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400 Cards in this Set
- Front
- Back
What is the most common freezing injury?
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Frostbite
|
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What is the most common non-freezing injury?
|
trench foot and immersion foot
|
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What injuries occur after exposure to dry cold?
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chilblains (pernio)
|
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What happens peripherally during cold stress?
|
peripheral vasoconstriction limits radiant heat loss
|
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What is cold-induced vasodilation?
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Recurring periods of vasodilation that interrupt cold-induced vasoconstriction in an attempt to protect the extremity
|
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When does frostbite occur?
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When the tissue temperature drops to less than 0C
|
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What are the putative mechanisms of tissue injury in frostbite?
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-architectural cellular damage from ice crystal formation
-microvascular thrombosis and stasis |
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What are the phases of freezing injury?
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Prefreeze phase (tissue cooling, microvascular vasoconstriction, endothelial plasma leakage)
freeze- thaw (ECF ice crystal formation, water exits the cell to maintain osmotic equilibrium, intracellular dehydration, cellular collapse and death) vascular stasis and progressive ischemia (microvascular collapse, rbc sludging, microthrombi formation, vascular endothelial cell damage, interstitial leakage, necrosis) |
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How long does the demarcation between viable and nonviable tissue in frostbite take?
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60-90 days (Frostbite in January, amputate in July)
|
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What are the categories of predisposing factors for cold injury?
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Physiologic (genetic, core temperature, previous cold injury)
Mechanical (constricting clothing, tight boots, immobility or cramped position) Psychological (mental status, fear, altitude) Environmental (ambient temperature, humidity, wind chill) Cardiovascular (hypotension, atherosclerosis, Raynaud's) |
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What is frost nip?
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A superficial cold insult manifested by transient numbness and tingling that resolves with rewarming (no tissue destruction)
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What is the most common presenting symptom of frostbite?
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numbness
|
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What specific locations are at risk for frostbite?
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fingers
toes nose ears penis |
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What are chilblains?
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A mild form of cold injury "cold sores" that appear less than 24 hours after exposure affecting facial areas, the dorsum of the hands and feet and the pretibial area
|
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What produces trench foot?
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Prolonged exposure to wet cold at temperatures above freezing
|
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What is the clinical hallmark of trench foot?
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After rewarming, the skin remains red, dry and very painful to touch
|
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What sign in frostbite is ominous?
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A residual violaceous hue after rewarming
|
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Discuss bleb formation and outcome?
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Early formation of clear large blebs that extend to the tips of digits is more favourable than delayed smaller hemorrhagic blebs
|
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What is the significance of edema in rewarmed frostbite?
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Post thaw edema usually develops in <3 hours
Lack of edema formation suggests significant tissue damage |
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What is the classification of frostbite?
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1st degree - anesthesia/erythema
2nd degree - superficial vesiculation surrounded by edema and erythema 3rd degree - deeper hemorrhagic vesicles 4th degree - extends into subcuticular, osseous and muscle tissues |
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Is classification of frostbite into degrees useful?
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No, it is often incorrect in relation to actual severity
|
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Can we predict actual tissue loss in frostbite? What is the best test?
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Not accurately
Scintigraphy may predict tissue loss |
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What should be done for frostbite in the field?
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Remove wet, constricting clothing
Insulate and immobilize extremities Avoid friction massaging Keep away from the dry heat (avoid a partial thaw) |
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Should tissue rewarming be initiated in the field?
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Not if there is any potential for interrupted or incomplete thawing
|
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How should frozen tissues be thawed?
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Rapid, active rewarming by immersion in gently circulating water 40-42debrees ideally circulating but a container is ok too
|
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Should the patient massage tissue during rewarming?
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NO, gentle motion should be encouraged
|
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What is the endpoint of thawing?
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Parts feel pliable and vital erythema is noted (usually 10-30 min)
|
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What is core-temperature after drop?
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Sudden return of cold, hyperkalemic, acidotic blood to the central circulation
|
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What is done after rewarming?
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dry
elevate gentle handling monitor tissue pressure consider thromboxane inhibition |
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What is the management of frostbite blisters?
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Broken blisters are derided
Clear blisters can be left intact, derided or aspirated Hemorrhagic blisters should not be derided (therefore you should aspirate them |
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What are organisms that can super infect frostbite?
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staph
strep pseudomonas |
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What is the management of chilblains?
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-supportive
-nifedipine (20-60mg QD) for perniosis -topical steroids -oral steroids -oral pentoxifylline -Limaprost |
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What are the only consensus treatments for frostbite?
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removal from cold
thawin gin 40-42 degree bath |
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What are potential adjunctive therapies for frostbite?
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Thrombolytics
heparin pentoxyfylline - decrease blood viscosity antiinflammatory steroids phenoxybenzamine (long acting alpha blocker) - decrease vasospasm HBO low molecular weight dextran sympathectomy medical sympathectomy with reserpine |
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What is the definition of hypothermia?
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Core Temp <35 degrees celsius
|
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How long can maximal heat production last?
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2 hours - b/c of fatigue and glycogen depletion
|
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What are the 5 mechanisms whereby heat is lost?
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radiation
conduction convection respiration evaporation |
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What heat conservation mechanisms are active at 32-37, 24-32, <24
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32-37 - vascoconstriction, shivering, non-shivering, endocrinologic thermogenesis
24-32 - decreased BMR without shivering thermogenesis <24 degrees autonomic and endocrinologic mechanisms become inactive |
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Are patients with hypothermia bradycardic or tachycardic?
|
tachy then brady
|
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Is the bradycardia of hypothermia responsive to atropine?
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No, because it is due to decreased spontaneous depolarization of pacemaker cells and not vagally mediated
|
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What are the ECG features of hypothermia?
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Osborn J waves at the junction of the QRS and ST segment
Atrial and ventricular dysrhythmiias prolonged PR, QRS and QT atrial fibrillation ventricular fibrillaiton and asystole |
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What is the "cold temperature after drop"?
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A further decline in an individuals core temperature after removal from the cold
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At what temperature does the EEG silence?
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19-20 degrees celsius
|
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What happens to the kidney in hypothermia?
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Cold diuresis of large amounts of dilute urine which does not clear nitrogenous waste
|
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What happens to the respiratory system in hypothermia?
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Decreased RR
CO2 retention Respiratory Acidosis Viscous bronchorrhea Decrease ciliary motility NCPE |
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What are the categories of predisposing factors to hypothermia?
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-decreased heat production (hypothyroid, hypoglycaemia, malnutrition)
-increased heat loss -impaired thermoregulation -miscellaneous |
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What are the 4 zones of hypothermia?
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Rosens
mild 32-35 moderate 28-32 severe 20-28 profound <20 ACLS >34 degrees - mild 30-34 - moderate <30 - severe |
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Describe reasons for decreased heat production?
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Endocrine failure (hypopituitarism, hypoadrenalism, hypothyroid, diabetes)
Malnutrition Large Surface area to volume ratio Extremes of age |
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Describe reasons for increased heat loss?
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Erythrodermas (dermatologic) - burns, psoriasis, ichthyosis
Environmental Exposure (iatrogenic) ethanol and drugs massive cold infusions |
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Describe reasons for impaired thermoregulation?
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CNS trauma
CVA Toxicologic Metabolic SAH Neoplasm Acute spinal cord transection (peripehral) |
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What is paradoxical undressing?
