Environment Flashcards
Burns
High Altitude Illness
Spectrum of illness from AMS -> HAPE/HACE
RF
- Rapid ascent
- Sleeping altitude
- Hypoxic ventilatory response
- Younger age
- Cardio-respiratory disease
- Previous altitude sickness, living at low altitude and return from low altitude if residing at high altitude
AMS
- > 2,500m
- “A little brain swelling”
- “Hangover” - loss of appetite, N/V, headache
- Sleep disturbance
- Last 2-3 days and usually self-limiting
HAPE
- Most common killer
- > 3000m
- PHTN => leaky capillaries => non-cardiogenic pulmonary oedema
- Sx like pneumonia - SOBAR, cough, crackles, hypoxia, fever
HACE
- Most severe, uncommon
- > 4500m
- Onset 2-3d
- “A lot of brain swelling”
- Sx: ataxia (early), lethargy, AMS, seizure
Mx
- O2
- Descent
- AMS: Analgesia, Dexamethasone, Acetazolamide
- HAPE: Nifedipine, PDE in hibitors, HBO
- HACE: Acetazolamide, dexamethasone, HBOT
- Never ascend until Sx resolve
High Altitude Physiology
Hypobaric hypoxia - high altitude => dec barometric pressure => low PaO2
Hypoxia => pulmonary vasoconstriction => PHTN => HAPE
Hypoxia => cerebral vasodilation => AMS / HACE
Acclimatisation
- Hypoxic ventilatory response = hypoxia stimulates carotid bodies => hyperventilation
- PaO2 rises, PaCO2 falls => resp alkalosis
- Kidneys compensate => dumping bicarbonate
- Acetazolamide
- Speeds up acclimatisation
- Carbonic anhydrase inhibitor
- HCO3 diuresis
- Creates metabolic acidosis
- Leads to hyperventilation
Radiation - ARS
Treatment for Radionuclides
- KCl - Iodine
- DTPA - Californium, Iridium, Cobalt, Plutonium, Americium
- HCO3 - Uranium
- Phosphorus - Phopshorus
- Prussian Blue - Cesium
- Water diuresis - Tritium
Oxygen Toxicity
> 24 hours after inhaling high [O2]
Muscle twitching esp lips/face
Nausea, agitation, confusion, vertigo
Seizures
Permanent CNS dysfunction
Resp failure
Ocular damage
Nitrogen Narcosis
Risk w/ dives > 100ft
> 150ft inc risk of drowning
Symptoms on descent and resolve on ascent
At increasing depths, inc PaN2 so N2 dissolves into tissues more readily
Rx
Ascent
Prevention
Dive safety reinforced
Basic divers limited to 40m depth
Deeper dives require dive partner + Heliox
Arterial Gas Embolism
Bubbles gas forced form alveoli -> pulmonary capillaries ->systemic circulation -> CVS or CNS complications
MAJOR NEURO Sx and signs within seconds to minutes of ascent
NEURO
Sudden AMS / LOC / seizure
CARDIAC
AMI or dysrrhytmias
Mx
Horizontal position to avoid reembolisation
100% O2
Hyperbaric oxygen
NEEDS FINISHING
Diving Reflex
The diving reflex -> peripheral vasoconstriction, bradycardia, and decreased cardiac output
When the face is submerged and water fills the nostrils, trigeminal nerve receptors relay info to the Medulla.
The vagus nerve produces bradycardia , bronchoconstriction
Other neural pathways elicit peripheral vasoconstriction.
Ultimately restricting blood flow to limbs and all organs to preserve blood and oxygen for the heart/brain/lungs
Allows diver to conserve oxygen -> longer dive time
Diving history - important factors
Number of dives
Depth
Bottom time
Decompression stops
Complications i.e rapid ascent
Eqpt used
Strenuous exercise within 4 hours of dive
Medical risk factors
- resp history
- altitude exposure
Hyperbaric oxygen
- Increases dissolved O2 delivery
- Reduction gas bubble size
- Antagonism CO
- Improved wound healing
Indications:
1. DCI
2. AGE
3. Necrotising soft tisuse infections
4. CO poisoning
Complications
1. Reversible myopia
2. Otic barotrauma
3. Pulmonary barotrauma
4. Pulmonary O2 toxicity -> resp failure
5. Seizures
Problems of Ascent
Problems of ascent
Due to gas bubbles forming in blood and tissues
Incidence 2-3/10,000 dives
Frostbite
Frostbite only occurs when the tissue gets below 0ºC. (Usually more likely -4º to -10º
C)
Tissue injury due to ice crystal formation, microvascular thrombosis and stasis.
