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SC Multidisciplinary > Disaster And Related Emergency > Flashcards

Disaster And Related Emergency Flashcards

1
Q

Disaster

A

Serious disruption of functioning of community / society causing widespread human, material, economic / environmental losses which **exceed ability of affected community to cope using its **own resources

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2
Q

Most common disasters and location

A

Flood, China

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3
Q

***Types of disaster (WHO)

A

Natural:

  1. Geophysical
    - Earthquake
    - Volcano
    - Mass movement (Dry)
  2. Climate-related
    - Hydrologic: Flood, Mass movement (Wet)
    - Meterologic: Storm, Extreme temp, Wildfire
  3. Biological
    - Epidemic disease
    - Pests infestations

Man-made:

  1. Technological
    - Chemical substance
    - Radiological agents
    - Transport crashes
  2. Societal
    - Conflict / War
    - Stampedes
    - Terrorism

Other classifications:
1. Duration (Brief, Short, Intermediate, Prolonged) + Onset (Sudden / Gradual / Slow)

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4
Q

***Disaster management cycle

A
  1. ***Response
    - Basic relief needs (water, food, sanitation, shelter)
    - Healthcare needs (trauma care, mental health care, chronic illness care, remains handling)
  2. ***Recovery
    - Primary care
    —> Children: nutrition, immunisation
    —> Women: child birth
    —> Chronic illnesses
    - Public health
    —> Mental health (Anxiety, Depression, PTSD)
    —> Disease surveillance
    —> Prevent / Control outbreak of infectious diseases
  3. Mitigation
  4. Preparation
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5
Q

Disaster medical response

A
  1. Search + Rescue
  2. Triage + initial stabilisation
  3. Definitive medical care
  4. Evacuation
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6
Q

Communicable diseases associated with natural disaster

A
  1. Water-related
    - Cholera
    - Leptospirosis
    - Hep A, E
  2. Overcrowding-related
    - Measles
    - Chicken pox
  3. Vector-borne
    - Malaria
    - Dengue
  4. Other diseases
    - Tetanus
    - Fungal infections
    - Pneumonia
    - Encephalitis
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7
Q

Emergency Response System in HK

A

Tier 1: **Isolated events (e.g. simple car crash) —> FSD (Ambulance), Police, GFS, HA
Tier 2: **Many casualties (e.g. fire) —> Security bureau duty officer / Emergency support unit
Tier 3: Severe + ***widespread consequences (e.g. typhoon) —> Emergency monitoring + support centre (involving CE)

FSD (Ambulance): On-site rescue + transport of casualties
Police: establish Command post at scene + secret outer cordoned zone surrounding the site
HA: provision of hospital services, dispatch medical teams for on-site triage + treatment
HAD: coordinate relief items with Social welfare department, Housing department / other agencies
EMSC: update Government senior officials

4”C”s + 2”T”s:

  • Coordination
  • Command (Emergency Executive Committee (EEC), Central Command Committee (CCC), Major Incident Control Centre (MICC))
  • Control
  • Casualty diversion
  • Triage
  • On-scene treatment
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8
Q

Common injuries seen in victims trapped in collapsed structures

A
  1. Fractures
  2. Multiple trauma
  3. Closed head injury
  4. Hypothermia
  5. Dehydration
  6. ***Crush injury / syndrome
  7. Laceration / punctures
  8. Dust inhalation
  9. Hazardous material issues
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9
Q

Initial assessment of patient under rubble

A

Airway: assume airway compromised
Breathing: assume ventilation impaired secondary to dust / noxious gases inhalation and direct trauma
Circulation: assume hypovolaemia, crush injury
Disability: assume neurologic examination incomplete
Exposure: assume hypothermia, expose body parts only if deemed absolutely necessary for saving life

