Enviro Flashcards

Question

Nommer 5 méthodes de refroidissement et autres traitement du coup de chaleur

Answer 1

Preferred Evaporative cooling with large circulating fans and skin wetting Ice water immersion Adjuncts Ice packs to axillae and groin Cooling blanket Peritoneal lavage (unproven efficacy in humans) Rectal lavage Gastric lavage Cardiopulmonary bypass Si tachyarythmies: éviter cardioversion, se résout avec refroidissement Éviter vasopresseurs - vasoconstriction empêche refroidissement et détériore fonction cardiaque Éviter atropine et autres anticholinergiques Alcalinisation des urines si rhabdo Benzo pour frissons Surveiller CIVD

Answer 2

En arc - kissing burns Thermiques Flash d'entrées et de sorties

Answer 3

Arrêt respiratoire: tétanie des muscles respiratoires ou atteinte du centre de la respiratoire a/n tronc cérébral Arrêt cardiaque 2nd arythmies: FV, asystolie.

Answer 4

tête/cou: atteinte oeil (brûlure cornée, conjonctive, saignement dans CA, détachement rétine, lésions maculaires, CATARACTE). Lésions des oreilles moins fréquentes.Vertige transitoire ou permanent. Lésions buccales + svt chez enfants lorsque brûlure via contact buccal. Typiquement: saignement de l'artère labiale lorsque chute de l'escarre 2 a 15 jr post événement MSK: lésions musculaires avec nécrose, lésions nerveuses, lésions vasculaires (thrombose, nécrose, dilatation anévrysmale), lésions osseuse (brûlures périostées, ostéonécrose), fx secondaire à la projection, syndrome de compartiment Nerveux: neuropathies périphériques, AEC/coma/convulsions, AVC/ sgmt IC 2 trauma/ thrombose veineuse, séquelles neuropsychiatriques, paralysie/SLA/myélite transverse

Answer 5

Élévation ST prolongation ST onde T aplaties ou inversées FA SCA sans séquelles

Answer 6

Neuro: hématomes intra/extracrâniens, convulsions, AEC, keraunoparalysis (paralysie flasque où le patient s'éveille sans être capable de bouger; associé à changements vasomoteurs a/n MI avec cyanose, récupération en minutes à jours), neuropsychiatriques, ataxie, névrites, névralgies... Peau: brûlures très fréquentes, mais rarement profonde. Lésion Lichtenberg - pathognomonique, forme de fougère Oreilles: rupture tympanique, surdité, accouphène, rupture mastoide, vertige, nystagmus Yeux: atteinte possible de toutes les structures, cataractes immédiates ou retardées, atteinte pupillaire avec mydriase/myosis/aréactivité Autres: myoglobinue rare, dysfonction autonomique/vasculaire qui simule syndrome du compartiment (vrai compartiment très rare), luxations,

Answer 7

Clothing wet from rain Tears or disintegration of clothing Multiple victims Typical arborescent pattern of erythema or superficial linear or punctate burns Tympanic membrane injury Cataracts, especially in a younger patient Magnetization of metallic objects on the body or clothing Electrocardiographic changes

Answer 8

high-risk indicators, such as 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.11

Answer 9

When was the first onset of symptoms? What type of equipment was used? Compressed air, mixed gas, enriched air, rebreather? What was the source of the gas? Did the dive approach or exceed decompression limits? Was a dive computer used? What were the number, depth, bottom time, total time, and surface intervals for all dives in the 72 hours preceding symptoms (the dive “profiles”)? Were decompression stops used? Was in-water decompression attempted? What was the time delay from the last dive to air travel? Did the diver experience difficulty with ear or sinus equilibration? Did the pain occur on descent or ascent? Was the diver intoxicated? Dehydrated? Working strenuously? How long after the dive did symptoms present? Were they present at surfacing? Delayed? Progressive? Is a medical history of ear or sinus infections or abnormalities present? Emphysema or asthma? Coronary artery disease? Patent foramen ovale (PFO)? Neurologic illness?

Answer 10

Barotrauma oreille moyenne Barotrauma oreille externe: protusion du tympan a/n CAE lorsque CAE partiellement obstrué avec pression négative Barotrauma oreille interne: lorsque équilibration impossible, pression négative a/n fenêtre ovale avec transmission pression a/n endolymphe de la cochlée, possible rupture membrane labyrinthique. Sx/ss: surdité, vertige, nystagmus, ataxie, sensation plénitude Barotrauma sinus Barotrauma facial (atteinte visage + oculaire 2nd masque)

Answer 11

Narcose à l'azote Toxicité à l'oxygène, lorsque la Ppartielle de l'oxygène dépasse 1.6 ata (à 220 ft pour air comprimé) ou en cas d'exposition prolongée à l'oxygène non concentré (plus de 24 hrs) Contamination: air contaminé par CO ou CO2. Particules de CaOH normalement présentes dans les circuits. Si fuite permet entrée d'eau, entraine une réaction avec les particules (soda lime) et brûlures 2nd

