Environmental Emergencies Board Review Mary Welch 2013

1. Environmental Emergencies
Mary Welch, DO

2. Electrical injuries
Types of Current
Direct:Electrons flow in one direction
Ex. Batteries
Alternating: Electrons flow back and forth (60 Hz)
Used in household outlets
Generally more dangerous

3. Electrical injuries
Mechanism of Injury
Thermal Injury: Damage caused by heat due to
resistance to current resulting in internal burns and
edema
Bone and fat have the highest resistance
Mechanical Injury: Fractures and dislocations
caused by muscle contractions or associated
trauma
Disruption of Depolarization
May cause Seizures or arrhythmias
Degree of injury related to voltage and duration of
exposure

4. Cutaneous Injury
Skin burns
Exit and entry wounds
“Kissing Burns”- burns in skin creases due
to opposition of skin during tetanic
contractions

5. Musculoskeletal injury
Direct Current
Powerful Muscle spasm results in fractures
More like to to cause traumatic fractures
Alternating Current
Causes sustained contractions
Flexor muscles more powerful than extensors resulting in
patient being brought closer to the source
More powerful internal rotators may result in posterior
shoulder dislocation

6. Vascular injury
Venous Thrombosis
More common due to slower flow and less ability to
dissipate heat
Delayed Arterial Thrombosis
May appear similar to compartment syndrome
Mesenteric artery thrombosis

7. CNS injury
Seizure
Loss of consciousness and amnesia
Median nerve injury
Autonomic dysfunction
Pupils may be fixed and dilated you cannot rely on
pupillary exam to cease resuscitation

8. cardiac
DC injury can cause asystole
AC injury may cause Vfib

9. complications
Compartment syndrome
Cataracts
Rhabdo
Labial artery bleeding
Depression
Delayed neurologic symptoms
Similar to ALS and transverse myelitis
Delayed Lower extremity weakness

10. Work up
ECG
Labs: CE, CHEM, Total CK
UA for myoglobinuria
Imaging PRN
Compartment checks and pressures
PRN

11. Management
Cardiac monitoring
Fluid management
Be aware of possible fluid losses
keep UOP to 1cc/kg/hr
Fasciotomy or carpal tunnel release PRN

12. Admission Criteria
ECG Changes
Loss of conciousness
Path of current possibly passed through
the heart
High voltage (>500V) injury
Transfer significant electrical injuries to
burn centers

13. Discharge
Low voltage injuries
No changes after 6 hours of monitoring
NO loss of conciousness

14. Lightening injuries
Massive unidirectional current
30% Mortality rate
70% Significant morbidity rate

15. Lightening injuries
Flashover burns are common
Ferning or Lichtenberg sign
Patient may be thrown significant
distances resulting in traumatic injuries
Tympanic membrane rupture (>50%)
Cataract formation is common
Deep tissue damage uncommon

16. Lightening injuries
Most common complications are related to
depolarization abnormalities:
Loss of consciousness
Seizures
Cardiac arrhythmias
Death caused by Vfib or asystole

17. management
Good prognosis if no respiratory or cardiac arrest
Massive fluid boluses not required due to little tissue
necrosis
If mass casualty highest priority are those in
respiratory or cardiac arrest
Continue resuscitation even if victims appear dead as
they be unresponsive with fixed and dilated pupils
Defibrillate to restore rhythm

18. High Altitude illness
acute mountain sickness
acute mountain sickness
Caused by hypoxia
Decreased oxygen pressure increases
cerebral blood flow resulting in cerebral
edema

19. acute mountain sickness
Signs and symptoms
Signs and symptoms
Headache
Nausea and vomiting
Insomnia
Decreased urination
Peripheral or facial edema
Retinal hemorrhage

20. acute mountain sickness
Treatment
Treatment
Halt ascent
Acetazolamide
carbonic anhydrase inhibitor which aids in
acclimatization
Take 12-24 hours before ascent for prophylaxis
Bicarbonate diuresis stimulates respiratory
compensation
Contraindicated in SSD and sulfa allergies
Steroids for cerebral edema
Descent for refractory cases

21. management
Descent
Supplemental oxygen
Acetazolamide
Steroids
Portable hyperbaric chamber if descent not
possible

22. High Altitude illness
High altitude cerebral edema
High altitude cerebral edema
Altered mental status
Ataxia, confusion
Retinal hemorrhages
Death due to brain-stem herniation
All patients with altered mental status
should be observed for ataxia

23. High altitude pulmonary edema
Most common cause of death from high
altitude illness
Due to hypoxia induced pulmonary
vasoconstriction

