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PEM Lectures dirigées > Environmental Emergencies + Mass casualties > Flashcards

Environmental Emergencies + Mass casualties Flashcards

1
Q

Risk factors for drowning

A

Male
Epilepsy
infants/toddlers

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2
Q

How does fresh water cause electrolyte/vascular volume abnormalities

A

aspirated - into circulation - hemodilution - can contribute to cerebral and pulmonary edema

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3
Q

How does salt-water aspiration affect intravascular volume

A

lowers, causes hemoconcentration
can cause massive hemolysis

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4
Q

What is the pathophysiology of drowning (fresh water)?

A

Fresh water - disrupts surfactant - increased surface tension - alveolar instability - fluid leak into alveoli - pulmonary edema

decreased pulmonary compliance, increased airway resistance + pulmonary artery pressure, diminish pulmonary flow
Non-ventilated alveoli are perfused = intrapulmonary shunt = decreased PaO2 = metabolic acidosis

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5
Q

What is the pathophysiology of drowning (salt water)?

A

no denaturing of surfactant
creates osmotic gradient - fluid accumulation in lungs - dilution of surfactant

decreased pulmonary compliance, increased airway resistance + pulmonary artery pressure, diminish pulmonary flow
Non-ventilated alveoli are perfused = intrapulmonary shunt = decreased PaO2 = metabolic acidosis

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6
Q

Risk factors for worse prognosis in drowning

A

duration of submersion
degree of pulmonary damage by aspiration
effectiveness of initial resuscitative measures
degree of hypothermia

Asystole on arrival in ED
Hyperglycemia
Fixed, dilated pupils on arrival

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7
Q

Target sat for drowning victim

A

92%+ for home
90% + for in-hospital

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8
Q

Management of drowning victim with normal O2 sat

A

observation 6-12 hours with repeat sat or abg

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9
Q

Investigations to order for drowning victim

A

CXR
ABG
CBC
Lytes
Urinalysis

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10
Q

Ways to improve gas exchange in drowning patient with resp compromise

A

fluid restriction (1/2 maintenance)
Diuretic eg. furosemide 0.5-1mg/kg (max 20mg/dose)

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11
Q

Characteristics of a fence for around the pool

A

4 sided fence
prevents direct access to the pool
4 feet high minimum
climb-resistance
distance between bottom of fence + ground < 4 inches
self-latching, self-closing

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12
Q

Effects of smoke inhalation on lower airway

A

loss of ciliary action
mucosal edema
bronchiolitis
alveolar epithelial damage
impaired gas exchange
ateletasis/air trapping
loss of surfactant activity - ventilation perfusion mismatch
later - sloughing of tracheobronchial mucosa, mucopurulent membrande formation

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13
Q

Burning of polyurethane, vinyl, wool, silk, plastic produces what toxic gas?

A

cyanide

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14
Q

What physical exam findings signal probable smoke inhalation?

A

facial burns
singed nasal hairs
pharyngeal soot
carbonaceous sputum

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15
Q

CXR findings of inhalation injury

A

diffuse interstitial infiltration
local areas of atelectasis and edema

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16
Q

Treatment of cyanide toxicity

A

hydroxycobalamin IV 70mg/kg (max 5g)

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17
Q

When should elective tracheostomy be considered in inhalation injury

A

if placing or securing ETT will further traumatize an edmatous airway or severe facial burns

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18
Q

Investigations for inhalational injury

A

ABG
CO level
cyanohemoglobin level
troponin
CXR

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19
Q

Indications for intubation with inhalation injury

A

Upper airway obstruction
PaO2 < 60mmHg on 60% O2
CNS depression with loss of cough+ gag reflexes

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20
Q

Preferred method of delivering humidified O2 in inhalation injury

A

mask or artificial airway - prevent inspissation of debris and occlusion of the airway

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21
Q

Medication adjunct to increase cardiovascular stability in inhalational injury

A

diuretics - furosemide 0.5-1mg/kg IV

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22
Q

Inhaled medication adjuncts to aid in inhalation injury

A

aerosolized heparin, NAC, tiotropium - decreased incidence of atelectasis, reintubation and moretality

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23
Q

Minimum amount of time to monitor someone in ED with suspected inhalation injury

A

6 hours

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24
Q

How does CO cause hypoxia?

