart?
HEAT EMERGENCIES
“IT’S TOO DARN HOT…”
• From imbalance of heat production and loss,
through: radiation, convection, conduction,
evaporation.
• Of note, with conduction there is a 25-FOLD
INCREASE in heat exchange in water
submersion
Minor illness
PT’S MENTAL STATUS & NEURO EXAM INTACT
All get DC’d home with outpatient follow up
• Heat edema
– Self limited, days to weeks
– Mild swelling hands/feet
• Prickly heat/Heat rash
– Pruritic, maculopapular, red rash over clothed areas
– Inflammation of sweat ducts, 2o to blocked ducts
• Heat syncope
– Cumulative: Periph. Dilitation, vasomotor tone, relative volume depletion
• Heat cramps
– Painful, involuntary, spasmodic contractions skeletal mm.( usu. LE)
– 2o deficiency Na, K, fluid at cellular level
• Heat tetany
– Hyperventilation
resp. alkalosis, paresthesias, carpopedal spasm
• Heat exhaustion
– Hyperthermia up to 40C/104F
– Nonspecific si/sx: Dizzy, weak, N/V, fatigue, HA, myalgia. Syncope, diaphoresis,
orthostasis, sinus tach, tachypnea.
HEAT STROKE
It doesn’t take long to fry an egg
or cook a neuron.
HEAT STROKE
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Heat exhaustion PLUS CNS dysfunction
Temp >40C/104F
Anhidrosis is classic, but not always present
Think this with any elevated body temp &
AMS (heat exhaustion is dx of exclusion)
• Order: CBC, CMP, Coags, UA, bld cxs, ABG,
CXR, EKG, pregnancy test ± CT/LP
TX of Heat Emergencies
• Initial stabilization, rapid cooling, evaluate underlying
injuries/illnesses
• ABCDE’s, high flow O2, monitor, continuous rectal temp
monitor, IVF, monitor CVP/UOP
• Evaporation cooling: Disrobe, spray with water, blast the
cooling fans. Ice packs to axillae/groin - treat shivering with
benzos or chlorpromazine 25 mg IM
• Active core cooling (gastric/peritoneal/cardiopulmonary
bypass only if recalcitrant to all others)
• **STOP** COOLING AT 40oC (avoid overshoot hypothermia)
• Admit all to ICU to observe for further end organ damage
– Admit pts at extremes of age or with comorbid dz who suffer
from heat exhaustion
Carbon Monoxide: CO
Fire, Fire…or sucking on the exhaust pipe…
• MYTH: SpO2 WILL BE DECREASED IN CO POISONING
• Pulse oximetry cannot differentiate between
hemoglobin bound O2 vs. CO
• Cherry red mucosa is a post mortem finding
• ORDER A CARBOXYHEMOGLOBIN LEVEL
– does not always correlate with severity
– if not available, call energy company for a gas test
CARBON MONOXIDE POISONING
THE GREAT PRETENDER
• “Flu”
– Consider CO poisoning when multiple family
members presents with afebrile “flu”
• headaches
• decreased LOC
• stroke like findings (surprisingly, CO can result in
lateralizing signs)
TREATMENT OF CO POISONING
• 100% O2 reduces ½ life from 4-5 hrs. to ~90 min
• hyperbaric O2 (HBO) reduces ½ life to 20 min
– controversial
– ACEP 2007:
• “optional – not mandatory” (C recommendation)
• neither clinical nor lab variables predict pts likely
to benefit from HBO
“POSSIBLE” INDICATIONS FOR HBO
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transient LOC or ongoing altered mental status
metabolic acidosis
hypotension
ataxia
evidence of cardiac damage
pregnant pts with any symptoms
carboxyhemoglobin levels >15%? >20%? >40%?
Phone Poison Control Center for advice
DELAYED NEUROPSYCHIATRIC SEQUELAE IN CO
POISONING
• widely reported incidence (12 – 68%)
• occurs 2- 21 days after recovery
• varies from mild cognitive changes on
neuropsych testing to dementia and psychosis
– also memory loss, difficulty concentrating, focal
neurological abnormalities, cortical blindness,
motor abnormalities (ataxia, Parkinson’s) etc.
• spontaneous recovery in up to ¾ over 2 years
• reduced by HBO
DYSBARISM
Exploring the Depths
• Refers to changes in environmental ambient pressure and breathing
compressed gases; commonly encountered in SCUBA diving.
• Pathophysiology… fire up those neurons to think of the gas laws…
– Boyle’s law: The volume of gas is inversely proportional to it’s pressure
at a constant temperature. THIS IS THE BASIC MECHANISM OF
BAROTRAUMA (WHEN THE DIVER IS UNABLE TO EQUALIZE THE PRESSURES IN AIR FILLED
CAVITIES WITH AMBIENT ENVIRON. PRESSURE)
– Dalton’s law: The total pressure exerted by a mixture of gases is equal
to the sum of the partial pressures of the component gases.
