toxicology 2: environmental ccrmc emergency medicine

Toxicology 2: Environmental

CCRMC Emergency Medicine

General Coverage

• 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– 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 onsetBe 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 NATURETreatment 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 NATUREArachnida: SPIDERS/SCABIES/MITES/CHIGGERS/SCORPIONS

Black Widow

Brown Recluse

Scorpion

Loxosceles bites are NOT seen in California


• 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


• 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.


• 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 NATURESnakes: Crotalidae (Pit Vipers) & Elapidae

Pygmy Rattlesnake Water Moccasin

Copper Head Coral Snake

PLAYING WITH NATURERattleSNAKES

• 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 NATURERattleSNAKES

• 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 NATURECoral 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 NATURERABIES 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 NATUREMARINE 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 NATUREMARINE 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 ABXMinor 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

HYPOTHERMIATHE PARADOX

Iatrogenic hypothermia can be protective(33-35o C for post cardiac arrest)

HOWEVERAccidental 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

HYPOTHERMIAOTHER 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

HYPOTHERMIACOMMON LAB FINDINGS

• Electrolytes variable– K >10.0 considered incompatible with survival;

however, exceptions have occurred• Hyperglycemia

• no insulin until To normal• Increased amylase, BUN, creatinine, LFS• Prolonged INR and PTT: IGNORE

HYPOTHERMIA

• 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 Cprobably 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!

HYPOTHERMIAKARLEE 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)

HYPOTHERMIAACTIVE EXTERNAL REWARMING

• 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

HYPOTHERMIAACTIVE INTERNAL REWARMING

• should be standard:– heated O2 to 40-44o C

– heated IV solution to 40-44o C• 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

HYPOTHERMIABECOME MORE AGGRESSIVE IF . . .

• hemodynamically unstable• cardiac arrest• DKA or other endocrine emergencies?

HYPOTHERMIAHOW? – 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

HYPOTHERMIAREWARMING 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

HYPOTHERMIAMONITOR DURING REWARMING

• 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 burnsAVOID• 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 illnessPT’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– Hyperventilationresp. 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

• 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: COFire, 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

• 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

DYSBARISMExploring 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.


• 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.


• 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.


• 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.


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 depletedPOPS: Tx PTX if present. Otherwise resolves with rest and supplemental O2, rarely requires recompression therapy


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.


• 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.


• 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


• Early recognition, descentEarly recognition, descent (at least 500-1000m) and treatment 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 40-

80mg).• HAPE: HAPE: Also use NifedipineNifedipine (10mg Q4-6o, or 30mg ER Q12o) as well as MorphineMorphine to

pull fluid off of lungs.• HACE/HAPE mandate immediate decent or evacuation.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 INJURYQuestion

• 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 INJURYAnswers

• 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• 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:

– 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.

toxicology 2: environmental ccrmc emergency medicine

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