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Removal of clothing in response to cold stress (peripheral vasoconstrictive changes) - this may occur in EtOH intox or the elderly
|
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How does hypothermia exacerbate blood loss?
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It induces a coagulopathy via 3 mechanisms: coagulation cascade of enzymatic reactions is impaired, fibrinolytic activity is enhanced, platelets are sequestered and poorly functional
|
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What is the significance of non-reactive dilated pupils above 22 degrees?
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They likely reflect inadequate tissue perfusion
|
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Which reflex is the last to disappear with hypothermia?
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knee jerk
|
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How does myxedema affect the ankle jerk?
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It prolongs the relaxation phase more than the contraction phase
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Why are ABG values not accurate in hypothermia?
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Blood gas analyzers warm blood at 37 degrees celsius which increases the partial pressure of dissolved gases. Therefore pO2 and pCo2 levels are higher and pH is lower
|
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Should ABGs be corrected for temperature?
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No, the ida and strategy is to have an uncorrected pH at 7.4 and paCo2 at 40mmHg
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How do you interpret hematocrit in the hypothermic patient?
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It is typically deceptively high therefore a low-normal level in a moderate to severely hypothermic patient should suggest acute blood loss or pre-existing anemia
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Why should you perform frequent evaluations of serum electrolytes during rewarming?
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because there are no safe predictors of their values
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What is important to remember about hyperkalemia and hypothermia?
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Hypothermia enhances cardiac toxicity and obscures the premonitory ECG changes associated with hyperkalemia
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How can blood sugar help determine the aetiology of hypoglycaemia?
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Acute hypothermia elevates blood sugar level by inducing glycogenolysis while chronic hypothermia produces glycogen depletion
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What should be suspected if hyperglycaemia persists during rewarming?
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hemorrhagic pancreatitis
DKA |
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What is important about the treatment of DKA in a hypothermic patient?
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Insulin is ineffective below 30 degrees celsius therefore the patient needs to be rewarmed
|
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What should you know about coagulation studies in hypothermia?
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The coag testsare performed at 37 degrees therefore there is a discrepancy between the clinically evident coagulopathy and the deceptively normal PT/PTT/INR
|
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What is the treatment of hypothermic coagulopathy?
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rewarming
not administration of clotting factors |
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At core temperatures <32 celsium what should a physician expect?
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Irritable myocardium
Temperature gradient between core and periphery Relative hypovolemia |
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What are oral temperatures unreliable?
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<35
uncooperative patients low ambient temperature tachypneic patients |
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What are concerns about rectal temperature?
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It can lag behind core changes
It can be influenced by lower extremity temperatures and probe placement |
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Where should the rectal temperature probe be placed?
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Up 15cm
not in cold feces |
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Why do some reports mention hypothermic pulmonary edema?
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Likely because cold depresses ciliary activity which allows secretory accumulation and frothy sputum
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Why is physical exam of the abdomen unreliable in hypothermia?
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Cold induced rectus muscle rigidity
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because physical exam of the abdomen is unreliable, what abdominal problems do you need to think about in hypothermia?
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ileus
pancreatitis occult trauma |
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What is the initial fluid choice in an adult patient with moderate to severe hypothermia?
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250cc-500cc D5NS heated
|
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To what temperature should fluids be heated?
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40-42 degrees celsius
(avoid rapid central venous administration) |
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How can you heat IV fluid?
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microwave in a plastic container for 2 min at high
|
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At what core temperature are defibrillation attempts usually successful?
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28-30 degrees or higher
|
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If a patient fails to rewarm and there is evidence of adrenocortical insufficiency, what should be done?
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Administer 30mg/kg of methylprednisolone or 250mg hydrocortisone
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When and how do you administer thyroxine?
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-in patients thought to be myxedematous
-draw thyroid function tests -250-500ug levothyroxine IV over several minutes (also add hydrocortisone 100-200 mg to fluid) If there is no improvement T2 PO 25ug q 6hours |
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How do you perform passive rewarming?
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-cover the patient with on insulating material in favourable atmospheric conditions
-ambient temperature >21celsius |
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At what temperature does shivering stop?
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<30 degrees celsius
|
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What is the purpose of shivering?
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It is the thermoregulatory neuromuscular response to cold that increases heat production from 250-1000kcal/hr
|
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What are recommended rewarming rates?
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0.5-2.0degrees celsius
|
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What is necessary for passive rewarming?
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Patient must be able to metabolically generate sufficient heat to maintain an acceptable rate of spontaneous rewarming
|
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What are indications for active rewarming?
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-CV instability
-Moderate to severe hypothermia (t<32.3) -Inadequate rate or failure to rewarm -Endocrinologic insufficiency (thyroid, pituitary, Wernicke's, DKA) -Traumatic or toxicologic peripheral vasodilation -secondary hypothermia impairing thermoregulation |
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What are methods for active external rewarming?
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Immersion in a 40C bath
plumbed garments hot water bottles heating pads forced air warming radiant sources arteriovenous anastomoses (immersion of distal parts of extremities in 44-45C) -negative pressure rewarming |
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What are ways to perform active core rewarming?
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Airway rewarming (heated humidified O2)
warmed IV fluids peritoneal dialysis heated irrigation (gastric or colonic, closed thoracic lavage with 2 CT in each side) mediastinal irrigation diathermy (delivery of large amounts of heat with ultrasonic and low frequency microwaves) extracorporeal blood rewarming |
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What are grave prognostic indicators in hypothermia?
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fibrinogen <50mg/dL
cell lysis (K+>10mEq/L) ammonia >250mmol/L |
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What should you consider in a hypothermic patient with tachycardia disproportionate to temperature?
|
hypoglycemia
OD hypovolemia |
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What should be considered in patients where there is a failure to rewarm?
|
infection
endocrinologic insufficiency futile resuscitation |
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What is conduction?
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The transfer of heat energy from warmer to cooler objects by direct physical contact
|
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What is convection?
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Heat loss to air and water molecules circulating around the body
|
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What is radiation?
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Heat transfer by electromagnetic waves
|
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What is evaporation?
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Conversion of a liquid to the gaseous phase
|
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What are apocrine glands?
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Those concentrated in the axillae that are adrenergically activated responding to emotional and heat stress
|
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What are eccrine glands?
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Cholinergically innervated glands distributed over the entire body which produce a colourless doorless sweat
|
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What is atmospheric cooling power?
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The ability of the environment to evaporate sweat (varies with humidity and wind velocity)
|
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What is the vascular response to heat stress?
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Cutaneous vasodilation and compensatory vasoconstriction of the splanchnic and renal beds
|
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How long does acclimatization take?
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Daily exposure, 100min/day for 7-14 days
|
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What happens in acclimatization?
|
Sweating
-earlier onset of sweating -increased sweat volume -lowered sweat electrolyte content Vascular -improved cutaneous vascular flow -expansion of plasma volume -enhanced CV performance Earlier release of aldosterone |
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What is the wet bulb globe temperature heat index?
|
-A meteorilogical measure of environmental heat stress
-It includes the effects of temperature, humidity and radiant thermal energy from the sun ->25 degrees celsius -> even health people are high risk if they choose to exercise ->28 degrees celsius -> exercise and strenuous work should be avoided or limited to extremely short periods |
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What is malignant hyperthermia
|
Hyperthermia, muscle rigidity and acidosis in patients under GA
|
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What is NMS?
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Muscle rigidity, severe dyskinesia/akinesia, hypothermia, tachycardia, dyspnea, dysphagia, incontinence caused by antipsychotic medication
|
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What is fever?
|
The product of a molecular interaction that establishes a new physiological thermal set point
|
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What are heat cramps?
