Environmental Emergencies + Mass casualties Flashcards
Risk factors for drowning
Male
Epilepsy
infants/toddlers
How does fresh water cause electrolyte/vascular volume abnormalities
aspirated - into circulation - hemodilution - can contribute to cerebral and pulmonary edema
How does salt-water aspiration affect intravascular volume
lowers, causes hemoconcentration
can cause massive hemolysis
What is the pathophysiology of drowning (fresh water)?
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
What is the pathophysiology of drowning (salt water)?
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
Risk factors for worse prognosis in drowning
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
Target sat for drowning victim
92%+ for home
90% + for in-hospital
Management of drowning victim with normal O2 sat
observation 6-12 hours with repeat sat or abg
Investigations to order for drowning victim
CXR
ABG
CBC
Lytes
Urinalysis
Ways to improve gas exchange in drowning patient with resp compromise
fluid restriction (1/2 maintenance)
Diuretic eg. furosemide 0.5-1mg/kg (max 20mg/dose)
Characteristics of a fence for around the pool
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
Effects of smoke inhalation on lower airway
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
Burning of polyurethane, vinyl, wool, silk, plastic produces what toxic gas?
cyanide
What physical exam findings signal probable smoke inhalation?
facial burns
singed nasal hairs
pharyngeal soot
carbonaceous sputum
CXR findings of inhalation injury
diffuse interstitial infiltration
local areas of atelectasis and edema
Treatment of cyanide toxicity
hydroxycobalamin IV 70mg/kg (max 5g)
When should elective tracheostomy be considered in inhalation injury
if placing or securing ETT will further traumatize an edmatous airway or severe facial burns
Investigations for inhalational injury
ABG
CO level
cyanohemoglobin level
troponin
CXR
Indications for intubation with inhalation injury
Upper airway obstruction
PaO2 < 60mmHg on 60% O2
CNS depression with loss of cough+ gag reflexes
Preferred method of delivering humidified O2 in inhalation injury
mask or artificial airway - prevent inspissation of debris and occlusion of the airway
Medication adjunct to increase cardiovascular stability in inhalational injury
diuretics - furosemide 0.5-1mg/kg IV
Inhaled medication adjuncts to aid in inhalation injury
aerosolized heparin, NAC, tiotropium - decreased incidence of atelectasis, reintubation and moretality
Minimum amount of time to monitor someone in ED with suspected inhalation injury
6 hours
How does CO cause hypoxia?
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
How does tissue hypoxia (eg. from CO) cause cerebral edema?
increases cerebral blood flow, cerebrospinal fluid pressure, cerebral capillary permeability
Symptoms of carbon monoxide poisoning
dull headache
weakness
dizziness
dyspnea
nausea
vomiting
confusion
blurred vision
loss of consciousness
Symptoms of CO poisoning at the following carboxyhemoglobin percentages;
20%
20-40%
40-60%
> 60%
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
Management of CO poisoning
Remove from contaminated environment
100% O2
Labs - ABG, CO level, troponin, CBC, Lytes, Urinalysis (myoglobin)
Monitoring
Keep HGB > 100
End point for O2 administration in CO poisoning
Carboxyhemoglobin < 5%
Metabolic acidosis with normal carboxyhemoglobin and methemoglobin suggests what?
coexistent cyanide pisoning
How does hydroxocooalamin work?
hydroxyl group of the vitamin (B12) binds to free cyanide forming nontoxic cyanocobalamin
Indications to consider hyperbaric O2 in CO poisoning
neurologic symptoms or signs
Signs of cardiac ischemia or metabolic acidosis
Pregnancy
Treatment of myoglobinemia or myoglobinuria in CO intoxication
vigorous hydration
diuresis with furosemide or mannitol to preserve renal function
Who needs admission from CO poisoning?
appear well on presentation to eD but have significant history (eg. LOC at scene) or elevated cO levels
What are poor prognostic indicators for CO poisoning
low GCS
high leuks
high Troponin
at presentation
Key differentiating factor between heat stroke vs heat exhaustion
presence of hyperpyrexia and anhidrosis with circulatory failure and/or severe CNS dysfunction
Why are children more susceptible to heat illnesses?
produce more metabolic heat
core temperature rises faster during dehydration
small organs less efficient at heat dissipation
Children with which conditions are more susceptible to heat stroke?
cystic fibrosis
congenital absence of sweat glands
receiving meds that cause oligohidrosis
eating disorders
diabetes insipidus
obesity
uncontrolled diabetes
young athletes
Where in the brain controls sympathetic tone + heat conduction?
posterior hypothalamus
What are the 4 ways for the body to reduce excess heat?
convection
conduction
radiation
evaporation
What precipitates heat cramps?
adequate water replacement without adequate salt replacement
What usually triggers heat cramps?
triggered by cold when relaxing after significant stress
Lab findings in heat cramps
low NaCl, urine Na
Increased BUN (slight)
What are the 2 types of heat exhaustion?