A

Binds to hemoglobin with an affinity 200 to 300 times greater than that of oxygen

Shifts the oxyhemoglobin dissociation curve to the left and changes the shape from sigmoidal to hyperbolic - only allows oxygen release at lower-than-normal tissue oxygen levels

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25
Q

How does tissue hypoxia (eg. from CO) cause cerebral edema?

A

increases cerebral blood flow, cerebrospinal fluid pressure, cerebral capillary permeability

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26
Q

Symptoms of carbon monoxide poisoning

A

dull headache
weakness
dizziness
dyspnea
nausea
vomiting
confusion
blurred vision
loss of consciousness

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27
Q

Symptoms of CO poisoning at the following carboxyhemoglobin percentages;
20%
20-40%
40-60%
> 60%

A

20% - headache, dyspnea, visual changes, confusion
20-40% - drowsiness, faintness, nausea and vomiting, tachycardia, dulled sensation, decreased awareness of danger
40-60% - weakness, incoordination, loss of recent memory
: 60% - coma, convulsions, death

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28
Q

Management of CO poisoning

A

Remove from contaminated environment
100% O2
Labs - ABG, CO level, troponin, CBC, Lytes, Urinalysis (myoglobin)
Monitoring
Keep HGB > 100

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29
Q

End point for O2 administration in CO poisoning

A

Carboxyhemoglobin < 5%

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30
Q

Metabolic acidosis with normal carboxyhemoglobin and methemoglobin suggests what?

A

coexistent cyanide pisoning

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31
Q

How does hydroxocooalamin work?

A

hydroxyl group of the vitamin (B12) binds to free cyanide forming nontoxic cyanocobalamin

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32
Q

Indications to consider hyperbaric O2 in CO poisoning

A

neurologic symptoms or signs
Signs of cardiac ischemia or metabolic acidosis
Pregnancy

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33
Q

Treatment of myoglobinemia or myoglobinuria in CO intoxication

A

vigorous hydration
diuresis with furosemide or mannitol to preserve renal function

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34
Q

Who needs admission from CO poisoning?

A

appear well on presentation to eD but have significant history (eg. LOC at scene) or elevated cO levels

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35
Q

What are poor prognostic indicators for CO poisoning

A

low GCS
high leuks
high Troponin

at presentation

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36
Q

Key differentiating factor between heat stroke vs heat exhaustion

A

presence of hyperpyrexia and anhidrosis with circulatory failure and/or severe CNS dysfunction

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37
Q

Why are children more susceptible to heat illnesses?

A

produce more metabolic heat
core temperature rises faster during dehydration
small organs less efficient at heat dissipation

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38
Q

Children with which conditions are more susceptible to heat stroke?

A

cystic fibrosis
congenital absence of sweat glands
receiving meds that cause oligohidrosis
eating disorders
diabetes insipidus
obesity
uncontrolled diabetes
young athletes

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39
Q

Where in the brain controls sympathetic tone + heat conduction?

A

posterior hypothalamus

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40
Q

What are the 4 ways for the body to reduce excess heat?

A

convection
conduction
radiation
evaporation

41
Q

What precipitates heat cramps?

A

adequate water replacement without adequate salt replacement

42
Q

What usually triggers heat cramps?

A

triggered by cold when relaxing after significant stress

43
Q

Lab findings in heat cramps

A

low NaCl, urine Na
Increased BUN (slight)

44
Q

What are the 2 types of heat exhaustion?

A

Predominant water depletion
Predominant salt depletion

45
Q

History + physical findings of predominant water depletion heat exhaustion

A

temp < 39
progressive lethargy
thirst
inability to work/play
headache
vomiting
CNS dysfunction
low BP
high HR

46
Q

Lab findings in predominant water depletion heat exhaustion

A

high Na, Cl, HCT
urine specific gravity high

47
Q

History + physical findings of predominant salt depletion heat exhaustion

A

temp > 39
weakness, fatigue
headache
GI symptoms
muscle cramps
tachycardia
orthostatic hypotension

48
Q

lab findings of predominant salt depletion heat exhaustion

A

low Na
HCT high
very low urine Na

49
Q

History + physical findings of heat stroke

A

temp 41+
hot, dry skin
circulatory collapse
severe CNS dysfunction
rhabdomyolysis
renal failure

50
Q

lab findings of heat stroke

A

high or normal Na, Cl
CK high
low Ca

51
Q

Treatment of heat cramps

A

rehydration with salt

52
Q

Labs to do for heat stroke

A

CBC
Lytes
BUN, Cr
CK
Ca, PO4
Urinalysis
ABG

53
Q

What needs monitoring for management of heat stroke?