Answer 12

Vertige alterno-barique: lorsque équilibration de l'oreille moyenne impossible à la montée, cause compression de l'oreille interne/ labyrinthe, cause un vertige transitoire, auto-résolutif. Barotrauma dentaire Barotrauma gastrointestinal Barotrauma pulmonaire: PTX, pneumomédiastin, emphysème sous-cutané, hémorragie alvéolaire Asthmatiques: risque double de barotrauma pulmonaire 1. Air contaminé au pollen ou autres allergènes 2. Asthme à l'exercice 3. Asthme au froid (air se refroidit lorsque s'expand dans le régulateur) 4. Bronchospasme et mucus engendre lésions pulmonaires focales 5. Diminution de la capacité pulmonaire en profondeur 6. Augmentation de la densité de l'air qui favorise un flot turbulent Recommandations aux plongeurs asthmatiques: A thorough history and physical by a trained physician The patient’s asthma should be well controlled Normal spirometry: FEV1 ≥80%, FEV1/FVC ≥75% Successful completion of a bronchial provocation challenge Cold, exercise, or emotion induced asthmatics should not dive Asthmatics requiring rescue medication with 48 hours should not dive Maladie de décompression: Spectre de maladie résultant de la formation de bulles d'azote a/n sang et des tissus durant l'ascension. FR: durée et profondeur de la plongée, age, obésité, fatigue, exercice physique intense, déshydratation, fièvre, froid après plongée, plongée en altitude, vol d'avion après plongée, sexe masculin (risk taking), peutêtre alcool + tabac, FOP Moyenne du début des dx: 60 min, 98% en 6 heures DCS 1: MSK, peau, lymphatiques (douleurs articulaires, stase veineuse, prurit, cutis marmorata, oedème des extrémités) DCS 2: autres (SNC, oreille interne avec sx vestibulaires plus que cochléaires, spinal, pulmonaire (bulles a/n circulations avec toux, dyspnée, douleur thoracique) Maladies reliées à la décompression: englobe type 1, type 2 et embolie gazeuse artérielle Embolie gazeuse artérielle: bulles forcées de passées de l'alvéole vers le capillaire pulmonaire, OG et la circulation artérielle ou résultant shunt D-G en cas de FOP. Embolie gazeuse peut se produire seul ou associée à DCS. Atteintes + sérieuses avec embolies a/n coronaires (infarctus, arythmies, arrêt cardiaque) et circulation cérébrale (AVC circulation antérieure ou moyenne le + svt, arythmies 2nd dysfonction autonomique

Answer 13

Barotrauma oreille moyenne Barotrauma oreille interne Vertige alterno-barique Lésion oreille interne associée à la décompression The differentiation of IEBT from inner ear neurologic DCS is crucial because the treatments differ. An IEBT is more likely when symptoms begin during descent or the diver relates a history of difficulty equilibrating or performing a vigorous Valsalva maneuver. If the dive profile is examined and the no-decompression limits are approached and symptoms began soon after surfacing, inner ear DCS is more likely. A history of difficulty in equalizing the ears on descent, or the onset of symptoms early in the dive, suggests barotrauma. A history of a dive that approaches decompression limits, or the onset of symptoms during or soon after ascent, and the presence of other neurologic findings suggest DCS. A trial of recompression therapy is prudent if concerns for DCS exist.

Answer 14

The differential diagnosis of pulmonary DCS includes AGE. Table 135.3 provides factors that differentiate the two conditions. Although the treatment of both requires recompression therapy, they may be differentiated by the timing of the onset of symptoms. Almost all cases of AGE present within the first 10 minutes of surfacing, whereas DCS presents more typically after 10 minutes: 40% of pulmonary DCS symptoms begin within 1 hour of surfacing, 60% within 3 hours, 80% within 8 hours, and 98% within 24 hours.

Answer 15

4 maladies: DCS 1, DCS 2, embolie gazeuse artérielle, contamination gazeuse avec CO Tx O2 100% Hydratation IV sauf si suspicion AGE avec sx SNC et risque d'oedème cérébral Hyperbare: pour augmenter délivrance O2 aux tissus, réduire l'obstruction mécanique des bulles, favoriser l'élimination de l'azote If air transportation must be used, it is important to maintain cabin pressure at less than 1000 feet. Commercial aircraft are typically pressurized to a cabin altitude of 5000 to 8000 feet in cruise flight (30,000 feet). Many of these aircraft are capable of near–sea level cabin pressures if flying no higher than 15,000 to 20,000 feet. Because helicopters are not pressurized, it is recommended that they maintain an altitude of no more than 500 feet above the departure facility. Lidocaine is not effective in DCS but may have neuroprotective effects in patients with AGE and serious neurologic symptoms. It is administered as an intravenous bolus of 1 mg/kg, followed by a drip infusion of 2 to 4 mg/min Gonfler ballonnet de TET et sonde avec salin (pas air). Éviter défibrillation dans chambre hyperbare Pas trendelenburg pour AGE - transport à 0deg

