KC Environment Flashcards
*What are the definitions of mild, moderate, severe and profound hypothermia?
- Mild: 33-35 degrees Celsius
- Moderate: 29-32 degrees Celsius
- Severe: 22-28 degrees Celsius
- Profound: 20 degrees and lower
*What are the indications for active external rewarming?
Previously healthy patients with acute hypothermia are optimal candidates for AER
*What are the indications for active core rewarming?
- Moderate or severe hypothermia (temperature <= 32 degrees Celsius)
- Cardiovascular instability
- Inadequate rate of rewarming or failure to rewarm
- Endocrinologic insufficiency (e.g. adrenal insufficiency, DKA, hypopit)
- Traumatic or toxicological peripheral vasodilation (e.g. spinal cord transection)
- Secondary hypothermia impairing thermoregulation
*Temperature doesn’t rise with interventions, why not?
(1) Adrenal insufficiency - give methylprednisolone or hydrocortisone.
(2) Myxedema - levothyroxine
(3) Sepsis - Ab
(4) Hypoglycemia - D50
*5 methods of heat loss
- Radiation
- Conduction
- Convection
- Respiration
- Evaporation
*5 methods of noninvasive rewarming
Rewarming options include plumbed garments that circulate warm fluids, hot water bottles, heating pads, forced air warming systems, and radiant sources.
*2 methods of invasive rewarming
Airway rewarming
Peritoneal dialysis
Heated irrigation
Endovascular rewarming
ECMO rewarming
*4 causes of failure to rewarm and interventions for each
(1) Adrenal insufficiency - give methylprednisolone or hydrocortisone.
(2) Myxedema - levothyroxine
(3) Sepsis - Ab
(4) Hypoglycemia - D50
*In the setting of hypothermia, please provide the temperature at which the following physiologic changes occur
1 Ataxia and apathy develop
2 Extinguishing of shivering thermogenesis
3 At this temperature the body assumes a poikilothermic state
4 Temperature above which ACLS medications are indicated for arrested patient
5 Onset of VF susceptibility; 50% decrease in 02 consumption
1 Ataxia and apathy develop -33
2 Extinguishing of shivering thermogenesis -31
3 At this temperature the body assumes a poikilothermic state -30
4 Temperature above which ACLS medications are indicated for arrested patient - 30
5 Onset of VF susceptibility; 50% decrease in 02 consumption - 28
*6 EKG changes in hypothermia
- Osborne waves
- Sinus Bradycardia
- Prolonged QT, PR, QRS
- VF
- Asystole
- Atrial fibrillation
*What effect does hypothermia have on the oxy-Hb dissociation curve
Left shift
*The ABG machine heats the blood to 37 C.
i) The result of the PO2 will appear higher/lower
ii) The result of the pH will appear higher/lower
i) Increases the partial pressure of blood gases – higher P02 and higher PC02
ii) Lower ph
*4 mechanisms of heat loss in the treatment of hyperthermia and list 1 example for each
- Conduction - cool water bath
- Convection - fan at bedside
- Radiation - take off clothes (facilitate radiation)
- Evaporation – spray with normothermic mist
*3 immediate treatments for core temp <28
Active rewarming, options listed above
2 end points for termination of resusciation of *hypothermic patient
Temp > 32 with asystole on monitor and no cardiac activity on US
Valid DNR order
obvious signs of irreversible death - non compressive chest, decapitation
conditions unsafe for rescuers
avalanche burial 35 min or +, airway packed with snow
serum K+> 12
*Risk factors for Hypothermia in elderly patients
-Poly-pharmacy / medications
-Dementia/ cognitive deficits
-Poor (low socioeconomic)
-Endocrine disease
-Malnourished
-Social isolation
-Age (impaired thermoregulation)
*What 3 things can be done in a pre-hospital environment for this patient specifically to lower core temperature?
Ice water immersion
Removal from hot environment (move to ac, shade…)
Fan
Remove clothes
ICe packs.