Grading
* 1 = no cyanosis on the extremity. This predicts no amputation and no sequelae
* 2 = cyanosis isolated to the distal phalanx. This predicts only soft tissue amputation and fingernail or toenail sequelae
* 3 = intermediate and proximal phalangeal cyanosis. This predicts bone amputation of the digit and functional sequelae
* 4 = cyanosis over the carpal or tarsal bones. This predicts bone amputation of the limb with functional sequelae.
Mx
Principles / Priorities
1. Prevent re-freeze injury & thaw
2. Analgesia
3. Wound care
4. Tetanus prophylaxis
5. Consider if there is a role for thrombolytic therapy (IV or IA)
6. Post-thaw wound care and follow-up
PRE-HOSPITAL
DO:
* Remove from the cold environment
* Prevent any thaw-refreeze cycles
* Remove constricting and wet clothing
* Insulate and immobilize the affected areas
* If unable to evacuate thaw in 37-39 degree water
DON’T
* Use dry heat sources / heat forced air / fire
* Rub the tissue vigorously
HOSPITAL
Prethaw
1. Attend to resus needs + core temperature stabilisation
2. Assess Doppler pulses and appearance.
Thaw
1. Analgesia
2. Immer part in circulating water at 37° C–39° C monitored by thermometer.
Postthaw
1. Vesicle Mx
a. Aspirate or débride clear vesicles.
b. Débride broken vesicles and apply topical ABx or sterile aloe vera ointment every 6
hours.
c. Leave hemorrhagic vesicles intact.
2. Tetanus prophylaxis
3. Streptococcal prophylaxis if high risk.
4. Consider phenoxybenzamine in severe cases.
5. Imaging, including angiography, if thrombolysis may be indicated.
Risk Factors for Cold and Heat injuries
Trenchfoot
Immersion injury or damp conditions over days
* Neurovascular damage, blistering and tissue loss can occur
Stages:
1. Cold exposure -> numbness
* Red -> pale -> white tissue
* Lasts until out of the cold
2. Rewarming - mottling, pale blue
* Cold and numb and progresses to pain and edema
* Can last days
3. Hyperemia:
* Hot, red and prolonged cap refill
* Vasomotor paralysis
* Severe pain, hyperalgesia
* Edema and bullae formation
* Can last weeks to months
4. Post-hyperemia
* Normal appearance unless tissue lost
* May have chronic pain
Chillblains
Chilblains (Perino)
* Due to repetitive exposure to cold conditions +/- underlying risk factors
* Look like cold sores that appear within 24 hrs after exposure to cold
o Face, hands, feet, tibia
* Risk groups: Young women, Raynaud’s / SLE / APLAb pts.
* Symptoms: burning, pruritus, erythema, edema.
* Resolves in 1-2 weeks.
* Analgesia; consider nifedipine
Heat Exhaustion vs Heat Stroke
Cooling techniques
Warming techniques
Lightening Injury
Voltage 2-100m V
DC shock causing Asystole (Household = AC -> VF)
Pregnancy = high change of IUD
Types of strike
1. Direct = current discharges through body
2. Side flash = primary strike to another object i.e. tree and then onto victim
3. Flashover = energy flows over surface of victim
4. Ground Current = stikes earth and spread via ground to victim
5. Blast Injury
Effects of Lightening Strike
1. CVS - Asystole w/ spontaneous reversiont to SR
2. CNS - Confusion, amnesia, Coma, ANS and PNS dysfunction
3. Resp - Apnoea - may need prolonged ventilation
4. Trauma
- Direct
- Blast
- Thermal
5. MSK
- Keraunoparalyis - vasopspasm -> glaccid paralysis, sensory loss and vascular compromise
6. Skin - Lichtenberg Flowers - may dvp slowly then disappear by 24 hrs
7. Other
- ENT - Vestibular dysfunction, senorineural deafness
- Ocular - optic nerve damage, retinal detachment, cartaracts
- Metabolic - rhabdomyolysis
Frostbite Grading / Prognosis
Drowning - Pathophysiology
Drowning results from respiratory impairment after submersion in a liquid.
The diving reflex – bradycardia, apnea, peripheral constriction – is thought to be protective, but few experience this.
Irreversible neuronal cell injury can start as early as 4-6 minutes into hypoxemia.
Pathophysiology
1. Voluntary breath holding
2. Involuntary laryngospasm secondary to liquid in oropharynx / larynx
3. Worsening hypoxia results in laryngospasm abating
4. Subsequent active aspiration of liquid
5. Results in loss of surfactant, pulmonary edema, and hypoxia, which in turn can lead to multiorgan dysfunction and cardiac arrest.