Answer 16

Tx conservateur Si petit PTX - mettre drain si VPP ou chambre hyperbare

Answer 17

Rapidité d'ascension, absence d'acclilmatation, altitude, sommeil à des altitudes élevées. Augmentation du risque HAPE chez jeunes inf 20 ans, même très rare inf 2 ans. Femmes moins à risque de HAPE Pas d'augmentation du risque AMS avec augmentation de l'âge modérée: 5000 à 8000 élevée: 8000 à 14 000 ft très élevée: 14 000 à 18 000 Désaturation rapide inf 90 % lorsque altitude sup 12 000 ft Pression barométrique plus basse à une même altitude dans les pays où la latitude est plus élevée et l'hiver p/r été

Answer 18

Hyperventilation réflexe, - réponse ventilatoire hypoxique Within minutes of exposure to high altitude, the peripheral chemoreceptors in the carotid bodies sense the decrease in the partial pressure of oxygen in alveolus (PAO2) and signal the respiratory control center in the medulla to increase ventilation. Increased minute ventilation causes a decrease in the partial pressure of carbon dioxide in alveolus As minute ventilation increases, carbon dioxide exhalation increases; and within minutes, a resulting respiratory alkalosis acts on the central respiratory center to limit further increases in ventilation. To compensate for this respiratory alkalosis, the kidneys begin to excrete bicarbonate. Acetazolamide enhances this excretion. Gradual, progressive renal excretion of bicarbonate allows ventilation to rise slowly, reaching a maximum after 6 to 8 days at a given altitude La réponse à l'hypoxie prédit l'acclimatation.

Answer 19

augmentation du nomre de globules rouges et de l'hémoglobine, sécrétion d'érythropoiétine Déplacement vers la droite de la courbe secondaire au 2,3, DPG (augmente libération de l'oxygène aux tissus), mais déplacement de la courbe vers la gauche 2nd à l'alcalose respiratoire. Changement nul de la courbe avec affinité de l'hb augmenté pour l'oxygène a/n poumons.

Answer 20

Rétention liquidienne secondaire à stimulation sympathique (aldostérone, rénine, BNP, parfois vasopressine) Hypertension pulmonaire secondaire à vasoconstriction hypoxique principalement Inflammation may “sensitize” the pulmonary endothelium to mechanical injury and increase susceptibility to alveolar fluid accumulation and HAPE during ascent.

Answer 21

Incidence: 12% to 67%, varies widely with elevation, rate of ascent and individual susceptibility; rare below 8000 feet, most common with rapid ascent to altitudes above 10,000 feet. Symptoms and signs: Headache, anorexia, nausea, fatigue, dizziness, difficulty sleeping. Treatment: Mild cases are usually self-limited and do not require treatment; discontinue ascent, rest. For moderate cases, administer acetazolamide (250 BID ou 2,5mg/kg/dose); ibuprofen, aspirin, or acetaminophen for headache; prochlorperazine (stimule HVR) for nausea; supplemental oxygen if available; descend if persistent or severe; add dexamethasone in severe cases. Prevention: Gradual ascent to allow acclimatization; high-carbohydrate diet, avoidance of ethanol or smoking; acetazolamide if ascent is rapid or known history of recurrent acute mountain sickness (AMS).

Answer 22

• Tension headache • Viral syndrome • Alcohol intoxication/toxidrome • Carbon monoxide (CO) poisoning • Dehydration • Caffeine withdrawal • Migraine headache • Infectious (meningitis, encephalitis/viral syndrome) • Intracranial hemorrhage or mass • Central nervous system aneurysm • Venous sinus thrombosis • Abdominal process (eg, gastroenteritis) • Acute angle closure glaucoma/ocular process

Answer 23

it has positive effects beyond its role as a carbonic anhydrase inhibitor (diurèse bicarbonate), with beneficial chemoreceptor effects on ventilatory drive, alterations of cerebral blood flow, relaxation of smooth muscles, and upregulation of fluid resorption in the lungs, diurétique qui limite la rétention liquidienne The most common adverse reactions to acetazolamide are paresthesias and polyuria. Less common reactions include nausea, diarrhea, drowsiness, tinnitus, and transient myopia. Carbonic anhydrase inhibition at the tongue causes dysgeusia, altering the flavor of carbonated beverages, including beer. Acetazolamide is a non-antibiotic sulfa compound that carries a low risk of cross-reactivity for individuals with an allergy to sulfa antibiotics. Éviter en grossesse et allaitement