*4 mechanisms of heat loss in the treatment of hyperthermia and list 1 example for each
-Conduction - cool water bath
-Convection - fan at bedside
-Radiation - take off clothes (facilitate radiation)
-Evaporation – spray with normothermic mist
*3 findings that differentiate heat stroke and heat exhaustion
Altered mental status
Core temperature >40.5 (loss of compensation)
End-organ damage
*6 pharmacologic causes of this presentation (different classes) (Hot and crazy)
- Anticholinergic
- Sympathomimetics
- EtOH withdrawal
- Benzo withdrawal
- ASA/clopidogrel
- NMS
- MH
*What are 3 management points for heat stroke
Cooling
Correct electrolyte imbalance/fluid deficit
Control seizure (benzo),
Limit shivering (paralysis and intubation PRN).
*List two early physiologic responses to heat stress
- earlier onset of sweating (ie at lower core temp)
- lowered sweat Na
- increased sweat V
- Expanded / increased plasma V
- Lower HR with higher stroke V
- earlier release of aldosterone (and lower amounts)
*One lab result most characteristic of heat stroke
Transaminitis
*Two ways of quickly cooling patients
- Evaporative cooling using fans and skin wetting (spraying)
- Ice water immersion (conduction)
*8 clinical features of heatstroke
• Exposure to heat stress, endogenous or exogenous
• Signs of severe central nervous system dysfunction (coma, seizures, delirium)
• Core temperature usually > 40.5° C (105° F), but may be lower
• Hot skin common, and sweating may persist
• Marked elevation of hepatic transaminase levels
- DIC
- Renal failure
- Rhabdo
- Diarrhea
- Pancreatitis …
*8 factors that impair the body’s ability to disperse or dissipate heat and which may predispose to heat stroke
No longer a table in new Rosens, but:
Pump: cardiac disease, beta blockers
Thermoregulation: age, chronci illness, CNS bleeding
Fluid: dehydration, inadequate fluid inatke
Evaporation: vaso-occlusive clothing, anticholinergic medication, burns
Increased production: fever, exercise, NMS, drugs, thyroid storm, malignant hyperthermia, seizures
*4 complications of heat stroke
CNS - cerebral edema, seizures, coma
CVS - peripheral vasodilation and central vasoconstriction
Liver - failure
Kidney - failure
Heme - DIC
Muscles - Rhabdo
Pancreas - itis
*4 examples of burns from electrical injuries
Entrance and exit site burns: deep tissue burns may be more significant than visible tissue burns
Arc burns, kissing burns: due to current jumping across flexed surfaces of the body
Thermal burns: due to fire started by lightning
Flash burns: skin burns caused by brief flashes of electrical current or radiation
*6 physical exam findings suggestive of a lightning strike, other than burns
CNS: Apnea, LOC, amnesia, peripheral nerve damage/paralysis, keraunoparalysis, seizures, cerebellar ataxia, cognitive dysfunction, facial nerve paralysis,
CVS: Asystole, dysrhythmias, vasospasm
HEENT: Tympanic membrane rupture, hearing loss, tinnitus, vertigo, nystagmus, cataracts
Resp: Respiratory muscle/centre paralysis
GI: Pancreatitis, solid organ injury, hepatitis, rhabomyolysis
MSK: Fracture, dislocation, rhabdomyolysis, compartment syndrome, osteonecrosis
*5 potential ECG findings after a lightning injury
ST segment elevation
QT interval prolongation
Atrial fibrillation
Inverted or flattened T waves
Myocardial infarction pattern without cardiac sequelae
*What is EMSs top priority in managing the scene of a lightening strike?
- Secure the scene
- Triage
- VSA first ** as pts rarely die from lightning unless present with cardiac arrest “At some point, the intrinsic pacemaker activity of the heart brings about a resumption of cardiac activity. However, if the respiratory center has not been reactivated, hypoxia follows, and the cardiac rhythm will deteriorate into ventricular fibrillation.”
*Injuries listed – more likely caused by electrical injury or lightning?