24. edema
Occurs a few days after ascent
Symptoms worse at night
Cough
Decreased exercise tolerance
Low grade fever
Tachycardia, Tachypnea
Rales and ronchi

25. edema
Immediate descent
Oxygen
Calcium channel blockers
Acetazolamide for prophylaxis
Portable hyperbaric chamber if descent not
possible

26. Diving Dysbarism
Pathology related to increases and decreases of
external pressure on the human body
Pressure and volume changes as a function of
depth
Boyle’s Law: pressure X volume = k (constant)
At a set temperature pressure and volume are
inversely related
Governs all gases under pressure
Atmospheric pressure doubles every 33ft under
water

27. Affects on
HEENT system
HEENT system
Middle Ear
Most commonly affected due to eustacian tube
dysfunction
Eustacian tube equalizes pressure in middle ear
Patients with eustacian tube dysfunction may
have: pain, hematoma, TM rupture, vertigo
Inner Ear
Rapid ascent may cause rupture of the round
window resulting in sudden hearing loss, vertigo
and tinnitus
Requires ENT consultation and surgical repair

28. Affects on
HEENT system
HEENT system
Sinus Squeeze
Frontal sinus most commonly affected
Inflammation or blockage of sinus ostia and
decreased sinus drainage may result in difficulties
On descent the air in sinuses contracts resulting in
negative pressure on sinus mucosa causing: edema,
hemorrhage and pain
On ascent expanding gas results in increased pressure in
the fixed space of the sinuses
Treat with decongestions, steroids and ABX if
necessary
Dental Pain due to air trapped in fillings

29. Affects on
pulmonary system
pulmonary system
Lung volume equalized by appropriate inspiration
and expiration
Complications due to rapid descent
Hemoptysis
Complications due to rapid ascent
Due to inadequate exhalation:
Lung volume doubles every 33 feet, exhalation
required to prevent injury
Inexperienced divers may hold their breath

30. Complications from ascent
Pneumothorax
May develop hypotension due to tension PTX
Pneumomediastinum
Arterial gas embolism
Management
Treat PTX
Hyperbaric treatment

31. Air embolism
Due to rupture of air or nitrogen into pulmonary
vein
May present similar to pulmonary embolism
Suspect in any diver who comes up unconscious
Air embolism into coronary artery may cause MI
Air embolism into brain presents similarly to CVA
Requires immediate hyperbaric treatment
and supportive care

32. Decompression sickness
Dysbarism due to reformation of dissolved
nitrogen into gas bubbles in tissues
During descent oxygen and nitrogen is
compressed
Oxygen continues to be consumed by the body
as nitrogen accumulates
During ascent nitrogen bubbles form in tissues
and joints resulting in vessel obstruction

33. Decompression sickness
risk factors
risk factors
Increased depth of dive and speed of ascent
Multiple dives in the same day
Nitrogen lasts for 12 hours
Air flight soon after dive
Obesity
Nitrogen is fat soluble
Poor physical conditioning and strenuous
exercise while under water

34. Decompression sickness
Symptoms and signs
Symptoms and signs
Onset within 6 hours
MSK: Joint pain (“The bends”)
Pulm: Chest pain, cough, dyspnea (“The
chokes”)
Inner Ear: Vertigo, hearing loss, and nausea
(“The staggers”)
Spinal Cord: pins and needles sensation
CNS: visual disturbances and HA
Derm: pruritis and burning of skin, mottling and
erysipelas-like rash over fatty areas

35. Decompression sickness
Diagnosis
Diagnosis
Clinical diagnosis
Severe illness and arterial gas embolism
may be difficult to differentiate
AGE presents suddenly with 10-20 min of
ascent
AGE only affects brain (NO spinal cord
involvement)
AGE can occur with short and shallow dives

36. Decompression sickness
management
management
Administer 100% oxygen
IV hydration
Aspirin if not bleeding
Hyperbaric treatment
Prevention
Slow ascent
Limit depth or dive time
No flying for 12-24 hours

37. Breathing gas under
high pressure
high pressure
Breathing oxygen or nitrogen at high partial
pressure is neurotoxic
Oxygen toxicity
Risk begins at 200ft
Tingling
Focal seizures
Vertigo
Nausea and vomiting

38. Breathing gas under
high pressure
high pressure
Nitrogen Narcosis
Risk begins at 100ft
Incapacitating at 300ft
Resembles alcohol intoxication
Prevention
Deep divers use mixtures lower in oxygen
mixed with helium or hydrogen
Management
Rabidly reversible with ascent