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Brief, intermittent, severe muscular cramps occurring in muscles that are fatigued by heavy work
|
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When do heat cramps occur?
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After exercise when the victim has stopped working and is relaxing
|
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What distinguishes heat cramps from hyperventilation tetany?
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The absence of carpopedal spasms and paresthesias
|
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What is the management of heat cramps?
|
Salt solutions 0.1-0.2% (2-4 10 gram salt tablets dissolved in 1 quart of H20)
or 0.9% NS Salt tablets alone are not recommended |
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What is heat edema?
|
Swollen feet and ankles in non-acclimatized individuals
|
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What is the management of heat edema?
|
leg elevation
thigh high support hose |
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What is heat syncope?
|
Syncope resulting from when an increased portion of the intravascular pool is located in periphery, decreased CO cerebral perfusion inadequate to maintain consciousness
|
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What is prickly heat?
|
An inflammatory disorder of the skin that occurs in tropical climates, it is the result of blockage of sweat gland pores by macerated stratum cornum and secondary staphylococcal infection
|
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What is the treatment for prickly heat?
|
Chlorhexidine in a light cream or lotion
|
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What is heat exhaustion?
|
A clinical syndrome characterized by volume depletion that occurs under conditions of heat stress. Body temp may be normal, below normal, or slightly elevated (37-<40), mental function is essentially intact
|
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What are the types of heat exhaustion?
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Water depletion - inadequate fluid replacement by individuals working in a hot environment
Salt-depletion - large volume of thermal sweat are replaced by water with too little salt |
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Over how long should free water deficits be replaced?
|
48 hours
|
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What is heat stroke?
|
On the spectrum of heat illness this is the catastrophic life-threatening emergency that is characterized by T>40.5C, multi system tissue damage and organ dysfunction
|
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What is the hallmark of heat stroke?
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Neurologic dysfuction
cerebral edema petechiae in the walls of the 3rd or 4th ventricle cerebellar Purkinje cell damage |
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What is a consistent feature of heat stroke?
|
Hepatic damage
|
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What are the usual manifestations of heat stroke?
|
Hyperpyrexia >40.5C
Profound CNS dysfunction Hot skin Pts exposed to heat stress marked elevation of hepatic transaminases |
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What are the 2 forms of heat stroke?
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classic (epidermic)
exertional |
|
Describe classic heat stroke?
|
Occurs during periods of sustained high ambient temps and humidity
-elderly -no airconditioning -limited access to fluids -often chronic illness -sweating ceases |
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Describe typical signs of exertional heat stroke?
|
Young, healthy patient
heat dispelling mechanisms are overwhelmed Athletes and military recruits Rhambolysis and ARF Sweating is often present hypoglycemia |
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Are commercial thermometers reliable in detecting hyperthermia?
|
No
|
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What is the differential diagnosis of heat stroke?
|
CNS hemorrhage
toxins/drugs seizures malignancy hyperthermia NMS SS thyroid storm sepsis encephalitis |
|
What tropical disease can manifest as heat stroke?
|
cerebral falciparum malaria
|
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What drug induced illness can manifest as heat stroke?
|
anticholinergic poisoning
|
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What physical examination findings can be used to differentiate anticholinergic poisoning from heat illness?
|
Pupils - mydriasis suggests anticholinergic whereas miosis suggests heat stroke
|
|
What is the classic triad of SS?
|
mental status changes
autonomic dysfunction neuromuscular abnormalities |
|
What is the ideal method of evaporative cooling?
|
Pt suspended while atomized H2O at 15 degrees celsius is sprayed and air 45-48degrees is blown over the skin
|
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At what body temperature should cooling measures be discontinued?
|
39 degrees to avoid overshooting
|
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What are preferred cooling modalities?
|
Evaporative cooling
Ice water immersion |
|
What are adjunct cooling modalities?
|
cold iv fluids
ice packs cooling blankets lavage (gastric or rectal) cardiopulmonary bypass |
|
What is the cause of hypotension in heat stroke?
|
Peripheral vasodilation resulting in high output cardiac failure
|
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Should patients with heat stroke have aggressive fluid resuscitation?
|
No, moderate because there is a possibility of pulmonary edema
|
|
Should antipyretics be given in heat stroke?
|
No, particularly salicylates can worsen hyperthermia by uncoupling oxidative phosphorylation
|
|
What should be the target UO in rhabdomyolysis?
|
2cc/kg/hr
|
|
What other treatment (other than hydration) should be provided for patients with rhabdo?
|
-urine alkalinization
-mannitol (after volume repletion) |
|
What should be given if patients have violent shivering during cooling?
|
BZD or chlorpromazine (25-50 mg IV)
|
|
Should alpha aminocaproic acid be given in coagulopathy of heat stroke?
|
No, it can be associated with rhabdomyolysis
|
|
Who are the most common victims of lightening fatalities and injuries?
|
Participation in sports and recreational activities
|
|
What is the significance of grauple?
|
It reflects a large difference in electrical potential in the atmosphere and is associated with lighting risks
|
|
What is the severity of electrical burn injury directly proportional to?
|
Current strength, resistance and duration of current flow
|
|
What is current strength?
|
The amount of energy flowing through an object expressed in amperes
|
|
What factors determine the severity of electrical injury?
|
type of circuit
duration resistance of tissues voltage amperage pathway of current |
|
What are the types of circuits?
|
DC or AC
|
|
What are differences between DC and AC circuits?
|
DC
-tends to cause a single muscle spasm -often throws the patients -results in shorter exposure with increased risk of blunt injury AC -continuous muscle contraction or tetanus can occur -longer exposure -more dangerous (for the same voltage) |
|
What is the let go threshold and what is its significance?
|
6-9 mA
It is the current at which the victims is prevented from releasing the current source (flexors are stronger than extensors: forcing the victim to grasp the current source) |
|
Which tissues in the body have the least resistance?
|
Blood
Nerves Mucous membranes muscle |
|
Which tissues in the body have the most resistance?
|
Tendon
fat bone |
|
What is the significance of increase resistance?
|
It prevents the flow of current and favours the transformation of electricity to thermal energy
|
|
How is amperage determined in human exposure?
|
It is estimated, it depends on the voltage (known) and resistance (varied)
|
|
What distinguishes a low vs a high voltage injury?
|
<1000V - low
>1000V - high |
|
What can current that passed through the heart cause?
|
dysrhythmia, direct myocardial damage
|
|
What can current that passed through the brain cause?
|
Respiratory arrest, seizure, paralysis
|
|
What can current that passes through the eye cause?
|
cataracts
|
|
What determines electrical field strength?
|
The pathway between source and ground contact points
|
|
What is the most important difference between lightening and high voltage electrical injury?
|
The duration of exposure
|
|
What are common manifestations of lightening injury?
|
Cardiac and respiratory arrest
vascular spasm neurologic damage autonomic instability |
|
What are the 4 types of electrical burns
|
electrothermal heating
arc flash flame |
|
What is the most destructive electrical injury?
|
Arc - the person is within the current spark formed by 2 objects of differing potential that are not in contact with each other
|
|
What is the histologic change in muscle from direct contact to electricity?
|
coagulation necrosis
|
|
What area of the vessel is most deranged in electrical injury?
|
the media
leading to vessel rupture and delayed hemorrhage |
|
What are the mechanisms of lightening injury?