- Rhabdo (E)
- TM perf (L)
- Keraunoparalysis (L)
- Vascular thrombosis (E)
- Pulmonary Contusion (L)
*5 ways in which lightening can injure a casualty
- Force of the strike
- Blunt trauma from being thrown
- Superheating of metallic objects in contact
- Blast-type effects and barotrauma
- Shrapnel
*Fernlike patterns of erythematous streaks
Lichtenberg figure
*6 indications for ECG monitoring in electrical injury
Not in new Rosen, but indications are listed for lightning: suspected direct strike, loss of consciousness, focal neurologic complaint, chest pain or dyspnea, associated traumatic injuries, pregnancy, and burns of the cranium or legs or on more than 10% of the total body surface area.
*4 ddx for chest and shoulder pain and mottling 24 hours post dive
DCS I
Lymphatic obstruction
Trauma?
Compartment syndrome?
?PTX
*3 things that can happen at depth
Nitrogen narcosis
Oxgen toxicity
Contaminated air
Hypothermia
Trauma
Drowning
*6 features of a dive profile
Depth
Length of the dive (bottom time)
Speed or time of ascent
Safety stop time and depth
Number of dives
Surface interval time
*1 thing you can do in the ED
100% oxygen
*Disposition
Hyperbaric chamber
*What are the formulas and descriptions for:
- Boyle’s law
- Dalton’s law
- Henry’s law
Boyle’s law: P1V1 = P2V2 (Pressure and volume are inversely proportional)
Dalton’s law: Pt = P1 + P2 + P3 … (Total pressure in a space is equal to the sum of all the gases)
Henry’s law: C=kPgas (The amount of a gas that will dissolve in a liquid at a given temperature is directly proportional to the partial pressure of that gas); this is the law that governs hyperbarics
*Scuba diver, unconscious, lateralizing to the right… 5 things on the differential
o AGE
o DCS II (involves CNS, inner ear, or lungs)
o SAH
o ischemic stroke
o CO toxicity
o post-ictal todd’s paralysis
*3 indications for hyperbaric oxygen after diving
o Decompression sickness Type 1
o Decompression sickness Type 2
o Arterial gas embolism
o Contaminated air (CO poisoning)
*One treatment to start before hyperbaric
100% oxygen
*One resource to consult
Diver Alert Network
*Diving stem: inexperienced divers dive to 130 feet (lost track of time/depth?), presents to ED with headache, malaise, lethargy onset right after surfacing, now neurologically normal. Choose the LEAST likely diagnosis:
a) DCS II
b) AGE
c) nitrogen narcosis
d) near drowning
*True or False
a At least 5% of near submersions have associated c‐spine injuries
b Antibiotics for submersion related aspiration are indicated
c DCS II commonly presents with loss of consciousness
a False
b False
c True
*Risk factors for DCS
age, obesity, fatigue, heavy exertion, dehydration, fever, cold ambient temperatures after diving, diving at high altitude, and flying after diving
*Contraindications for HBO
Not in new Rosen
-pneumothorax (untreated)
-pacemaker (can malfunction)
-claustrophobia
-history of seizures (decreases seizure threshold)
*Treatment options for DCS I
Fluids, analgesia, oxygen, HBO
*Patient is spending time at 4000 m, s/s: headache, fatigue, anorexia, dizziness: What is the diagnosis ?
AMS
*2 physiologic EARLY adaptations and what their mechanism is?
Hypoxic ventilatory response: increase in minute ventilation decreases the partial pressure of carbon dioxide in the alveolus and increases the partial pressure of oxygen in the alveolus. This results in a respiratory alkalosis; which limits the response
Hypoxemia also results in an increase in 2,3-diphosphoglycerate, causing a rightward shift of the oxyhemoglobin dissociation curve, which favors a release of oxygen from the blood to the tissues. This is counteracted by the leftward shift of the oxyhemoglobin dissociation curve caused by the respiratory alkalosis from hyperventilation.
Rapid release of catecholamines, increasing cardiac output and elevations in heart rate, stroke volume, blood pressure, and venous tone.