39. Radiation Injuries
Radiation: energy emitted when
change from higher energy state to
lower energy state in the form of
atomic particles or waves

40. Radiation Injuries
ionizing radiation
ionizing radiation
Energy released from unstable atoms as
they decay to more stable state
Able to break chemical bonds and form ion
pairs
May be electromagnetic or particulate
Causes cellular injury by cleaving DNA
strands and producing free radicles
Induces genetic mutations and cancer

41. Radiation Injuries
non-ionizing Radiation
non-ionizing Radiation
All forms of electromagnetic radiation
except:
High energy UV, Xray, gamma ray
Includes radio wave, microwave infrared
visible light and low energy UV

42. Radiation Injuries
electromagnetic radiation
electromagnetic radiation
Self-propagating waves of energeny with
electric and magnetic components
Ionizing or non-ionizing
Ionizing electromagnetic radiation includes:
high energy UV, Xray, Gamma ray
UV radiation

43. Alpha
Radiation Injuries
Particulate radiation
Particulate radiation
Consists of 2 neutrons and 2 protons
Cannot penetrate skin
Dangerous if internalized (ingested or inhaled), id decays when inside
the body
Beta
High energy electrons
Can penetrate skin and cause burns
Penetration may be prevented by heavy clothing
Internalization is dangerous
Neutrons
Generally from nuclear explosion
Penetrates tissue causing radioactivity and damaging tissue

44. Radiation Injuries
signs and symptoms
signs and symptoms
Early vomiting correlates with radiation
exposure
c
LD 50/30: Dose causing 50% mortality in 30 days is
4.5 Gy
No documented survival with >10 Gy
Dermatologic
Cutaneous burns from localized exposure
Delayed blistering and desquamation weeks later

45. Radiation Injuries
signs and symptoms
signs and symptoms
Hematopoietic Syndrome:
Destruction of bone marrow
Pancytopenia resulting in anemia, bleeding and infections
Gastrointestinal Syndrome:
Prodrome of N/V/D
Symptoms worsen after 1 wk with dehydration, bloody diarrhea
and sepsis
Death within 3-10 days
CNS Syndrome:
Nausea, vomiting, ataxia
Seizures, AMS
Death within hours to days

46. Radiation Injuries
Diagnosis
Diagnosis
CBC
Lymphocyte count at 48 hours is prognostic
Good prognosis >1500
Poor prognosis <1500

47. Radiation Injuries
signs and symptoms
signs and symptoms
Decontamination
Removal of clothing, showers, and water
Blocking agents to reduce amount of absorbed
radiation
Potassium iodine prevents absorption by the thyroid
Close wounds early to decrease infection risk
Supportive care
IVF
Anti-emetics
Leukocyte reduced blood transfusion if necessary
Antibiotics and antivirals if neutropenic

48. Animal bites
Human
Human
Direct bite or “Fight Bite”
Look for lacerations of the knuckle due to
contact with teeth
Xray
For closed fist injuries to rule out fractures
which may require inpatient antibiotics
Rule out foreign body

49. Human Bites
Management
Management
Fight Bites
Irrigation and wound exploration in full range of
motion
Admit all infected bites
Consider admitting uninfected fight bites to
ensure close follow up
Antibiotics for all wounds with or without
infection

50. Human Bites
treatment of infection
treatment of infection
Cover skin flora and oral flora
Eikenella corrodens
Augmentin is recommended
Other options:
Clinda or erythromycin + doxy, keflex or
cefuroxime
Wounds on extremities should not undergo
primary repair
Consider prophylaxis for communicable

51. cat and dog bites
Dogs and large animals cause crush
injuries
Look for underlying tissue damage and
fractures
Cats and smaller animals cause puncture
injuries
Wounds appear benign but have higher risk of
infection

52. cat and dog bites
causes of infection
causes of infection
Dogs: Staph>Strep>Eikenella>Pasteurella
Cats:
Pasteurella>Actinomyces>Bacteroides>F
usobacterium
Infection rate of 50-80%

53. cat and dog bites
management
management
Thorough neurovascular and tissue exam
Treat underlying injury
If bite to the head in young children consider
penetrating injury to the skull
Neurosurgery consultation and admission if
suspected
Update Td
Assess risk for rabies

54. cat and dog bites
Antibiotics
Antibiotics
Most cat bites should be treated
Dog bites should be decided on a case-bycase basis
Regimens
Augmentin
Clinda + Cipro
Clinda + Bactrim