Drowning - Prognosticators
Prognosis
*no clinical score 100% accurately predicts which patients will survive the drowning event
Submersion Time
-85% of survivors with good neurological recovery are submerged < 6 minutes
-7.5% for 6–10 minutes
-5% for 11–59 minutes
-<1% greater than 60 minutes
-> 10 minutes is considered a possible cut-off point for non-survival
Efficiency of initial resuscitation influences outcome
Water temperature no longer believed to influence outcome
Non-reactive pupils and a GCS of 5 on arrival in ICU are the best independent predictors of a poor neurological outcome
Time of first spontaneous respiratory effort
-if < 15 - 30 minutes, < 10% have significant neurological deficit
-if 60 - 120 minutes, 50 - 80% chance serious neurological damage
Orlowski scale
*age < 3 years
*estimated submersion > 5 minutes
*no attempted resuscitation in the first 10 minutes after rescue
*coma on arrival at the ED
*metabolic acidosis on arrival with pH < 7.10
-90% chance of good recovery if < 3 of the above present
-5% recovery if > 3 present
Other prognostic factors
* On arrival to ED good prognosis with
- Spontaneous respiration and heart beat
- VT / VF on initial ECG (compared to asystole)
* Poor prognosis
- Resuscitation duration > 25 minutes
- Fixed dilated pupils
- Cardio or respiratory arrest
CPR Futility in Drowning
- Water temperature > 6C and immersion time > 30 min
- Water temperature < 6C and immersion time > 90 min
- Submersion > 10 min without hypothermia
- Persistent apnoea and asystole after 1 hour of post-rescue CPR provided not hypothermic
- Serum K+ > 11 mmol/L
- Blood is frozen
Crush Syndrome
CRUSH INJURY = Compression of extremitites or part of the body causing muscle swelling +/- neurovascular distubance
Lower limbs > upper limbs > thorax
CRUSH SYNDROME = crush injury + systemic manifestations
Causes
Trauma
Limb #
Severe compression of limb
Electrocution
Severe burns
Prolonged immobilisation
Drugs / Alcohol
Neurological events
External compression - plasters / bandages
Complications
* Compartment syndrome
* Metabolic
* Rhabdomyolysis
* ARF
* Direct effects of myoglobin
* Hyperkalaemia / hyperphosphataemia / hypocalcaemia
* Lactoc acidosis
* Coagulopathy
* K/Ca causing dysrrhythmias / cardiac arrest (worsened by lactoc acidosis)
* Hypotension from massive 3rd spacing
* Skin ulceration and wound complications
Prehospital Mx
* Tourniquet of affected limb
* IVF prior to release affected limb/region (aim UO 1-2ml/kg/hr)
* Mx metabolic abnormalities
* NaHCO3 for acidosis
* Ca gluconate / insulin dextrose for Hyperkalaemia
* Monitor for cardiac arrhythmias
* Monitor for compartment Syndrome / vascular or neurological compromise
Hospital
* Resuscitation of shocked patient
* IVF - CSL - aiming for MAP 65 and OU 1-2ml/kg/hr
* NaHCO3 for acidosis
* Staged Tourniquet Release
* Rx metabolic complications such as those listed above
* Mx all other injuries
* Early analgesia, IV ABx and tetanus
Suspension Injury Pathophysiology
Suspension Injury Reperfusion Injury
Suspension Cardioplegia
Myocardial stunning occurring from uncontrolled release of compression force, harness or tourniquet
All pooled “cold” blood rushed to Right heart -> sudden inc preload and sudden right atrial stretch
Destabilises myocardium into aystole or AF
Simultaneous sudden dec in SVR and afterload as blood rushed back into reperfusing limb = cardioplegic solution
Metabolic abN may devlop over time
Tourniquet
Tourniquet
Crush / Suspension syndromes
Arterial bleeding
Max time: 2 hours
Max pressure
UL - 250 mmHg
LL - 350 mmHg
Complications
Neuropraxia
Limb ischaemia
Compartment Syndrome
Reperfusion Injury
Rhabdomyolysis
CI
Vascular grafts - PVD
High risk DVT - multi-system trauma
Taser
Major Concerns
1. Inducing cardiac arrhythmias
2. PPM interferance
3. Risk of sudden death
Considerations
Penetrating injury / wounds from barb
Trauma from fall
Cardiac injury - PPM, multiple shocks
Reason for taser - MH, drugs, medical illness
Pregnant pt
Mx
ECG
PPM check
Bloods - Trop, CK
Xray
- CXR - trauma, PTx, pneumomediastinum
- Trauma assessment
ADT
Wound closure if appropriate
CTG if pregnant
Electrical Injury