Erythropoietin is secreted in response to hypoxemia within hours of ascent, which in turn stimulates the production of red blood cells, leading to new circulatory red blood cells in 4 or 5 days.
*Two ways the Hb-oxygen dissociation curve changes at altitude and why?
2,3 DPG to the right to compensated by the decrease in CO2 (alkalosis) which shifts to the left
*3 non-pharmacologic ways to prevent AMS
- Slow ascent (gradual introduction of higher altitude)
- Allow time for acclimation period (ie, stay at basecamp to acclimate prior to ascent)
- Stay well hydrated
*2 treatments, their class, and mechanism of effect
Acetazolamide (carbonic anhydrase inhibitor): increases minute ventilation and enhances renal bicarb diuresis
Dexamethasone (steroid): anti-inflammatory, reduces cerebral blood flow and the release of inflammatoyr growth factors
*you decide to go on a relaxing weekend getaway vacation to the base-camp of K2. At 12,000 ft, a 28 year old male on vacation himself presents to you with headache, nausea, fatigue and malaise.
a. What could prevent this? (3)
- Gradual ascent
- Mild exercise
- Maintain hydration (not over hydrate, use balanced solution)
- Acetazolamide: 250mg BID 24H before and 1st 2 days
- Dexamethasone: 8mg first then at 4mg Q 6H if Acetaz not available
- Oxygen
*you decide to go on a relaxing weekend getaway vacation to the base-camp of K2. At 12,000 ft, a 28 year old male on vacation himself presents to you with headache, nausea, fatigue and malaise. You note that he is desating, has developed crackles and is looking more unwell. Please outline your further management of this patient.
- Immediate descent 1,500-3,000 feet
- Supplemental oxygen/Gamow Bag/Hyperbaric oxygen
- Nifedipine*
- Sildenafil*
- Acetazolamide**
- Rx with Abx if cant r/o pneumonia
- DO NOT give lasix, bc not CHF, and probably already dry
*Lower pulmonary artery pressure, pulmonary blood volume, and pulmonary vascular resistance or enhance alveolar fluid clearance
**Enhances acclimatization by promoting renal bicarbonate diuresis, thus improving renal correction of ventilation- related respiratory alkalosis encouraging enhanced ventilation and arterial oxygenation
*How does acetazolamide work to prevent/treat AMS?
Increased minute ventilation,
HCO3 diuresis,
decreases nocturnal period breathing
also
It lowers CSF volume and pressure
upregulation of fluid resorption in the lungs
*3 drugs that can be used for AMS
Acetazolamide, O2, NSAIDs, tylenol, dexamethasone
*2 symptoms that would warrant immediate descent
ataxia, altered mental status, seizures, slurred speech, hallucination (ataxia is
most specific)
*4 physiologic changes involved in acclimatization to altitude
● increased RR (HVR)
● increased HR
● Increased EPO and resulting RBC production and blood volume
● Relase of catecholamines resulting in increased cardiac output
● bicarbonate diuresis
● Increase in 2,3-DPG
Hypoxic ventilatory response
*6 risk factors for altitude sickness
Travel details: rapid ascent, sleeping altitude, duration of stay, weather (ex. low pressure front), seasonal variations (lower barometric pressures during winter, making lower altitude ‘physiologically higher’), durating of stay
Patient details: underlying medical issues, genetic susceptibility (NOT older age), exercise tolerance
*4 treatment strategies for HACE
Descent
Hyperbarics
Pharmacologic (acetazolamide, dex, O2); caution with diuretics
Evaluate for trauma, CVA, intox
*Describe THREE pathophysiological injuries to the lung that contribute to hypoxia post- drowning
- Loss of surfactant due to wash out
- Alveolar collapse/atelectasis
- Non-cardiogenic pulmonary edema
- Intrapulmonary shunting (ventilation:perfusion ratio of 0)
*Define immersion syndrome
Syncope resulting from cardiac dysrhythmias on sudden contact with water that is at least 5 degrees Celsius lower than body temperature
*FIVE of the MOST important factors affecting outcome (ie survival) in drowning/near-drowning.