|
Direct orifice entry
Contact (person touching an object that is part of the lightning current pathway) side flash or "splash" - lightning jumps from its primary strike object to a nearby person on its way down step voltage - difference in electrical potential between a person's feet as the lightening electricity spreads through the ground blunt trauma |
|
What are the most common sites of source contact?
|
hands and skull
|
|
What is the most common site of ground contact?
|
heel
|
|
Is it possible to predict underlying tissue damage from the cutaneous involvement?
|
no
|
|
What is a kissing burn?
|
Burns at the flexor creases where the electrical current arced and caused burns
|
|
What is the most common electrical injury seen in children?
|
mouth burns
|
|
What is a delayed risk of children's mouth burns?
|
Delayed bleeding from the labial artery
|
|
What is pathognomic for lightening injury?
|
feathering burns (from electron showering)
|
|
WHat type of injury causes the extremities to appear cold, blue, mottled and pulseless? WHat is the management
|
lightening
watch and wait |
|
What is keranoparlysis
|
unique temporary paralysis secondary to lightening strike, it is in the lower +/- upper extremities being blue/mottled/cold and pulseless
|
|
What is the focus of history of patients with taser injuries?
|
wounds
retained fragments secondary injury |
|
Which types of electrical burns have the best prognosis?
|
flash
|
|
Should fluid formulas for burns be used in electrical injury management?
|
No, these injuries are more like crush injuries than burns
|
|
What are indications for ECG monitoring post electrical injury?
|
Cardiac:
-Cardiac arrest -ECG changes -document dysrhythmia -chest pain -History of CAD -History of cardiac risk factors Non-cardiac -loss of consciousness -significant injury -hypoxia -conductive injury |
|
When can electrical injury patients be discharged?
|
Normal physical exam
mild burns, if ECG normal and no urinary heme pigment |
|
What is the definition of moderate altitude?
|
8,000-10,000 feet
|
|
What is the definition of high altitude?
|
10,000-18,000 feet
|
|
At what altitude do people usually encounter the steep portion of the oxygen hemoglobin dissociation curve?
|
12,000 feet
|
|
What is the definition of extreme altitude?
|
>18,000 feet
|
|
What physiological changes occur during acclimatization?
|
Increase minute ventilation (decreased pCO2) resulting in increased p02 (hypoxic ventilatory response)
excretion of bicarbonate (within 24-48hours) increased cardiac output increased Hgb and rbcs generalized fluid retention increased 2,3 DPG |
|
Descrive the CXR findings in HAPE?
|
Patchy infiltrates (the result of uneven distribution of pulmonary vasoconstriction)
|
|
How do you diagnose AMS?
|
In the setting of a recent gain in altitude HA and at least 1 other symptom (GI upset, weakness, fatigue, light headedness, difficulty sleeping)
Lake Louise Consensus definition |
|
How long does AMS last?
|
~24-48 hours followed by gradual resolution
|
|
What is an early indicator of HAPE?
|
dyspnea at rest
|
|
What symptoms in AMS mandate immediate descent?
|
Ataxia or altered mentation or evidence of severe pulmonary edema
|
|
What can be done for AMS?
|
Stop further ascent and wait for acclimatization to occur
|
|
What distance of descent should reverse high altitude illness?
|
1500-3000 ft
|
|
What is effective therapy for AMS?
|
acetazolamide 250mg at the onset of symptoms and repeated BID
or dexamethasone 8mg x 1 then 4 mg q6. (this resolves AMS but does not have a role in acclimatization) |
|
How does acetazolamide work?
|
It is a carbonic anhydrase inhibitor therefore it causes a renal bicarbonate diuresis resulting in a metabolic acidosis that increases ventilation
|
|
Is gingko biloba effective in AMS?
|
No, a well-designed study showed no evidence of effectiveness
|
|
What is the most common fatal manifestation of severe high altitude illness?
|
HAPE
|
|
WHat is the treatment for mild/moderate cases of HAPE?
|
Bed rest and oxygen for 1-2 days
|
|
How do portable hyperbaric chambers work?
|
They generate 103mmHg pressure above ambient pressure therefore simulating a descent of 4000-5000ft
|
|
What medications may be useful in HAPE?
|
nifedipine - a pulmonary vasodilator
phosphodiesterase-5 inhibitors may have a told but have not been studied |
|
What are prophylactic therapies to prevent HAPE?
|
acetazolamide
nifedipine phosphodiesterase-5 inhibitors dexamethasone |
|
What is the management of HACE?
|
O2
descent dexamethasone intubation/hyperventilation diuresis/hypertonic saline |
|
What is the definition of drowning?
|
The process of experiencing respiratory impairment from submersion/ immersion in a liquid (the therm near-drowning or drowning with fatal outcomes are no longer used)
Drowning injuries are qualified by death, morbidity or no morbidity |
|
What is immersion syndrome?
|
Syncope resulting from cardiac dysrhythmias on contact with water that is at least 5 degrees celsius less than body temperature
|
|
In what proportion of submersion injury or death is acute alcohol intoxication a contributing factor?
|
30-50%
|
|
What medical conditions confer an increased likelihood of drowning or submersion injury?
|
seizure disorders
autism prolonged QT developmental or behavioural disorders |
|
What is the pathophysiology of drowning?
|
initial breath holding and panic
air hunger and hypoxia develop which result in involuntary gasps that result in aspiration. Aspiration of 1-3mL/kg destroys the integrity of the pulmonary surfactant leading to alveolar collapse and atelectasis |
|
What is the diving reflex?
|
it is a reflex in children and infants
immersion of the face in cold water shunts blood centrally to the heart and brain, resulting in apnea and bradycardia |
|
Why do most submersion victims vomit?
|
Victims swallow a significantly greater volume of water than is aspirated and the distension of the stomach causes them to vomit. The aspiration of stomach contents and water is worse that just aspiration of water.
|
|
What findings on ED arrival in submersion victims are associated with unfavourable prognosis?
|
submersion >5 minutes
Age <3 years Delay in CPR >10 minutes after rescue hypothermia severe acidosis unreactive pupils GCS 3 asystole need for ongoing CPR |
|
Should you perform maneuvers to remove H2O from the lungs of a submersion victim?
|
No, such maneuvers may be ineffective and dangerous unless there is reason to suspect FBA
|
|
How long should you observe an asymptomatic submersion victim?
|
6 hours
|
|
To what temperature must submersion victims be warmed before cerebral death can be diagnosed?
|
30-35 degrees Celsius
|
|
Which patients with submersion injury should be admitted?
|
History of apnea, unconsciousness or hypoxia
dysrhythmia abnormal CXR |
|
Where may you find hazardous levels of Radon gas?
|
Basements and lower levels of buildings
|
|
Patients in which occupations have the highest levels of occupation exposure to radon?
|
uranium mines
|
|
What is the definition of radioactivity?
|
the loss of particles (alpha/beta) or energy (x-rays/ gamma rays) from an unstable atom that is spontaneously decaying
|
|
What are the primary adverse effects of non-ionizing radiation?
|
local heat production
|
|
How does ionizing radiation induce injury?
|
By damaging DNA and other cellular components
|
|
How is ionizing radiation emitted?
|
Alpha and Beta particles
gamma rays x-rays |
|
What does it mean when an object has been irradiated?
|
radiation has passed through it
|
|
What is radioactive contamination?
|
Radioactive particulate matter (alpha and beta), covering an exposed surface
|
|
What 4 types of radiation have the potential to contaminate?