A

temperature
HR
ECG
BP
Perfusion
U/O
CNS function

54
Q

Treatment of Heat stroke

A

Active cooling
Fluids
Inotropic support -
Dobutamine 5–20 mcg/kg/min or
Diuresis for myoglobinuria
Maintain urine output >1 mL/kg/hr
Consider furosemide 1 mg/kg
Consider mannitol 0.25–1 g/kg

55
Q

why is dobutamine the vasopressor of choice in heat stroke?

A

beta-agonist - increases contractility and maintains peripheral vasodilation

56
Q

Definition of hypothermia

A

core temp < 35

57
Q

Temps to classify hypothermia as mild, moderate, severe

A

mild: 32-35
moderate: 28-32
severe: 25-28

58
Q

Why are younger children (esp newborns) at higher risk of hypothermia?

A

large surface:volume ratio
small amount of subcutaneous fat
can’t shiver (neonates)

59
Q

Risk factors for hypothermia

A

physical disability (esp if immobilized)
drug or alcohol ingestion
working/playing to exhaustion in cold environment

60
Q

How does the body combat hypothermia

A

increase muscle tone
increase metabolism
shivering
no sweating
vasoconstriction of cutaneous and subcutaneous vessels

61
Q

Cardiac conduction abnormalities in hypothermia

A

decreased sinus rate
T-wave inversion
prolongation of intervals
J-waves (pathognomonic)
afib (<33 degrees)
vfib (<28 degrees)

61
Q

Treatment for hypothermia at the following temperatures:
> 32
< 32 (Acute)
< 32 (chronic)

A

≥32°C (89.6°F): passive rewarming or simple external rewarming
<32°C (89.6°F) (acute): external or core rewarming
<32°C (89.6°F) (chronic): core rewarming

61
Q

Reason for hyperglycemia with hypothermia

A

insulin release stops
can cause frank pancreatic necrosis

61
Q

before respiratory depression, what factors predispose a hypothermic patient to airway obstruction and aspiration?

A

impaired mental status
cold-induced bronchorrhea

61
Q

Hematologic abnormalities in hypothermia

A

plasma loss - increased hct
splenic sequestration - fall WBC and PLT
DIC

61
Q

Labs for hypothermia

A

CBC
INR/PTT
Lytes
BUN + Cr
glucose
amylase
ABG (corrected for temp)
Urine (drug screening)

61
Q

Temperature at which BP falls in hypothermia

A

33

61
Q

To what temperature should NS / RL be warmed for a hypothermic patient?

A

43 degrees

61
Q

At what temperature does defibrillation become more likely to be effective?

A

30 degrees

61
Q

How do you adjust the ventilatory rate for a hypothermic patient?

A

put to 1/2 normal (decreased metabolic rate = less CO2 = resp alkalosis if at normal minute-ventilation rate)

61
Q

What are passive rewarming strategies?

A

removal of patient from cold environment
use of blankets

62
Q

What is the temperature “afterdrop”

A

external rewarming causes early warming of the skin and extremities - peripheral vasodilation - shunting of cold, acidemic blood to the core - dip in temp and BP

63
Q

What are the 3 phases of frostbite treatment?

A
  1. prethaw - take patient out of the cold environment and remove wet clothing. apply soft padding to the affected area. DO NOT RUB.
  2. rewarm over 15-30 mins by immersing the affected area in 40-42 degree water. likely need IV analgesics
  3. Post-thaw - wound management and application of loose, sterile dressings. Digits separated with cotton and extremities splinted
64
Q

What are the factors that influence the severity of electrical injuries?

A

-resistance of skin, mucosa and internal structures
- type of current (AC or DC)
- frequency of the current
- intensity
- duration of contact
- pathway taken by the current

65
Q

In comparing lightning vs high-voltage electrical injury:

  • type of current
  • shock wave
  • cardiac arrhythmia
  • burns
  • renal failure
  • fasciotomy/amputation
A

lightning
- direct
-present
-asystole
-superficial/minor
-rare
-rare

high-voltage
- AC
-absent
-vfib
-deep (frequently obscured)
-common (2 to myoglobinuria)
- common

66
Q

Why is alternating current more dangerous than DC?