Environmental: water temperature, submersion time
Vitals: hypoxia, hypothermia
Rescue: initial rescue efforts, need for CPR
Patient: neurologic status (GCS), acidosis, pupils
*What are three criteria for discharge of a patient after a submersion injury?
- Asymptomatic
- Normal room air oxygen saturation
- Normal chest X-ray
- Normal blood gas
*Why should you never hyperventilate before diving?
Blackout
*Define: drowning, immersion syndrome, diving reflex
Drowning: “the process of experiencing respiratory impairment from submersion/immersion in liquid” (WHO)
Immersion syndrome: syncope from cold water + arrhythmia
Diving reflex: Activation of the diving reflex by fear or immersion of the face in cold water shunts blood centrally to the heart and brain. Apnea and bradycardia ensue, prolonging the duration of submersion tolerated without central nervous system (CNS) damage.
Describe the stages of freezing injuries
Prefreeze 0-10 degrees: superficial cooling and vasoconstriction, plasma leakage
Freeze-thaw (0 degrees): ice crystals form extracellularly -> osmotic diuresis -> intracellular dehydration -> cellular collapse
Vascular stasis and progressive ischemia (>10 degrees): inflammatory reaction leads to stasis coagulation, platelet aggregation, AV shunting, leukocyte immobilization, and damage to the microvasculature
List 10 predisposing risk factors
[Box 131.2]
Physiologic: poor physical condition, dermatologic disease, EtOH, diabetes, genetics, psychiatric illness, previous cold injury, trauma, dehydration, hypoxia
Mechanical: constrictive wet clothing, inadequate insulation, immobility
Psychological: mental status, fear, panic, peer pressure, attitude, fatigue, hunger, malnutrition, intoxicants
Environmental: temperature, wind chill, humidity, duration of exposure, heat loss through conduction (ex. through water), altitude, exposed surface area,
PmHx: atherosclerosis, arteritis, raynaud’s syndrome, cold-induced vasodilation, anemia, sickle cell disease, diabetes, vasoconstrictors, vasodilators
List 3 good prognostic signs in freezing injuries
Normal sensation/warm/colour after rewarming, soft pliable tissue, early formation of large blebs with clear fluid
What is frostnip
Superficial freezing injury with transient numbness and tingling that resolves after rewarming, no tissue destruction, sensory deficits in light tough/pain, temperature
How are freezing injuries classified
Superficial, deep
List 10 sequelae in freezing injuries
[Box 131.3]
Neuropathic: pain, complex regional pain, paresthesias, thermal sensitivity, autonomic dysfunction, Raynaud’s
MSK: compartment syndrome, rhabdo, ATN, atrophy, tenosynovitis, necrosis, amputation
Dermatologic: edema, lymphedema, ulcers, hair and nail deformities, squamous cell
Misc: cold temperature after drop, ATN, electrolyte fluxes, psychological stress, gangrene, sepsis
What is cold temperature after drop
Acute thawing causes cold, hyperkalemia, acidotic blood to rush back to the heart. May cause arrhythmia and Vfib
What are the stages of trench foot
Occurs without freezing of tissue due to prolonged exposure to wet and cold environments
Stage 1: cold exposure, extremities are white with vasoconstriction, feels numb but no pain or swelling
Stage 2: post cold exposure/rewarming: peripheral blood slowly returns and extremities become mottled and blue
Stage 3: hyperemia weeks-months: increased blood flow, hot and red extremity, severe pain, bullae can form
Stage 4: stabilization of skin, gangrege of tissue
(remember white -> blue -> red -> black)
What is pernio
Non Freezing injuries that cause cold sores, typically in susceptible individuals (ex. Raynaud’s)
List 10 factors that predispose patients to hypothermia
Box 132.1
- Decreased heat production
- Lack of fuel: hypoglycemia
- Endocrine failure: hypothyroid, hypoadrenalism, hypopituitarism
- Poor homeostasis: elderly (poor sensation, behavioral reaction, autonomic dysfunction)
- Increased heat loss
- Poor insulation: malnutrition, neonates
- Increased peripheral blood flow(erythroderma): psoriasis, dermatitis, eczema, burns
- Ethanol: less shivering, increased peripheral blood flow, poor adaptive behavior; paradoxical undressing
- Iatrogenic: exposure during resuscitation, cold fluids
- Impaired thermoregulation