|
Alpha
Beta Gamma (and x -rays) Neutron |
|
Describe alpha particles?
|
Helium nuclei produced by alpha emission from radioactive isotopes (plutonium and uranium decay)
Alpha particles dissipate energy quickly and travel only a few cm (penetrate the thickness of the epidermis). They cannot penetrate paper. |
|
When does alpha radiation present a biohazard?
|
When it has been internalized
|
|
Do Geiger-Muller counters detect alpha particles?
|
Not all of them
|
|
What is the tissue penetration of beta particles?
|
8mm
|
|
What is in primary danger of beta particles?
|
exposed skin
|
|
What is the primary cause of acute radiation syndrome?
|
gamma rays
|
|
What is external radiation?
|
It results from partial body or whole body irradiation from an outside source
|
|
What is external contamination?
|
surface exposure to radioactive materials that remain in contact with skin
|
|
What can be used as a screening tool to detect those who require urgent medical investigations after exposure to radiation?
|
Timing of nausea and vomiting
|
|
What is the earliest indicator of significant radiation exposure?
|
Absolute lymphocyte count
|
|
What is the LD50 of whole body irradiation exposure?
|
4.5Gy
|
|
What is the maximum survivable dose of whole body irradiation?
|
10Gy
|
|
Who should be contacted in the event of a radiation disaster?
|
The radiation control officer
|
|
How do you decontaminate radioactively contaminated patients?
|
-remove clothing
-wash with water and soap -shampoo hair -collect all waste and waste water |
|
Should interventions be delayed for decontamination of radiation exposed patients?
|
No, the risk to the providers is low, life saving therapies should not be delayed
|
|
What does SCUBA stand for?
|
Self contained underwater breathing apparatus
|
|
What are dysbarisms?
|
Illnesses that result directly or indirectly from exposure to increased ambient pressure
|
|
What is Pascals law?
|
Pressure applied to any part of a liquid is transmitted equally throughout
|
|
What is Boyle's law?
|
P proportional to 1/v
At constant temperature the pressure and volume of gas are inversely proportional PV=K |
|
What is Charles' law?
|
At a constant pressure volume is proportional to the change in temp
v1/T1 = V2/T2 |
|
What is the general gas law?
|
P1V1/T1 = P2V2/T2
|
|
What is Dalton's law?
|
Total pressure exerted by a mixture of gases is equal to the sum of their partial pressures Pt = P1+P2+Pn
|
|
What is Henry's law?
|
The amount of gas that is dissolved in a liquid at a given temperature is directly proportional to the partial pressure of each component
|
|
What are dysbarisms?
|
Illnesses that result directly or indirectly from exposure to increased ambient pressure
|
|
What is the standard atmospheric pressure at sea level?
|
760 mmHg
|
|
What is absolute pressure or atmospheres absolute (ATA)?
|
It is the total pressure on a diver -> therefore the sum of the gauge and atmospheric pressure
|
|
What is decompression sickness (DCS)?
|
Spectrum of clinical illness resulting from the accumulation of bubbles (especially nitrogen) which disrupts body tissues and systems
|
|
What is barotrauma?
|
Injury caused by pressure changes
|
|
Where is the greatest risk of barotrauma in diving and why?
|
In shallow water, because fractional changes in volume are greater near the surface
|
|
What is middle ear barotrauma (MEBT)?
|
TM rupture caused by the pressure difference as a diver descends and the inability to equalize pressure
|
|
What signs may be associated with MEBT?
|
-nystagmus and vertigo from cold H20 in middle ear
-facial paralysis is the 7th nerve is exposed |
|
How does external ear barotrauma occur?
|
If air is trapped in the external auditory canal during descent - resulting in outward TM bulge
|
|
What is inner ear barotrauma?
|
Inward deflection of the TM transmitted to the oval window resulting in rupture of the round window (it tends to occur with Valsalva maneuver or equalization of pressures)
|
|
What are symptoms of IEBT?
|
Variable hearing loss
severe vertigo nausea tinnitus fullness in the affected ear |
|
Which condition may be difficult to distinguish from inner ear barotrauma?
|
DCS type II (one should treat was DCS if there is any doubt in the diagnosis)
|
|
Which sinus is most commonly affected in barosinusitis?
|
The frontal sinus
|
|
What causes facial barotrauma?
|
Negative pressure generation within the artificial air space created by a dive mask over the face and the nose
|
|
What is a potentially dangerous injury caused by facial barotrauma?
|
optic nerve damage
|
|
What is nitrogen narcosis?
|
Intoxicating effects of increased tissue nitrogen concentration at depth. Symptoms include euphoria, confusion, loss of judgement, disorientation
"Rapture of the deep" |
|
At what depth of diving is compressed air not recommended?
|
>120ft
|
|
What are symptoms of CNS oxygen toxicity?
|
V - visual symptoms (tunnel and blurred)
E - ear symptoms (tinnitus) N - nausea, spasm, vomiting T - twitching/tingling I - irritability, confusion D - dizziness C - convulsion |
|
How do deep divers prevent oxygen toxicity?
|
By breathing mixed gases wing decreased oxygen content
|
|
What are potential contaminants of compressed air?
|
-carbon dioxide
-carbon monoxide -"soda lime" (calcium hydroxide) |
|
What is decompression sickness?
|
A spectrum of clinical illnesses that result from the formation of small bubbles of nitrogen gas in blood and tissues
|
|
What are RF for DCS?
|
-increased depth of dive
-increased length of dive -age -obesity -fatigue -heavy exertion -dehydration -fever -PFO -cold temperature post dive -dive at high altitude -flying after a dive |
|
What is Type I DCS?
|
That which affects the MSK, skin and lymphatic vessels
|
|
What is Type II DCS?
|
That which involves any organ system other than Type I (skin, muscle and lymph)
|
|
What is the other name for DCS type I?
|
"the bends"
|
|
Which systems can be involved in type 2 DCS?
|
CNS, inner ear and lungs
|
|
What is another term for inner ear DCS?
|
"the staggers"
|
|
What is another term for pulmonary DCS?
|
"the chokes"
|
|
What 5 conditions may result from pulmonary barotrauma?
|
-AGE (arterial gas embolus)
-pneumothorax -pneumomediastinum -subcutaneous emphysema -alveolar hemorrhage |
|
How do AGE occur?
|
Air bubbles are forced across the alveolar-capillary membrane and escape into the pulmonary venous circulation ->left atrium ->left ventricle -> arterial circulation or PFO
|
|
When should you suspect AGE?
|
Any diver who has breathed compressed air and surfaces unconscious or loses consciousness within 10 minutes of ascent
|
|
Under what circumstances is IEBT more likely than DCS?
|
-symptoms began during descent
-difficult equalization or vigorous valsalva |
|
Within what time frame does AGE present?
|
Almost always within 10 minutes of surfacing
|
|
What is the only definitive treatment for DCS I and II and AGE?
|
Recompression
|
|
What is the immediate treatment for diving disorders?
|
100% O2 - reduces bubble size by increased differential pressure for nitrogen diffusion
|
|
What is the mortality of AGE?
|
If recompression within 5 minutes then 5 %
If decompression within 5 hours then 10% |
|
How long after the onset of DCS should recompression still be considered?
|
Even 10-14 days post-exposure
|
|
Which diving disorders require recompression therapy?
|
DCS type I
DCS type II AGE Contaminated air (CO) |
|
What type of transport is recommended for transfer to hyperbaric facility?