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10
Q

Crush injury

A

At risk:
- All patients crushed / immobilised for ***>=4 hours

Consequence of muscle injury:
1. Disintegration of striated muscles
—> Swelling of muscles
—> Pressure effect on surrounding structures
—> ***Compartment syndrome
—> Further ischaemia
—> Further muscle damage
—> Further muscle swelling
—> Vicious cycle
  1. Rhabdomyolysis
    —> Release of muscular cell contents into ECF
    —> Systemic manifestations = ***Crush syndrome
  • **Metabolic consequences:
    1. HyperK
    2. HyperPO4
    3. HypoCa
    4. Hyperuricaemia
    5. Myoglobinaemia —> Red discolouration of urine
    6. ↑ CK
    7. ↑ Creatinine / Urea (∵ Acute kidney injury)
    8. Metabolic lactate acidosis —> further deteriorate HyperK
  • Systemic effects:
    1. Hypovolaemia
    2. Electrolyte imbalance
    3. **    Acute renal failure
    4. **    Arrhythmia
    5. Sepsis (∵ wound)
    6. **ARDS (prodrome for death)
    7. **    DIC (∵ massive bleeding / sepsis)
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11
Q

Acute renal failure

A

Causes:

  1. ***↓ Intravascular volume —> Acute tubular necrosis
  2. **Myoglobin + Uric acid (potentiated by acidosis + urine concentration) —> **Cast —> Tubular damage
  3. ***Microthrombi (∵ DIC) —> deposited in glomerular tufts

Prevention of Acute renal failure:

  1. ***Normal saline (1L / hour (a lot)) (10-15 ml/kg/hour)
  2. Monitor BP + urine output
  3. ***Never give K containing solution (∵ patient already HyperK)
  4. ***Forced alkaline diuresis
    - NaHCO3
    - Mannitol
  5. Urine volume + pH maintenance
    - volume **300 mL/hr
    - pH **    >6.5
  6. Dialysis
    - 50% of crush syndrome develop ARF —> 50% of ARF require dialysis
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12
Q

“Rescue Death”

A

Metabolic causes:

  1. Influx of plasma into muscles
  2. Efflux of muscle breakdown products —> Acidosis, HyperK
  3. Influx of Ca into cells

Bleeding causes:
1. Tamponade effect removed in Pelvic fracture / Abdominal bleeding

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13
Q

***Causes of cardiac arrest

A

5H:

  1. Hypoxia
  2. Hypovolaemia
  3. HyperK
  4. Hydrogen (Acidosis)
  5. Hypothermia

5T:

  1. Tension pneumothorax
  2. Tamponade
  3. Thrombosis (Coronary)
  4. Thrombosis (Pulmonary)
  5. Toxin
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14
Q

HyperK treatment

A

Acute:

  1. ***CaCl
    - counter adverse effect of HyperK on myocardium
  2. ***Glucose insulin drip / Beta agonist (e.g. Ventolin) / NaHCO3
    - shift K back to cell
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15
Q

Compartment syndrome

A

Compartment pressure > Filling pressures of arterioles of muscle

6P:

  1. Pain
  2. Pallor
  3. Paresthesia
  4. Paralysis
  5. Perishing cold
  6. Pulselessness

Treatment:
1. Fasciotomy
- if pressure ***>40 mmHg
—> NO need anaesthetic (∵ already numbed)
—> Stop until bleeding (i.e. indicate reperfusion)

  1. Amputation
    - must for urgent life saving
    —> difficult decision (life saving vs limb saving)
    - depend on salvageability of the trapped limb
    —> is vascular injury reparable?
    —> can skeletal injury be reconstructed?
    —> is the soft tissue viable / can adequate soft tissue coverage be achieved?
    —> is innervation present / possible?
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16
Q

Physiological changes at high altitude

A

Altitude↓
—> Barometric pressure↓, Ambient PO2↓, PiO2↓

***PiO2 = (Pb - SVP) x FiO2

  • PiO2: Partial Pressure of Inspired Oxygen
  • Pb: Barometric pressure
  • SVP: Saturated vapour pressure at body temp (47 mmHg)
  • FiO2: Fraction of inspired oxygen (normal: 21%)

How body function with low SaO2 + PaO2?
**O2 delivery = O2 content x CO
- O2 content in 100ml blood
= O2 combined with Hb + O2 dissolved in plasma
= (Hb x 1.36 x SaO2) + (0.0031 x PaO2)
- O2 content can be maintained despite fall in SaO2 and PaO2 if **Hb is adequate
- Hb will ↑ as an adaptation

17
Q

High altitude illness

A

High altitude:

  • ***2500-3500m
  • Arterial saturation ***>85-90%

High altitude sickness:

  • common when individuals when ascend rapidly
  • HACE: High altitude cerebral edema
  • HAPE: High altitude pulmonary edema
  • Cause: ***Hypobaric hypoxia
Early symptoms:
- Headache (different from other causes of headache by giving O2)
- Loss of appetite
- Dizziness
- Fatigue on minimal exertion
—> ***Don’t go higher, ***Rest, ***Fluid
—> Symptoms go away —> Continue go up
—> Symptoms get worse —> Go down
Worsening symptoms:
- Severe headache
- Vomitting
- Walking like a drunk
- Increasing tiredness
—> ***Descend with accompaniment
18
Q

High altitude cerebral edema (HACE)

A 
Pathophysiology:
Hypoxia
—> Hypoxaemia
—>
1. ***↑ Cerebral blood flow
—> ↑ Capillary pressure
—> Brain swelling
  1. ***↑ Cerebral blood volume
    —> Brain swelling
  2. ***↑ Permeability of BBB
    —> Brain swelling

—> Inadequate buffering by CSF
—> AMS (Acute mountain sickness i.e. mild)
—> HACE (severe)

Diagnosis of AMS:
- **Lake Louise AMS score
—> questionnaire on symptoms during ascent
—> scoring system to assess severity of illness
1. Headache
2. GI symptoms
3. Fatigue
4. Dizziness
5. AMS clinical functional score
- AMS = **Altitude gain + **Headache + **Total symptom score >=3

Diagnosis of HACE:
- ***Lake Louise Criteria for HACE
- HACE: >=2 of following:
1. AMS
2. ***Altered mental status
3. ***Ataxia
(是但兩個)
Cautions:
- need to assess whole situation:
—> Altitude
—> Ascent rate
—> Alternative Dx (e.g. flu)
19
Q

Management of HACE

A

Mild AMS:

  • ***Descend >=500m
  • Acclimatisation for 1-2 days
  • Avoid ascent until S/S subsided
  • ***Acetazolamide 125-250 mg BD

Moderate AMS:

  • Descend
  • ***O2 (1-2 L/min)
  • ***Portable hyperbaric therapy (2-4 psi) x 6 hours
  • Acetazolamide 125-250 mg BD
  • ***Dexamethasone 4mg Q6H IM/PO (for cerebral edema)

HACE:

  • Immediate descend / evacuation >=1000m
  • O2 to keep SpO2 >=90%
  • Dexamethasone 8mg STAT IV/IM/PO —> then 4mg Q6H
  • Portable hyperbaric therapy if cannot descend

Hyperbaric therapy SE: Hyperbaric trauma (e.g. Pneumothorax, Pneumotympanum)

20
Q

Acetazolamide

A
  • Diamox
  • Carbonic anhydrase inhibitor
  • Induce renal excretion of HCO3 —> induce ***Metabolic acidosis —> trick body to hyperventilate —> speed up acclimatisation process to relieve symptoms
  • Counter respiratory alkalosis due to hyperventilation
  • SE: GI upset, Tingling in hands, Abnormal taste in tongue
(From SC008: Carbonic anhydrase inhibitor:
Altitude sickness
Prevent carbonic acid breakdown
—> Accumulation of carbonic acid 
—> Lower blood pH
—> Hyperventilation
Carbonic anhydrase:
- in RBC, Proximal tubule —> reabsorb Na, Cl, HCO3, Ciliary body —> Aqueous production
- when inhibited
—> Na, Cl, HCO3 excreted
—> diuresis
—> excretion of excess water
—> ↓ BP, ICP, IOP)
21
Q

High altitude pulmonary edema (HAPE)

A

DDx of High altitude SOB:

  • Asthma
  • Bronchitis
  • Heart failure
  • Hyperventilation syndrome
  • Mucus plugging
  • MI
  • Pneumonia
  • PE
Pathophysiology:
Rapid ascent
—> Lack of acclimatisation
—> Accentuated ***alveolar hypoxia
—> Accentuated ***pulmonary HT (also induced by cold, exercise)
—> Mechanical stress on endothelium
—> Vulnerable endothelium / epithelium (also induced by viral infection)
—> Fluid leak
—> ***Interstitial and Alveolar edema
—> ***HAPE
—> Hypoxia
—> Worsen pulmonary HT (+ potentially HACE)
—> Vicious cycle