Predominant water depletion
Predominant salt depletion
History + physical findings of predominant water depletion heat exhaustion
temp < 39
progressive lethargy
thirst
inability to work/play
headache
vomiting
CNS dysfunction
low BP
high HR
Lab findings in predominant water depletion heat exhaustion
high Na, Cl, HCT
urine specific gravity high
History + physical findings of predominant salt depletion heat exhaustion
temp > 39
weakness, fatigue
headache
GI symptoms
muscle cramps
tachycardia
orthostatic hypotension
lab findings of predominant salt depletion heat exhaustion
low Na
HCT high
very low urine Na
History + physical findings of heat stroke
temp 41+
hot, dry skin
circulatory collapse
severe CNS dysfunction
rhabdomyolysis
renal failure
lab findings of heat stroke
high or normal Na, Cl
CK high
low Ca
Treatment of heat cramps
rehydration with salt
Labs to do for heat stroke
CBC
Lytes
BUN, Cr
CK
Ca, PO4
Urinalysis
ABG
What needs monitoring for management of heat stroke?
temperature
HR
ECG
BP
Perfusion
U/O
CNS function
Treatment of Heat stroke
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
why is dobutamine the vasopressor of choice in heat stroke?
beta-agonist - increases contractility and maintains peripheral vasodilation
Definition of hypothermia
core temp < 35
Temps to classify hypothermia as mild, moderate, severe
mild: 32-35
moderate: 28-32
severe: 25-28
Why are younger children (esp newborns) at higher risk of hypothermia?
large surface:volume ratio
small amount of subcutaneous fat
can’t shiver (neonates)
Risk factors for hypothermia
physical disability (esp if immobilized)
drug or alcohol ingestion
working/playing to exhaustion in cold environment
How does the body combat hypothermia
increase muscle tone
increase metabolism
shivering
no sweating
vasoconstriction of cutaneous and subcutaneous vessels
Cardiac conduction abnormalities in hypothermia
decreased sinus rate
T-wave inversion
prolongation of intervals
J-waves (pathognomonic)
afib (<33 degrees)
vfib (<28 degrees)
Treatment for hypothermia at the following temperatures:
> 32
< 32 (Acute)
< 32 (chronic)
≥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
Reason for hyperglycemia with hypothermia
insulin release stops
can cause frank pancreatic necrosis
before respiratory depression, what factors predispose a hypothermic patient to airway obstruction and aspiration?
impaired mental status
cold-induced bronchorrhea
Hematologic abnormalities in hypothermia
plasma loss - increased hct
splenic sequestration - fall WBC and PLT
DIC
Labs for hypothermia
CBC
INR/PTT
Lytes
BUN + Cr
glucose
amylase
ABG (corrected for temp)
Urine (drug screening)
Temperature at which BP falls in hypothermia
33
To what temperature should NS / RL be warmed for a hypothermic patient?
43 degrees
At what temperature does defibrillation become more likely to be effective?
30 degrees
How do you adjust the ventilatory rate for a hypothermic patient?
put to 1/2 normal (decreased metabolic rate = less CO2 = resp alkalosis if at normal minute-ventilation rate)
What are passive rewarming strategies?
removal of patient from cold environment
use of blankets
What is the temperature “afterdrop”
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
What are the 3 phases of frostbite treatment?
- prethaw - take patient out of the cold environment and remove wet clothing. apply soft padding to the affected area. DO NOT RUB.
- rewarm over 15-30 mins by immersing the affected area in 40-42 degree water. likely need IV analgesics
- Post-thaw - wound management and application of loose, sterile dressings. Digits separated with cotton and extremities splinted
What are the factors that influence the severity of electrical injuries?
-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
In comparing lightning vs high-voltage electrical injury:
- type of current
- shock wave
- cardiac arrhythmia
- burns
- renal failure
- fasciotomy/amputation
lightning
- direct
-present
-asystole
-superficial/minor
-rare
-rare
high-voltage
- AC
-absent
-vfib
-deep (frequently obscured)
-common (2 to myoglobinuria)
- common
Why is alternating current more dangerous than DC?
able to induce tetanic muscle contraction - creates a “locking on” phenomenon
nervous system injuries resulting from electrical injury
LOC
seizure
amnesia
disorientation
deafness
visual disturance
sensory deficit
hemiplegia/quadriplegia
Subdural/epidural/intraventricular hemorrhage
SIADH (leading to cerebral edema)
Ocular damage secondary to lightning strikes
corneal lesion
hyphema
uveitis
iridocyclitis
vitreous hemorrhage
choroidal rupture
retinal detachment
chorioretinitis
GI consequences of electrical injury
gastric dilation
ileus
diffuse GI hemorrhage
visceral perforation
When is risk of bleeding highest in electrical burns around the mouth?
2-3 weeks post-injury with eschar separation
Bacteria that infect electrical injury wounds
- extremities
- mouth
extremities - staph, pseudomonas, clostridium
mouth - strep, oral anaerobes
Management of electrical injury
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
Labs for electrical injury
CBC
BUN, Cr, urinalysis
Lytes
Troponin
ECG
When is the greatest risk related to whole-body radiation exposure?
3-4 weeks after exposure when bone marrow depression reaches nadir
3 steps that can be taken to minimize adverse effects of a nuclear reactor accident to the public
public should be sheltered or evacuated
administer potassium iodide (to prevent uptake of radioactive iodine)
monitor the food supply to prevent further ingestion
Steps to external decontamination
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
How can you tell cyanide poisoning from nerve-agent poisoning?
nerve agent more likely to have - miosis, cyanosis, copious oral and nasal secretions, bronchorrhea, bronchospasm [cholinergic toxidrome]
3 zones to have to manage chemically contaminated victims
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
Which chemical agents cause a primarily neurologic syndrome?
nerve agents, cyanide
Which chemical agents cause a primarily respiratory syndrome?
Phosgene, Chlorine
Which chemical agents cause a primarily mucocutaneous syndrome?
Lewisite, mustard
What should a decontamination centre look like?
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
Antidotes for nerve-agent toxicity
atropine
pralidoxime
Mustard gas - clinical findings
erythema, vesicles of skin
eye inflammation
epithelial denudation with airway obstruction
bone marrow suppression
Lewisite/arsenic toxicity - clinical findings
eye inflammation
ARDS with hypotension
Phosgene toxicity - clinical findings
bronchospasm, pulmonary edema
Cyanide toxicity - clinical findings
hyperpnea, collapse, seizures, muscle rigidity, apnea, coma