|
Ground
|
|
Under what conditions should air transport to hyperbaric therapy be undertaken?
|
Cabin pressure <1000ft
|
|
What is the cabin pressure of commercial aircrafts?
|
5000-8000ft
|
|
What are the goals of decompression therapy?
|
-decreased mechanical obstruction of air bubbles
-facilitate nitrogen washout by increased tissue-blood nitrogen gradient -increased oxygen delivery to ischemic tissues |
|
What are adjunctive treatments for DCS and AGE?
|
-O2
-IVF, maintain UO at 1-2 cc/kg/hr -treat/prevent hypothermia |
|
In what position should patients with AGE be transported?
|
Supine
not trendelenberg |
|
Explain the physiologic response to acute cold exposure of an extremity
|
15 degrees -> maximal peripheral vasoconstriction
10 degrees -> hunting response (recurring vasodilation cycles lasting 5-10 min that interrupt vasoconstriction and serve to protect the extremity) |
|
What is the ultimate determinant of progressive tissue damage in cold injury?
|
injury to the microvasculature
|
|
What tissue is the most susceptible to freezing injury?
|
endothelial cells
(nerve and muscle cells are more susceptible than connective tissue) |
|
How long does the edema progress after thawing?
|
Develops in <3h and progresses for 48-72h
|
|
What are the clinical features of frostbite?
|
numbness
sensory deficit clumsiness violaceous-white waxy or pale yellow appearance |
|
Who is at risk for chilblains?
|
Young women with a history of Raynaud's phenomenon, SLE or antiphospholipid antibodies
|
|
When does trench foot occur nowadays, how does it present and how can it be prevented?
|
When - recreational activities and expeditions in cold, wet climates, develops while a person is wearing sweat-dampened or neoprene socks, vapor-barrier boots or constrictive gaiters
Presentation - initially cool, pale feet with numbness later becoming cold, cyanotic, oedematous. Bullae may develop followed by ulceration and gangrene Prevention: continual drying of socks |
|
Why do children cool faster than adults?
|
Elevated raios of surface area to mass
|
|
How does the body respond to acute cold exposure?
|
Skin thermoreceptors signal to the hypothalamus an exposure to cold
Hypothalamus triggers the following (5) -increased muscle tone -shivering thermogenesis -peripheral vasoconstriction secondary to release of NE -increased release of TSH -adaptive behaviour |
|
How should core temperature be measured?
|
Ideally: rectal or esophageal probe with continuous reading
If not available: rectal digital thermometer (advance 15cm) Avoid: mercury thermometer |
|
What is the differential for osborn J waves?
|
Hypothermia
Sepsis CNS lesions Cardiac ischemia Brugada syndrome Hypercalcemia |
|
What is the lowest core temperature of a child and an adult that survived to hypothermia neurologically intact?
|
Child 14.2 degrees celsius
Adult 13.7 degrees celsius |
|
What is the clinical presentation associated with each level of hypothermia?
|
35 - maximum shivering and respiratory stimulation
32 - 25% decrease O2 consumption, stupor 31 - extinguished shivering 30 -afib 29 - vfib risk 26 - no reflexes or response to pain 25 - pulmonary edema 24 - significant hypotension 22 - max risk vfib 19 - flat EEG 18 - asystole |
|
What lab abnormalities are expected in hypothermia?
|
Hyperglycemia followed by hypoglycemia
Renal failure secondary to hypovolemia from cold diuresis or rhabdo Increased CK if rhabdo Hyperkalemia due to cell lysis Metabolic acidosis Respiratory acidosis Increased hematocrit cold induced thrombocytopenia normal INR, PT, PTT despite clinical coagulopathy which is treated with rewarming |
|
Explain the prehospital management of hypothermia?
|
-Evaluate pulse and respiration for 30-45 seconds
-Remove from the wind and cold. Bring patient to a heated ambulance -Remove wet clothes -Insulate with blankets -Transport in the horizontal position -Minimize movements and transfers -avoid brisk movements which could trigger VF -measure core temp if possible -administer warm humidified O2 -active external rewarming in truncal area |
|
What is the in-hospital management of hypothermia?
|
-ABCs - evaluate pulse and respiration for 30-45s
-Measure core temperature and determine the severity of hypothermia -Passive rewarming: increase temperature in the resuscitation room, remove wet clothes, insulate with blankets -Active external rewarming of truncal areas -Active internal rewarming: volume resuscitation 500mL of heated D5NS then 150mL/hr, warm humidified O2 and other active internal techniques as needed. -Intubation in cases of severe hypothermia |
|
When do you use passive, active external and active internal rewarming?
|
Passive: mild hypothermia only
Active external: mild and moderate hypothermia Active internal: severe hypothermia |
|
When is temperature afterdrop a concern and what should be done to mitigate it?
|
With active external rewarming of cold extremities
When this is a concern (frostbitten extremities or severe hypothermia) make sure to apply a heat source to truncal areas only. |
|
How is closed thoracic lavage performed?
|
2 large chest tubes (36F) inserted on the same side
Drain 1: 2nd or 3rd intercostal space (mid clavicular) Drain 2: 5th or 6th intercostal space (posterior axillary line) Infuse warm NS into inferior tube |
|
What are the disadvantages of gastric/vesicle/colonic lavage?
|
All three: limited surface area for heat exchange resulting in a very slow rate of rewarming
Also gastric and colonic lavage can cause fluid and electrolyte fluxes |
|
What are the advantages of peritoneal lavage over other lavages? What are contraindications to this?
|
Rewarming of the liver -> reactivates the detoxification and conversion enzymes
CI: abdominal trauma, peritoneal signs, surgical abdomen |
|
When should mediastinal and direct myocardial lavage be considered?
|
Hypothermic cardiac arrest patients
|
|
What are extracorporeal rewarming methods?
|
Venovenous rewarming
Arteriovenous rewarming Hemodialysis Cardiopulmonary bypass |
|
Why should Ringers lactate be avoided in cases of hypothermia?
|
The cold liver is unable to metabolize lactate efficiently
|
|
If CV access is required in hypothermia where should it be inserted?
|
Femoral, because of the risk of irritating the myocardium with SC or IJ access
|
|
What are the modifications to ACLS in hypothermia situations?
|
-Evaluate pulse and respiration for 30-45 seconds
-If T<30 degrees defibrillate only once and no other shocks until T>30 -Withhold IV medication if T<30 (because it is not efficacious, there is decreased metabolism and you could have toxic accumulation) -Rewarm the patient -If the T>30 then increase the intervals between ACLS drug doses |
|
What is the treatment of heat exhaustion?
|
Rest
Cool environment Assess volume status Fluid replacement (NS, replace slowly to avoid cerebral edema) Healthy young patients can generally be treated as outpatients Elderly should be considered for admission if severe electrolyte disturbance or risk for recurrence |
|
What are the zones of injury in frostbite?
|
Central irreversible injury
Zone of stasis - potential area of salvageable cells Zone of hyperemia |
|
Who is at greatest risk for chilblains?
|
Young women with Reynaud's phenomenon
It is suggestive of connective tissue disease |
|
What is immersion foot?
|
Severe variant of trench foot seen in downed pilots and shipwrecked sailors exposed for extended period in life rafts
|
|
What are good prognostic features of frostbite?
|
normal sensation
normal warmth normal color soft pliable subcutaneous tissues early formation of clear blebs |
|
What are bad prognostic features of frostbite?