– Henry’s law: The amount of gas dissolved in a fluid is proportional to
the pressure of the gas with which it is in equilibrium.
– SO… Decompression sickness occurs because  ambient pressure as a
diver descends causes an in the partial pressure of the inspired
nitrogen in the breathing air. Due to Henry’s law, nitrogen dissolves
and accumulates in tissues. If the ascent is too rapid, nitrogen comes
out of solution abruptly, leading to bubble formation.
DYSBARISM
Exploring the Depths
• Barotrauma is the MC diving related affliction
– MC form= Barotitis media (“middle ear squeeze”),
if pressure not equalized or dive aborted ,
eardrum can rupture and cause nausea and
vertigo. May see hemorrhage at ear or mouth.
– Sinus squeeze, MC in frontal and maxillary
– Inner ear trauma, rare; Usu after forceful valsalva
or very rapid descent.
Clinically= tinnitus, vertigo, sensorineural hearing
loss, feeling of ear fullness, N&V.
DYSBARISM
Exploring the Depths
• Pulmonary overpressurization syndrome (POPS)
during ascent may result in mediastinal and SQ
emphysema. After the dive there may be gradual
onset of hoarseness, neck fullness, substernal
chest pain, dyspnea and dysphagia. Severe cases
may present with syncope/PTX.
• Air embolism with rapid ascent, gas bubbles
enter systemic circulation from ruptured pulm.
vv. and occlude distal circulation. Thus can cause
cardiac arrest and dysarrythmias, signs of stroke,
seizures.
DYSBARISM
Exploring the Depths
• Decompression sickness (DCS) is not a form of barotrauma,
It is due to gas bubble formation as nitrogen comes out of
blood and tissues if ascent too rapid.
– SX: Aching joint pain, neurologic abnormalities (bladder dysfxn,
LE paraplegia, parasthesias, paraparesis), chest pain, cough,
dyspnea, pulmonary edema and shock can be seen.
– RF: Advanced age, obesity, dehydration, recent etoh use, cold
water diving, underwater exercise, multiple repetitive dives
• Nitrogen narcosis: due to anesthetic effect of nitrogen,
similar to alcohol, at elevated pressures.
RESOLVES WITH ASCENT. But common cause of accidents
underwater and may cause amnesia of the circumstances.
DYSBARISM
Exploring the Depths
DIFFERENTIAL…After surfacing,
– Severe sx onset within 10 min is an air embolism until proven otherwise
– Onset of sx after 10 min is DCS until proven otherwise. Most cases present 1-6
hrs after, but can be delayed up to 48 hrs.
Mild POPS and other forms of barotrauma may also present hours after the
dive, but usually at descent and ascent.
TREATMENT:
ABCDE’s, high-flow O2, treat hypothermia and life-threatening injuries.
Air embolism: place supine.
DCS/Air embolism: Recompression-chamber therapy initiated ASAP.
(aeromed. transport at altitude of less than 1000 ft, or on craft that can be
pressurized to 1 atm.)
DCS: IVF, if not contraindicated for other reasons, b/c usu. volume
depleted
POPS: Tx PTX if present. Otherwise resolves with rest and supplemental
O2, rarely requires recompression therapy
DYSBARISM
Exploring the Depths
Treatments continued…
• Squeeze syndromes: Stop diving until resolve.
Decongestants/Antihistamines may help.
• If TM ruptured, Amoxicillin. Obviously no diving
until healed.
• Antibiotics are usually indicated for frontal sinus
squeeze.
• Inner ear barotrauma mandates otolaryngology
consult (may require surgery), avoid straining,
recommend bed rest with head elevated.
ALTITUDE
“Climb every Mountain…”
• AMS (Acute Mountain Sickness) is much more common than HAPE
(High Altitude Pulmonary Edema) which is more common than
HACE (High Altitude Cerebral Edema). All are caused by hypobaric
hypoxia on different scales.
• Hypoxemia  CBF & cerebral capillary hydrostatic pressure,
resulting in fluid shifts and either mild cerebral edema in AMS or
severe in HACE. Hypoxemia also raises pulmonary artery pressure.
•  ICP s sympathetic nervous system activity, which in turn
compliance of pulmonary aa., promotes venous constriction, & 
pulm. capillary permeability
• PLUS  Sympathetic activity is associated with decreased urine
output (mediated by renin, angiotensin II, aldosterone, vasopressin)
which leads to fluid retention and elevated capillary pressure in
lung, brain and peripheral tissues.