- CNS: skull fractures (basal), chronic subdural hematoma, stroke, neoplasm
- Psych meds: antidepressants, antimanic, antipsychotics, anxiolytics
- Spinal cord transection
- Other
- Infection: sepsis, pneumonia, meningitis/encephalitis, atypicals
- Trauma: hypotension jeopardizes thermostability, hypothermic coagulopathy worsens bleeding”
List the stages of hypothermia and the clinical features associated with each stage
“Stage 1 mild: 33-35 degrees - increased shivering, increased metabolic rate, confusion but conscious i.e. amnesia and ataxia at 33 degrees, blood pressure and HR normal
Stage 2: moderate 29-32 degrees - decreased shivering (31 degrees), afib and other dysrhythmias, decreased LOC/stupor, decreased HR, RR
Stage 3: severe 20-28 degrees - fib, 50% decreased in O2 consumption, decreased LOC, decreased cerebral blood flow, loss of reflexes, major acid-base disturbances, hypotension
Stage 4: profound <20 degrees - asystole, vital signs absent”
List 3 cardiac symptoms of hypothermia
Bradycardia, J/Osborn waves, T wave inversions, prolonged PR/QRS/QTc, afib, v fib, asystole
List 3 CNS symptoms of hypothermia
Decreased LOC, decreased reflexes (initially increased), nystagmus, EOM abnormalities
List 5 differences in ACLS for the profoundly hypothermic patient
Longer pulse checks >1 min, max 1-3 doses of epi (consider withholding if <30), no evidence for other antiarrhythmics, max 1-3 shocks (defib usually unsuccessful if temp <30), transcutaneous is preferred over transvenous pacing, atropine in effective, do not terminate until warm and dead at 32 degrees
“Epi x 3, defib x 3, then no further until 30”
List 5 causes of J waves on ECG
Hypothermia, hypercalcemia, STEMI, sepsis, increased ICP, Brugada
List 3 types of rewarming strategies
Passive external (patient must be able to generate their own heat)
Active external: non invasive
Active internal: invasive
List 3 ways our body control heat regulation
Thermosensors in skin and hypothalamus
Central integrative area that receives info from thermosensors
Thermoregulatory effectors ex. sweat glands, vasodilation
4 types of minor heat illness
Prickly heat rash, heat cramps, heat syncope, heat edema
How does prickly heat rash develop
Blockage of sweat glands cause them to fill with keratin plugs, leads to pruritic vesicles
Presents with an intensely pruritic rash without sweating over clothes areas”
List 2 treatment strategies for heat rash
Chlorhexidine lotion or topical salicylate (avoid in children), wear light loose fitting clothing
What is the mechanism for the development of heat cramps
Thought to be related to salt content; treated with salt solutions. Usually occurs after exertion with copious sweating and replacement with isotonic fluid
What is the mechanism for the development of heat edema
Vascular leak due to increased peripheral blood flow and vasodilation
What is the mechanism for the development of heat syncope
Vasodilation and poor venous return; often from standing outside for long periods in warm weather
What are the two types of heat exhaustion
Water depletion: inadequate fluid intake with progressive hypovolemia
Salt depletion: large volumes of sweat are replaced with free water but no salt
What is the clinical presentation of heat exhaustion
Malaise, fatigue, headache, Hyponatremia and hypochloremia with low urine sodium
NO CNS dysfunction temp <40
What are the two types of heatstroke
Exertional: healthy young patients with exercise. Present with diaphoresis, hypoglycemia, DIC, rhabdo, renal failure, high lactate
Classic: older, sedentary individuals with high environmental temperatures. Present in heat waves with anhidrosis and normal labs in comparison to exertional heat stroke
List 7 differentials for the hot and altered patient
CNS hemorrhage, tox (ex. anticholinergic poisoning), seizures, malignant hyperthermia, meningitis/encephalitis, serotonin syndrome, NMS, thyroid storm, sepsis
What is our cooling target in heat stroke
39 degrees
List 5 ways to cool the patient
Remove clothing, fans + mist with cold water,* ice packs to the neck/groin/axilla*, cooling blankets, ice water immersion, peritoneal lavage/rectal lavage/gastric lavage (low evidence) *preferred
List that factors affect the degree of electrical injury
Voltage Can Cause ARCs: voltage, current, current type (AC/DC), amps, resistance, contact