|
Residual violaceous hue
lack of edema formation delayed appearance of small hemorrhagic blebs early black dry eschar |
|
What is the ED treatment of frostbite?
|
Prethaw
Assess doppler pulses and appearance protect the part stabilize core temperature address medical and surgical conditions rehydrate prevent partial thaw and refreeze Thaw Provide analgesia Block prostaglandin and thromboxane formation (administer ibuprofen 400mg q8rs PO) Thaw - immerse in circulating water bath 37-40 degrees Post-thaw protect the limb aspirate or debride clear vesicles apply topical antibiotic ointment leave hemorrhagic vesicles intact (or aspirate them without debriding) tetanus provide hydrotherapy at 37 degrees TID Monitor compartment pressures and possible decompressive escharotomies prn amputation |
|
What are the tissue damaging contents of frostbite clusters?
|
Arachadonic acid breakdown products (prostaglandins and thromboxane)
|
|
What are sequela of frostbite?
|
Pain - phantom, causalgia
Sensation - hypesthesia Thermal sensitivity to heat and cold MSK - atrophy, compartment syndrome, tenosynovitis, necrosis, amputation Derm - edema, lymphedema, ulcers Miscellaneous - ATN, sepsis |
|
What is the typical progression of cardiac arrhythmias that occur as temperature decreases?
|
Bradycardia - atrial fibrillation - ventricular fibrillation - asystole
|
|
What are the target ABG values in hypothermia?
|
pH 7.4, PaCO2 40
Do not correct the values despite the fact that the machine warms the blood to 37 degrees |
|
What causes the frothy sputum seen in hypothermia?
|
Cold depression of ciliary activity produces bronchorrhea
|
|
What are extracorporeal rewarming options?
|
Venovenous rewarming
Hemodialysis CAVR (arteriovenous re-warming) Cardiopulmonary bypass |
|
What is venovenous rewarming?
|
CV catheter to CV or peripheral catheter
no oxygenator/circulatory support Rate of rewarming 2-3degrees/hr |
|
What is HD rewarming?
|
single or dual vessel cannulation
stabilizes electrolyte or toxicologic abnormalities ROR 2-3 degrees/hour |
|
What is CAV rewarming?
|
Perculaneous femoral catheters
No perfusion/pump or anticoagulation RPR 3-4 C/hr |
|
What is CPB rewarming?
|
Full circulatory support with pump and oxygenator
ROR up to 9.5degrees/hour |
|
What are 3 functions required to regulate body temperature?
|
Thermosensors (thermosensitive neurons in the thalamus are activated when blood exceeds a certain set point)
Central integrative area - thermostat Themoregulatory effects (things that regulate heat loss) |
|
What are risk factors for heat illness?
|
Elderly
Chronic illness that interferes with heat loss Chronic medication that interferes with heat loss Young children CNS disease Diarrheal illness Alcoholics Past history of heat stroke |
|
What are 2 categories of heat-related illness
|
Minor syndrome
Heat edema Heat syncope Heat cramps Prickly heat Major syndromes Heat exhaustion Heat stroke |
|
What is the clinical hallmark that differentiates heat exhaustion and heat stroke?
|
CNS dysfunction
|
|
What is the approach to hypotension in heat stroke?
|
Check CVP +/- Wedge pressure
If CVP is low then the patient is hypovolemic - bolus the patient, until BP 90/60 or CVP >12 If CVP elevated and low wedge pressure - the patient is hypodynamic and may benefit from a trial of catecholamines If the CVP and wedge pressure are both elevated then the patient is hyperdynamic and will benefit from continued cooling and modest IV fluids ~300cc/hr |
|
What is the treatment for heat stroke?
|
ABCS
Cooling Manage hypotension based on CVP and wedge Seizures are managed with BZD Cardiac - Try to avoid shocks until the myocardium is cooled, adrenergics and anticholinergics can worsen things Try to avoid over hydration because of pulmonary edema |
|
What is Joules' Law?
|
P = I^2Rt
I - current R - resistance t - time, in seconds |
|
What is Ohms Law?
|
I = V/R
V = potential in volts |
|
What are other names for entry and exit site of electrical injury?
|
Entry: source contact point
Exit: group contact point |
|
Why must amperage be estimated in human electrical exposure?
|
Resistance varies according to the involved tissue
As tissue changes secondary to the energy, resistance may change markedly |
|
What is the threshold of perception of current?
|
0.2-0.4mA
|
|
What amperage is associated with ventricular fibrillation?
|
60-120mA
|
|
What is different about lightening mass casualty events?
|
Treat the patients that are labeled as "black" first as they are easily treated with rescue breathing. Non "black" triaged patients usually do well
|
|
What are contraindications to scuba diving
|
Neuro: seizures, vertigo, panic disorder
Resp: asthma, COPD CVS: syncope HEENT: sinus or ear disorder Poor training |
|
Classify injuries that a scuba diver is at risk for?
|
1. due to environmental exposure (hypothermia, sunburn, physical trauma)
2. common to aquatic environment (submersion, motion sickness, marine envenomations) 3. Dysbarisms (exposure to increased ambient pressure) |
|
What injuries is Boyle's law important for?
|
Squeeze syndromes
|
|
What injuries is Dalton's law important for?
|
Nitrogen narcosis and oxygen toxicity
|
|
What is the significance of Henry's law to scuba divers?
|
Nitrogen accumulates in tissues and blood in proportion to the depth and length of a dive
If a diver ascend too rapidly to the surface, nitrogen comes out solution, forming gas bubbles in tissues and blood |
|
What is the presentation of facial barotrauma?
|
Facial edema
Conjunctival edema Diffuse petechial hemorrhages on the face Subconjunctival hemorrhages Optic nerve damage |
|
What is the treatment of nitrogen narcosis?
|
Resurfacing allows nitrogen to be cleared
(persistent symptoms should lead a search for DCS, AGE, contaminated air or near drowning) HBO is not needed |
|
What two organ systems are most affected by oxygen toxicity?
|
Pulmonary
CNS |
|
How is oxygen toxicity prevented and treated?
|
On deep dives, oxygen toxicity is prevented by breathing in gases with decreased oxygen content like hypoxic trimix.
Treatment is ascent and supportive, HBO is not needed |
|
List the presentation of type II DCS?
|
These illnesses present gradually and most present within 24 hours
Spinal DCS -limb weakness or paralysis, parethesia, numbness -back and abdo pain -sensory and motor loss -bladder and bowel symptoms CNS DCS -headache -blurred vision -dysarthria -unusual fatigue -inappropriate behaviour -sense of detachmen -LOC Inner ear DCS -nausea, dizziness, vertigo, nystagmus Pulmonary DCS -progressive dyspnea, cough, chest pain |
|
List 6 mechanisms by which asthmatics are at higher risk for pulmonary barotrauma?
|
Bronchospasm and mucus plugging
Compressed air has greater turbulent flow There is a reduction in breathing capacity related to depth Effort of scuba diving may aggravate effort related component Contamination of compressed air by allergens |
|
What two organ systems are most at risk of AGE?
|
Coronary
Cerebral |
|
How is AGE differentiated from DCS II?
|
It is an acute event occuring within 10 min of resurfacing. DCS takes longer to present
|
|
What are contributors to pulmonary edema in the setting of diving?
|
Increased after load
Increased pre load |
|
What dive injuries occur on descent?
|
Middle ear barotrauma
inner ear barotrauma External ear barotrauma facial barotrauma sinus barotrauma |
|
What dive injuries occur at depth?