ALTITUDE
“Climb every Mountain…”
• Risk factors include: heavy exertion, rapid ascent, cold,
excessive salt intake, use of sleeping medication, low vital
capacity & low hypoxic ventilatory response, prior history
of HAPE/HACE. (Usually seen at elevations >2000m)
• Earliest sx AMS: light headedness & mild breathlessness.
– Other sx are similar to a hangover: bifrontal HA, anorexia,
nausea, weakness, fatigue.
– Progression is indicated by worsening HA, vomiting, oliguria,
dyspnea, and weakness. May see postural hypotension,
peripheral and facial edema, fever. Localized pulmonary rales
seen in 20%.
– Retinal hemorrhages are seen at altitudes over 5000m.
ALTITUDE
“Climb every Mountain…”
• HACE is usually seen with HAPE. Presents with
AMS, ataxia, stupor, and progression to coma.
Can see focal neuro abnormalities (ie: CN 3/6
palsies). Also remember in the mountains you
can still get TIAs, strokes, and cerebrovascular
spasm (migraine equivalent) but these will
have more focal findings than HACE.
• HAPE is the most lethal of all of them
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ALTITUDE
“Climb every Mountain…”
Early recognition, descent (at least 500-1000m) and treatment are essential to
prevent progression.
Oxygen (0.5-1L+/min) is helpful.
Acetazolamide helps in prevention and treatment. As a CAI, it causes a bicarbonate
diuresis, leading to a mild metabolic acidosis, stimulating ventilation and thus
produces acclimatization.(125 mg BID, until sx resolves- or 3-4 days as prophylaxis.
Restart if sx reoccur.)
Dexamethasone (4mg PO/IM/IV Q6o for moderate/severe AMS;8 mg 1st dose, then
4mg Q 6o in HACE/HAPE ) If used over several days, taper off.
ASA or Tylenol for HA
Prochlorperazine (5-10mg IM/IV) can help with N/V
Use diuretics with caution in AMS, but definitely use with HAPE/HACE (Lasix 4080mg).
HAPE: Also use Nifedipine (10mg Q4-6o, or 30mg ER Q12o) as well as Morphine to
pull fluid off of lungs.
HACE/HAPE mandate immediate decent or evacuation.
IN THE FIELD: An expiratory positive pressure mask can increase oxygen saturation
by 10-20% without supplemental O2. Gammow bags are great, but are expensive,
and few people carry them.
ELECTRICAL INJURY
Question
• Which of the following is true regarding electrical
injury?
– DC (Direct Current) is more dangerous than AC
(Alternating Current)
– In high voltage injuries, the extent of cutaneous burns
is a good predictor of internal tissue damage
– Asystole is the most common dysarrythmia resulting
from low voltage electrical injury
– In contrast to other multi-victim tramatic events,
patients without signs of life should be resuscitated
first
ELECTRICAL INJURY
Answers
• For a given voltage, AC is thought to be 3 times more dangerous than DC.
This is due to the fact that AC current causes repetitive muscle contraction
or tetany once the “let-go current” is exceeded. This results in prolonged
exposure and more severe injury. High voltage AC & DC curents will often
cause a single violent contrature and thus victim is thrown from source of
contact, thus increasing risk of blunt trauma and blast injuries.
• High voltage injuries should be treated like crush injuries, because there is
often a large amount of tissue damage underneath normal appearing skin.
It is impossible to predict the degree of underlying damage from the
extent of cutaneous burns.
• Fewer than 10% of pts experiencing a low voltage injury experience a
dysarrythmia. In those pts who do suffer cardiac arrest from the incidence,
V fib is the most common dysarrythmia.
• Triage priorities in high voltage electrical injury and lightening strikes are
different, because pts with obvious signs of life tend to do well, and can
afford a small delay in delivery of care; and due to the possibility of good
outcome with CPR, pts without signs of life should receive immediate care.
Electrical and Lightning Injuries
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As current flows through body greatest damage is to skin, nerves, blood vessels,
muscles
Investigations: ECG, CBC, UA, CK-MB, CMP, Lipase/Amylase, Mg, ABG, Coags. CTs
and XRs for trauma patients.
C-spine immobilization for any unwitnessed event or obtunded patient. IVF bolus,
O2, Monitor, Foley. Tetanus.
If rhadomyolysis present, alkalizine urine with 50 mEq sodium bicarb per 1 L of IVF.
Maintain blood pH at 7.45, and UOP 2mL/kg/h.
Admission criteria:
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High voltage (>600 V) exposure
Systemic injury
Neurologic or vascular injury to an extremity or digit
Deep burns
Dysarryhtmia or abnormal ECG
High-risk exposure
Abuse or suicidal intent
Presence of comorbid diseases
Associated injuries requiring admission
If brief, low-intensity current exposure, who are asx., and have normal ECG, UA
and no evidence of signif. burns or trauma, may be discharged after 6-8 hours
observation.