55. Snake envenomations
25 poisonous species of 2 major
families native to North America
Viperidae
Elapidae

56. Viperidae
Subfamily: crotalids or pit vipers
Subfamily: crotalids or pit vipers
Includes: rattlers, cottonmouths,
copperheads, and the western
diamondbacks
98% of all US envenomations
Identified by:
Triangular-shaped head
Nostril pits anteroinferior to eye
Elliptical pupils
Single row of plates at distal tail

57. viperidae

58. Viperidae envenomation
signs and symptoms
signs and symptoms
Most bites are “dry”
Systemic Effects
Weakness, paresthesias
Metallic taste
Chest pain and dyspnea
Local Effects
Pain, erythema, edema, bullae
Compartment syndrome and rhabdo
Hematologic consequences
Coagulopathy, thrombocytopenia, bleeding

59. Viperidae envenomation
diagnosis
diagnosis
CBC
Coags
UA
Total CK
Check compartment pressures
XRay to rule out foreign bodies

60. Viperidae envenomation
management
management
Antivenin
CroFab (Crotalidae polyvalent immune Fab)
Sheep product with few allergic manifestations
Administer to most patients
Antivenin (Crotalidae) polyvalent
Horse serum with higher risk of anaphylaxis and serum
sickness
Only for moderate to severe envenomations
Consider fasciotomy for compartment syndrome
Observe “dry bites” for 8 hours
Admit all true envenomations

61. Elapidae Family
Includes: Coral snakes, cobras and
mambas
Identified by:
Round pupils
Double row of plates at distal tail
Brightly colored
“Black on yellow kill a fellow, red on black venom
lack”

62. Elapidae

63. Elapidae envenomation
signs and symptoms
signs and symptoms
Delayed for up to 13 hours
Patients may look deceptively well
Local Symptoms
Pain and edema may be limited
Neurotoxicity causes predominate symptoms
Blurred vision, ophthalmoplegia, ptosis, fasiculations,
paresthesias and hypersalivation
Late symptoms: paralysis of face, palate, jaws and vocal
cords
Respiratory failure from neuromuscular blockade

64. Elapidae envenomation
management
management
Do not underestimate degree of
envenomation due to lack of initial symptoms
All Eastern and Texas coral snake bites
should be treated with antivenin
Micrurus fulvius antivenin
Symptoms completely reversible
Admit all coral snake bites

65. Spider Bites
Black Widow
Black Widow
Identification: red hourglass shape on ventral
abdomen
Symptoms and signs
Systemic
Autonomic instability
Hypertension and tachycardia
Nausea and vomiting
Neurologic
Muscle cramps, Headache
Severe abdominal pain
Fasiculations and ptosis

66. Black Widow Bite
Management
Management
Supportive Care
Analgesia
Treat cramps with benzos
IV calcium is discouraged
Antivenin only for severe symptoms
Horse serum derived, may cause anaphylaxis and
serum sickness

67. Spider Bites
Brown Recluse
Brown Recluse
Identification: violin-shaped markings on back
Symptoms and signs
May cause fever, chills, malaise, and hemolysis
“Bull’s eye” lesion: red and white, with a necrotic
center
May become so severe it requires plastic surgery
Rarely hemolysis and renal failure result in mortality

68. Brown Recluse
Diagnosis
Check labs for hemolysis, renal failure and DIC
Management
Consider anthrax in the differential
Local wound care
Some evidence for dapsone (remember side effects)
Supportive care

69. Scorpion Stings
The “Bark scorpion” is the only potentially
letal scorpion species in the US
Found in: AZ, NM, CO
Signs and Symptoms
Localized pain and inflammation (most common)
Neurotoxic
Roving eye movements
Opisthotonic posturing
Paresthesias

70. Scorpion Stings
treatment
treatment
Antivenin available for severe symptoms
Supportive care

71. Lethal jellyfish stings
Box jellyfish
Box jellyfish
Carry the most lethal marine toxin
Over 5000 deaths worldwide
Severe pain and spasms
Parasympathetic overstimulation
leads to cardiac arrest
Paralysis, respiratory weakness
and drowning

72. Lethal jellyfish stings
Portugese man-of-war
Portugese man-of-war
Severe pain as if
being struck by
lightening
Rarely deadly

73. Lethal jellyfish stings
management
management
Remove and prevent unfired nematocysts
Wash with seawater or sterile saline
Fix nematocyst with household vinegar
Remove tentacles with gloves and forceps
Coalesce nematocyst with talcum powder or shaving cream
then scrape off skin with knife
Antivenin exists for box jellyfish from Australia but
ineffective after symptom onset
Supportive and local wound care
Apply topical anesthetic, antihistamine or steroid
Update TD