|
Nitrogen narcosis
hypothermia contaminated gas oxygen toxicity |
|
What dive injuries occur on ascent?
|
Rapid ascent
AGE Pulmonary overpressure syndrome Barodentalgia GI barotrauma Long/deep DCS I DCS II |
|
How do you differentiate DCS from AGE on dive history?
|
DCS
depth and length dependent decompression limits approached flying after diving diving at altitude AGE independent of dive profile rapid ascent inexperience out of air |
|
How do you differentiate DCS from AGE based on risk factors?
|
DCS
fatigue dehydration fever, hypothermia obesity strenuous activity AGE Obstructive lung disease emphysema mucous plugging patent foramen ovale |
|
How do you differentiate DCS and AGE based on signs and symptoms?
|
DCS
progressive onset spinal symptoms predominate limb weakness or paralysis AGE Rapid onset cerebral symptoms predominate LOC |
|
What are recommendations about flying after diving?
|
<2hours total dive time in 48hour -> >12 hours
Multiple day, unlimited diving -> >24 delay DCS or AGE -> 72 hours |
|
What variables influence the incidence of altitude related illness?
|
Rate of ascent
Sleeping at altitude Final altitude Duration of stay at altitude Individual susceptibility Use of sedatives |
|
Define acclimatization?
|
Series of integrated adaptations that take place at high altitudes which tend to restore oxygen pressures within the tissues toward normal sea levels
|
|
What is the principle of management of AMS?
|
After the symptoms of altitude illness occur, further ascent to a higher sleeping altitude is contraindicated
|
|
How is AMS prevented?
|
-Slow ascent allowing acclimatization - stop at 2500m for sleep, then no more than 600m ascent per day
-mild to moderate exercise -high carbohydrate diet -maintain hydration -acetazolamide -dexamethasone (typically rescue teams that don't have time to acclimatize) |
|
What a specific signs suggesting that a patient has progressed from AMS to HACE?
|
Ataxia
Seizures Slurred speech Rare focal deficits Altered mentation |
|
What is the definition of HAPE?
|
Recent gain in altitude
2 of the following: -dyspnea at rest -cough -decreased exercise performance -chest tightness or congestion 2 of the following PE signs -central cyanosis -rales -tachypnea -tachycardia |
|
What are chest xray findings of HAPE?
|
Alveolar and patchy infiltrates
Right middle lung fields Areas of clearing |
|
When does HAPE usually begin?
|
Insidiously on day 2-4 at altitude
|
|
What are symptoms of high altitude retinal hemorrhage?
|
Asymptomatic
Scotoma |
|
What is a submersion victim?
|
Anyone who has submersion distress requiring medical support and transport to an emergency facility
|
|
What is the most important characteristic about aspirated water with regard to pulmonary derangements?
|
Volume
(not composition ie salt or fresh) |
|
What is dry drowning?
|
Death from a non-submersion event or post submersion event
|
|
What is the effect of hypothermia on a submersion victim?
|
Lowers cerebral metabolic rate and is neuroprotective to some extent
|
|
List important precipitants of a submersion injury to consider?
|
Drug and alcohol intoxication
Cardiac arrest hypoglycemia seizure attempted suicide or homicide child abuse or neglect head or c-spine injury |
|
Is the initial CXR in submersion injuries prognostic?
|
It may underestimate the severity of the pulmonary injury or may already show pulmonary infiltrates and edema
|
|
What is the management of a submersion victim?
|
On scene
-mouth to mouth -do not perform the heimlich ED -ABCs, immobilize if trauma possible -consider rewarming -intubation if desaturating, pCO2>50, make sure there is CPAP with the vent settings -consider CPAP in alert patients -antibiotics and steroids do not improve outcomes |
|
What is the minimum recommended observation period for submersion victims?
|
6 hours
|
|
What are discharge criteria for submersion victims?
|
Asymptomatic on presentation
Normal room air saturation No CXR abnormalities Normal ABG |
|
What are 4 causes of injury from nuclear explosions?
|
Blast and penetrating trauma from a blast/blast wave
thermal burn effects ioninzing radiation radioactive fallout |
|
What is non-ionizing radiation?
|
-All forms of the electromagnetic spectrum except xrays and gamma rays
-long wavelength, low frequency and high energy -primary adverse effects are related to transformation of energy to local heat |
|
What is incorporation?
|
Radioactive material is ingested, inhaled, or absorbed through an open wound
|
|
When are gamma rays emitted?
|
Most radioisotopes emit a gamma ray after beta decay
|
|
What form of radiation is the cause of acute radiation syndrome?
|
Gamma rays - they are emitted from radioisotopes after beta decay and penetrate tissues deeply
|
|
What is radioactive fallout?
|
Neutrons captured after emission cause a previously stable atom to become radioactive
|
|
What is external radiation?
|
Partial body or whole body irradiation from an outside source - no radioactive hazard to other people or environment
|
|
What is incorporation and internal contamination?
|
inhalation or ingestion of radioactive substances or absorption via open wound
|
|
What is external contamination?
|
surface exposure to radioactive dirt or liquids
|
|
What is acute radiation syndrome?
|
Symptom complex that occurs after whole-body irradiation
|
|
What factors determine the severity of acute radiation syndrome?
|
Dose
Dose rate Dose distribution Individual susceptibility |
|
How is the dose of radiation absorbed expressed (units)?
|
Gray - Joules of radiation per Kg of tissue
Rad - 1 rad - 100 erg/gram or 0.01 Gy Rem - 1 rad of x-radiation (100rem - 1 Sv) |
|
What tissues are more sensitive to radiation?
|
Those with greater rates of cellular turnover
(hematopoietic, GI, reproductive) |
|
What are clinical syndrome that result from radiation exposure?
|
CNS syndrome: HA, mental status changes, vertigo, tinnitus, sensory and motor changes
GI syndrome: NV to bloody diarrhea Hematopoietic manifestations: pancytopenia Skin burns |
|
In MCI how are radiation victims categorized?
|
Survival probable: <2Gy, initial lab studies and serial CBC reveal no depression in leukocyte count, not necessary to hospitalize
Survival possible 2-10Gy, brief nausea and vomiting, hematologic changes after 24-48 hours, protective isolation recommended, surgical treatment within 48 hours, administer hematopoiesis stimulating agents Survival improbable >10Gy: rapid onset fulminant nausea, vomiting, diarrhea, early CNS symptoms, made comfortable |
|
What kind of head and neck injuries do you see in electrical injuries and lightning injuries?
|
Electrical: burns and cataracts
Lightening: skull fracture, c-spine fractures, TM rupture, deafness, disruption of the ossicles, disruption of the mastoid, otorrhea, ocular injuries, cataracts |
|
What kind of CVS injuries do you see in electrical injuries and lightning injuries?
|
Electrical: arrest, sinus tach, transient ST elevation, reversible QT prolongation
Lightening: cardiac arrest, non specific ST changes, prolonged QT interval |
|
What kind of skin injuries do you see in electrical injuries and lightning injuries?
|
Electrical: Burns - contact, ground, kissing, electrical, flame, mouth
Lightening: superficial, deep - linear, punctate, feathering, thermal |
|
What kind of extremity injuries do you see in electrical injuries and lightning injuries?
|
Electrical: muscle necrosis, compartment syndrome, myoglobulinuric renal failure, joint damage, vascular damage
Lightening: transient vasopasm |