Inherent characteristics for pulmonary HT:

  1. Blunted hypoxic ventilatory response
  2. Brisk hypoxic pulmonary vascular response (i.e. vasoconstriction)
  3. Decreased NO synthesis
  4. Increased sympathetic tone
  5. Genetic determinants
Diagnosis of HAPE:
***Lake Louise Consensus Definition
Symptoms (>=2):
- SOB at rest
- Cough
- Weakness / Decreased exercise performance
- Chest tightness / congestion

Signs (>=2):

  • Crackles / wheezing in >=1 lung field
  • Tachypnea
  • Tachycardia
  • Central cyanosis (desaturation)
22
Q

Management of HAPE

A
  1. ***O2 (4-6 L/min until improved —> then 2-4 L/min to keep SpO2 >=90%)
  2. Minimise exertion
  3. Descend / Evacuation >=1000m
  4. ***Portable hyperbaric therapy if cannot descend
  5. ***Nifedipine 10mg PO (pulmonary artery vasodilation) —> then 30mg SR QD/BD
  6. ***Inhaled Beta agonist (e.g. Ventolin)
  7. EPAP mask
  8. Dexamethasone (only if HACE develops)
23
Q

Hypothermia

A

Rule of 3 in survival:

  • 3 mins without air
  • 3 hours without shelter (Hypothermia)
  • 3 days without water
  • 3 weeks without food

Hypothermia:

  • Core body temp ***<35oC (95oF)
  • Mild: 32-35oC
  • Moderate: 28-32oC
  • Severe: <28oC

Environmental temp determined by:

  1. Ambient temp
  2. Wind speed (protected by shelter) —> Wind Chill Chart

Causes:

  1. Environmental
  2. Sepsis
  3. Hypothyroidism
  4. Alcohol (diuretic + vasodilation)
  5. Opioid (sedation)
24
Q

Physiological response to cold

A
  1. Vasoconstriction
  2. Lateral Spinothalamic tract —> Hypothalamus
    - Shivering
    - Stress hormone release (ACTH, TSH, Insulin, Catecholamine)
  3. Behavioural
    - Put on more clothing
25
Q

Pathophysiology of Hypothermia

A

All cells + tissues affected —> Organ dysfunctions

  1. CNS depression
  2. Cardiac depression / arrhythmia
  3. Respiratory depression
  4. Metabolic acidosis (∵ Inadequate perfusion)
  5. Volume depletion (∵ cold-induced diuresis)
(Cold-induced diuresis:
- Peripheral vasoconstriction
—> ↑ Central blood volume
—> Inhibition of ADH release
—> Diuresis)
26
Q

***Diagnosis of Hypothermia

A
  1. Clinical S/S (***”Umbles”)
    - Stumble (ataxia, unsteady gait)
    - Grumble (dysarthria)
    - Mumble (cannot express clearly)
    - Fumble (clumsiness of hand)
    - Marble (torso feels like cold marble)

35oC: **maximum shivering thermogenesis
34oC: **maximum respiratory stimulation
33oC: **ataxia + apathy
32oC: stupor
31oC: **extinguished shivering thermogenesis
30oC: ***dilated + less reactive pupil, arrhythmia (e.g. AF)
29oC: decrease in level of consciousness, paradoxical undressing
28oC: decreased VF threshold
27oC: loss of reflexes
26oC: major acid-base disturbance
25oC: cerebral blood flow 1/3 of normal, loss of cerebrovascular autoregulation, CO 45% of normal, pulmonary edema may develop
24oC: significant hypotension + bradycardia

  1. Low reading thermometer
    - Rectal (time lag ~30 mins, but ***more accurate)
    - Tympanic
    - Mid-esophagus (real time but invasive)
27
Q