A

able to induce tetanic muscle contraction - creates a “locking on” phenomenon

67
Q

nervous system injuries resulting from electrical injury

A

LOC
seizure
amnesia
disorientation
deafness
visual disturance
sensory deficit
hemiplegia/quadriplegia
Subdural/epidural/intraventricular hemorrhage
SIADH (leading to cerebral edema)

68
Q

Ocular damage secondary to lightning strikes

A

corneal lesion
hyphema
uveitis
iridocyclitis
vitreous hemorrhage

choroidal rupture
retinal detachment
chorioretinitis

69
Q

GI consequences of electrical injury

A

gastric dilation
ileus
diffuse GI hemorrhage
visceral perforation

70
Q

When is risk of bleeding highest in electrical burns around the mouth?

A

2-3 weeks post-injury with eschar separation

71
Q

Bacteria that infect electrical injury wounds
- extremities
- mouth

A

extremities - staph, pseudomonas, clostridium

mouth - strep, oral anaerobes

72
Q

Management of electrical injury

A

Remove from source of current
Cardiopulmonary resuscitation as needed
Provide mechanical ventilation until spontaneous ventilation is adequate
Immobilize neck and spine

assess + Get labs

Maintenance fluids: 5% dextrose in normal saline
Volume expansion in presence of thermal burns or extensive deep tissue injury: 0.9% sodium chloride or lactated Ringer’s solution
Fluid restriction for central nervous system injury
Maintain urine output >1 mL/kg/hr
Treat arrhythmias
Treat seizures
Tetanus toxoid; consider penicillin/other antibiotics
Consider general, oral, or plastic surgical consultation

73
Q

Labs for electrical injury

A

CBC
BUN, Cr, urinalysis
Lytes
Troponin
ECG

74
Q

When is the greatest risk related to whole-body radiation exposure?

A

3-4 weeks after exposure when bone marrow depression reaches nadir

75
Q

3 steps that can be taken to minimize adverse effects of a nuclear reactor accident to the public

A

public should be sheltered or evacuated
administer potassium iodide (to prevent uptake of radioactive iodine)
monitor the food supply to prevent further ingestion

76
Q

Steps to external decontamination

A

Try to do this outside the hospital. if not possible, wrap patient in a cotton sheet to transport them inside the hospital

Remove clothes
Wash with a damp cloth
Pay special attention to skin folds and fingernails
Cover clean wounds to prevent contamination
Prevent external and tepid water contamination from becoming internal
Do not abrade the skin

77
Q

How can you tell cyanide poisoning from nerve-agent poisoning?

A

nerve agent more likely to have - miosis, cyanosis, copious oral and nasal secretions, bronchorrhea, bronchospasm [cholinergic toxidrome]

78
Q

3 zones to have to manage chemically contaminated victims

A

hot zone = on scene
warm zone = receiving area for chemical casualties
cold zone = in the ED, separated by a “hot line” after which no liquid contamination is permitted to pass and anyone that comes in is already thoroughly decontaminated

79
Q

Which chemical agents cause a primarily neurologic syndrome?

A

nerve agents, cyanide

80
Q

Which chemical agents cause a primarily respiratory syndrome?

A

Phosgene, Chlorine

81
Q

Which chemical agents cause a primarily mucocutaneous syndrome?

A

Lewisite, mustard

82
Q

What should a decontamination centre look like?

A

Outdoor facility is best but must ensure adequate water, temperature control, curtains separating males/females showers

OR
another enclosed facility adjacent to the ED with a separate and high-volume ventilation system vented directly outdoors

surface of decontamination facility should allow drainage to prevent slipping

83
Q

Antidotes for nerve-agent toxicity

A

atropine
pralidoxime

84
Q

Mustard gas - clinical findings

A

erythema, vesicles of skin
eye inflammation
epithelial denudation with airway obstruction
bone marrow suppression

85
Q

Lewisite/arsenic toxicity - clinical findings

A

eye inflammation
ARDS with hypotension

86
Q

Phosgene toxicity - clinical findings

A

bronchospasm, pulmonary edema

87
Q

Cyanide toxicity - clinical findings

A

hyperpnea, collapse, seizures, muscle rigidity, apnea, coma

88
Q
A

PEM Lectures dirigées (28 decks)

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