What is the difference in the pattern of injury between DC and AC electrical exposures
DC: single, strong muscular contraction, limited exposure but force of fall can cause other injuries
AC: alternating current, tetany contractions can result in prolonged exposures
Compare tissues in terms of their resistance to current
Good conductors (low resistance): nerve -> blood vessel -> muscle -> dry skin -> tendon -> fat -> bone -> poor conductors (high resistance)
List 5 signs of a lightning strike
How is ACLS modified for lightning injuries
Reverse triage; those who appear dead get medical attention first
Compare the presentation of electrical vs lightning burns
Electrical: V fib >asystole, skin burns/kissing burns more common, joints and extremities more commonly affected, higher risk of muscle injury/compartment syndrome, may have transient LOC
List 4 mechanisms of injury in lightning strikes
Direct contact, side flashes, ground strike
List 5 injuries that occur on descent
Middle ear barotrauma, external ear barotrauma, inner ear barotrauma
Barosinusitis, facial barotrauma
What is the mechanism of external ear barotrauma
Obstruction of the auditory canal (wax, earplus) traps air, causing relative negative pressure and the tympanic membrane to rupture
What is the mechanism of middle ear barotrauma
As the diver descends, water exerts pressure on the tympanic membrane. Sx include pain, tinnitus, vertigo. Managed with equalization during descent
What is the mechanism of inner ear barotrauma
Pressure is transmitted from the middle ear down the oval window of the cochlea and through the ossicles; which can cause the round and oval window to rupture. Clinical similar to middle ear barotrauma; but may present with more vertigo
What injuries occur at depth
Nitrogen narcosis, oxygen toxicity
What gas law is relevant on ascent/descent
Boyle’s law
What gas law is relevant on depth
Dalton’s law
What is nitrogen narcosis
Increased ambient pressure increased the concentration of nitrogen at depth. Sx include euphoria, confusion, disorientation. This should resolve as the diver ascends and partial pressure of nitrogen increases
What is oxygen toxicity
Partial pressure of oxygen increases at depth; toxic level is beyond where most sport divers can go >218 feet
What gas law explains the pathophysiology of the bends
Henry’s law
What are 7 injuries that occur on ascent
Vertigo
Barodontalgia, GI barotrauma, pulmonary barotrauma
Decompression sickness, arterial gas embolism
When is the highest risk of barotrauma
Within the first 10 ft of water. As the pressure decreased volume in the alveoli increases; beyond their limit they rupture causing pneumothorax, pneumomediastinum, subcutaneous emphysema
What are 6 factors that increase the risk of barotrauma in asthmatics and COPDers
Box 135.2
- Bronchospasm and mucus plugging predispose certain area of the lung to injury
- Dense, compressed air results in turbulent airflow
- Breathing capacity is reduced due to the effects of immersion
- Scuba air is chilled and may trigger bronchospasm
- Scuba diving is effortful and exertional
- Compressed air may be contaminated by pollen and other allergens
What is decompression sickness
As the partial pressure of nitrogen decreases bubbles come out of solution. If this happens too quickly nitrogen accumulates and disrupts body tissues. A slow ascent allows gas to be carried to the vascular bed and exhaled
What are risk factors for decompression sickness
Dive factors: length and depth of the dive, flying after diving, type of gas used
Patient factors: age, obesity, fatigue, heavy exertion, fever
What is the no decompression limit
The maximum dive time based on the expected amount of dissolved nitrogen for a dive’s length and depth
What are the types of decompression sickness
Type 1: MSK (joint pain), skin (cutis marmorata), lymph
Type 2: any other organ system
Vertigo/cochlea: the ‘staggers’
Pulmonary ‘chokes’
CNS: limb weakness, spinal cord injuries (CNS has high limit content and more susceptible to nitrogen)
What is an arterial gas embolism
Air bubbles precipitate from the alveolar capillary membrane and into the venous system. Sx of cerebral embolism include altered LOC, headache, dizziness. Sx of pulmonary embolism include dyspnea, chest pain, hemoptysis.