Initial management of Hypothermia

A
  1. ABC resuscitation
  2. Monitoring CVS system, Deep rectal temp
  3. Prevent heat loss
    - move patient to warm environment
    - create good shelter to protect from wind
    - insulate from ground
    - insulate the patient
    - remove wet clothing (to eliminate evaporative heat loss)
    - cover with vapour barrier (e.g. garbage bag)
  4. Rewarm
    - ***Passive (for mild hypothermia)
    —> wrap up patient for insulation
    —> provide drink with glucose
  • **Active external (for moderate / severe hypothermia)
    —> hot pad (beware of excessive heat causing burn)
    —> lying by side of normothermic person in a sleeping bag
    —> do **    NOT rub / massage —> damage to skin —> worsen thermodamage
  • ***Active core
  1. Treat underlying problems
    - e.g. sepsis, metabolic disorder, drug overdose
  2. Consider evacuation
    - all patients other than mild hypothermia (esp. those with trauma / other problems)
28
Q

ED management of Hypothermia

A

Mild (32-35oC):

  • Thermoregulatory mechanism intact
  • Keep away from cold environment
  • ***Passive rewarming
  • May consider External rewarming
  • Warm IV fluid replacement if prolonged exposure (X Dextrose solution ∵ bacterial growth in thawed solution)

Moderate / Severe:

  • ***Active external rewarming (for moderate hypothermia)
  • **Active core rewarming (necessary for **cardiovascular instability)
  • Target >1oC / hour (depending on CVS status)
29
Q

External + Core rewarming rate

A

External:

  • Simple blanket: 0.5 oC/hr
  • Space blanket: 0.6 oC/hr
  • Warmed blanket: 0.9 oC/hr
  • Whole body immersion: 2.2 oC/hr
  • Forced air: 2.4 oC/hr

Core:

  • Chest tube lavage (500 mL/min): 6.1 oC/hr
  • Chest tube lavage (2 L/min): 19.7 oC/hr (SE: infection, organ bleeding, injury)
  • Peritoneal lavage: 1-3 oC/hr
  • Extracorporeal: 2.1 oC/hr
  • Cardiopulmonary bypass: 6.9 oC/hr
  • Heated O2 by mask: 0.7 oC/hr
  • Heated O2 by ETT: 1.2 oC/hr
  • Warmed IV fluid: 0.3 oC/hr
  • Gastric lavage: 1-1.5 oC/hr
  • Bladder lavage: 1-1.5 oC/hr
30
Q

Complications of rewarming

A
  1. Rewarming ***shock (∵ marked vasodilatation by rewarming)
  2. Rewarming ***acidosis (∵ recirculation of pooled lactic acid)
  3. ***Afterdrop effect (∵ cold peripheral blood rapidly returns to heart —> minimised by core rewarming before external rewarming)
31
Q

Pre-hospital management of apparent cardiac arrest

A
  1. Ventilate for ***3 mins if no pulse detected initially after 30-60s (long period pulse detection required ∵ profound bradycardia)
    - Avoid hyperventilation (∵ alkalosis may precipitate VF)
  2. Start CPR if no pulse detected ***after ventilation, optimal rate unknown
    - do NOT start CPR immediately after no pulse detected ∵ CPR may precipitate VF / asystolic (∵ cardiac membrane sensitive to movement)
32
Q

Frostbite

A

Cold exposure, particular temp ***< -15oC
—> Tissue hard, pale, anaesthetic

Grading:

  • 1st degree: only outer part of skin, no lasting problems
  • 2nd degree: clear blister
  • 3rd degree: haemorrhagic blister
  • 4th degree: full thickness skin damage —> no blister

Management:

  1. Treat hypothermia first
  2. Prevent further cold injury
  3. Maintain hydration
  4. Protect frostbitten tissue with ***dry, bulky dressing
  5. ***Ibuprofen (for anti inflammatory + analgesic effect)
  6. Thawing
    - circulate warm (    37-39oC) water around frozen tissue in a bath for 30mins
    - analgesic for pain during rewarming

Don’t:

  1. Rub frozen part
  2. Apply ice / snow
  3. Thaw frostbitten part in cold water
  4. Thaw frostbitten part with high temp (e.g. stoves)
  5. Break blister
  6. Alcohol / Tobacco

Prevention:

  1. Keep skin dry + warm
  2. Extremity at risk for frostbite (e.g. numb, poor dexterity, pale colour) —> warmed with adjacent body heat

SC Multidisciplinary (10 decks)

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