Patient presents with ear pain during descent. Most likely diagnosis?
Middle ear if transient vertigo
Inner ear if more severe vertigo, nausea, nystagmus
Both can have ear pain, hearing loss
Patient presents with ear pain during ascent. Most likely diagnosis?
Alternobaric vertigo
Patient presents confusion after a dive. Most likely diagnosis?
“Decompression if delayed onset, longer and deeper dive, joint and neurologic pain
AGE if sudden onset (within 10 mins of ascent) independent of dive profile with more CNS sx”
List 5 potential injuries in scuba diving other than dysbarism
Environmental exposures: hypothermia, sunburn, trauma
Aquatic exposure: drowning, motion sickness, marine envenomations
List 5 risk factors for drowning injuries
Infants, men, alcohol, seizure disorder, autism or other behavioural health issues, prolonged QtC
How is ACLS modified for a drowning patient
No role for compressive only CPR; needs positive pressure ventilation. Intubation if PCO2 >50 or PaO2 <60
What is ionizing radiation and how does it cause damage
Particle: particles carry an electric charge ex. alpha particles, protons
Electromagnetic: ionizing radiation occurs in the form of high energy particles or rays ex. gamma rays
List 3 mechanisms of radiation exposure
Particles or high frequency have enough energy to producing ionization of the particles they encounter. This can cause direct damage (ex. damage to the DNA) or indirect (ex. free radical damage)
List 4 ways to quantify radiation
Irradiation, contamination (exposure to particles), and incorporation (ingestion or absorption)
List 4 ways to reduce radiation
Time, distance, shielding, quantity
What is acute radiation syndrome
Syndrome that occurs after exposed to whole body radiation. Includes stages:
Prodromal: non specific nausea, vomiting, fatigue, anorexia, diarrea
Latent: symptom improvement
Manifest: sub systems
Describe the hematopoietic syndrome and when does it occur?
Bone marrow suppression with lymphocyte suppression, thrombocytopenia, and immunosuppression. Occurs after 1-2 Grays. Treated with supportive care (prophylactic antibiotics), cytokine treatment, bone marrow transplant
Describe the GI syndrome and when does it occur?
N/V, GI bleeding, malabsorption, fluid losses.hypovolemia. Occurs at 5-7 days. Treated supportively
Describe the neurovascular syndrome and when does it occur?
Altered mental status with multiorgan failure, seizures, irritability, death. Occurs at 10-12 Grays. Comfort care
Describe the manifestations of local radiation injury that occur at the following levels: 3 Gy, 6Gy, 10 Gy, 15Gy, 25 Gy
Hair loss, erythema, dry desquamation, wet desquamation, necrosis
What is the best predictor of radiation injury
Lymphocyte count at 48 hours
List the antidotes for each of the following exposures: iodine, uranium, caesium, plutonium
Potassium iodide, bicarbonate, prussian blue, DTPA
List 6 universal precautions that should be taken by the health care provider when treating a patient with a radiation injury
1- Wearing rubber gloves x2
2- Patients outer clothes —> removed—> plastic container
3- wash with water and soap
4- The water to be collected in plastic containers ( radioactive waste)
5- Wound should be decontamination with high pressure irrigation
6- Decontamination should continue until the radiation reading is only 2 times background radiation
What score can you use to triage patients with hypothermia who may benefit from ECLS? What are the components and cut-off?
HOPE score