Answer 24

For treatment, use should be limited to patients with acetazolamide intolerance or more advanced cases of AMS, especially to help facilitate descent Decadron 8mg, puis 4mg q 6 hrs

Answer 25

Incidence: 0.01% to 15%, varies with elevation and rate of ascent; rare below 8000 feet and more common above 14,500 feet; typically occurs 2 to 4 days after arrival at high altitude. Symptoms and signs: Dyspnea at rest, cough, anorexia, cyanosis, rales, tachypnea, tachycardia. Treatment: Patients with mild cases may recover with bed rest. Moderate cases can be treated with bed rest and supplemental oxygen if clinical monitoring is available. Severe cases require oxygen and descent; use hyperbaric therapy if available; if oxygen or descent is unavailable, then nifedipine 30 mg slow-release every 12 hours; consider acetazolamide (125–250 mg every 12 hours) and tadalafil 10 mg every 12 hours (unstudied). Alveolar fluid clearance is upregulated by beta-adrenergic agonists in animal models, and inhaled beta-agonists have been used anecdotally for therapy of HAPE (salmeterol 125 µg inhaled twice daily). Prevention: Gradual ascent and recognition of early AMS symptoms so that ascent is stopped before HAPE develops; with previous HAPE history, use nifedipine 30 mg slow-release every 12 hours during ascent, then continue for 3 days (monitor for hypotension). Sildenafil (40 mg every 8 hours) and tadalafil (10 mg every 12 hours) are effective in preventing HAPE. Limited data suggest that dexamethasone (8 mg every 12 hours) started 2 days before ascent may prevent HAPE salmeterol 125 µg inhaled twice daily may be used as an adjunct to nifedipine in patients with a history of HAPE, although side effects are common at this high inhaled dose. Finally, clinical experience suggests that acetazolamide aids in acclimatization and prevents HAPE, and it has utility in reduction of hypoxic pulmonary vasoconstriction.

Answer 26

Carbon monoxide (CO) poisoning • Pneumonia • Pneumothorax • Pleural effusion • Pulmonary embolism (PE) • Acute coronary syndrome • Acute congestive heart failure (CHF) • Acute exacerbation of preexisting pulmonary hypertension • Acute flare of chronic obstructive pulmonary disease (COPD) • Acute asthma flare • Acute exacerbations of valvular disease (insufficiency and stenosis)

Answer 27

Incidence: Lower than 1% or 2%, uncommon as a pure entity; usually associated with the presence of severe AMS and HAPE. Symptoms and signs :ataxia cérébelleuse et AEC = 2 + sensibles, slurred speech, and altered mental status, which can range from mild emotional lability or confusion, to hallucinations and worsening obtundation that may advance to coma and death. Less commonly, generalized seizures and rarely, focal neurologic deficits may occur.Papilledema and occasionally cranial nerve palsy also occur in the setting of increased intracranial pressure. Treatment: Immediate evacuation to a lower altitude; oxygen, bed rest, dexamethasone (The initial dose of dexamethasone is 8 mg parenterally or orally in mild cases, followed by 4 mg every 6 hours.). Hyperbaric therapy if unable to immediately descend. Hyperventilation, diuretics (eg, furosemide), and hypertonic solutions (eg, mannitol) have been used to manage severely elevated intracranial pressure, but grave caution is warranted. Many patients with HACE are already volume depleted from poor fluid intake; diuretic use could compromise adequate intravascular volume and reduce cerebral perfusion pressure.

Answer 28

Acute cerebral vascular accident (CVA)/transient ischemic attack • Intracranial hemorrhage • Hypoglycemia • Carbon monoxide (CO) poisoning • Meningitis/encephalitis • Hypothermia • Intracranial mass • Vertebral/carotid dissection or stenosis • Acute toxidrome—alcohol, other • Acute alcohol withdrawal/delirium tremens • Seizure • Transient global amnesia

Answer 29

Rétinopathie la + fréquente des visiteurs en altitude Lorsque altitude sup 17 000 Physiopatho imprécise, FR imprécis Auto-résolutif sans traitement

Answer 30

**Bas risque:** Young and old Fit and unfit Mild obesity Diabetes Previous coronary artery bypass grafting (without angina) Mild chronic obstructive pulmonary disease (COPD) Asthma (moins à risque - diminution allergènes et polluants, diminution du flot turbulent) Low-risk pregnancy Controlled hypertension Controlled seizure disorder Psychiatric disorders Neoplastic diseases Inflammatory conditions **Moyen risque** Moderate COPD Asymptomatic pulmonary hypertension Compensated congestive heart failure (CHF) Morbid obesity Sleep apnea syndromes Troublesome arrhythmias Stable angina or coronary artery disease (CAD) High-risk pregnancy Sickle cell trait Cerebrovascular diseases Any cause of restricted pulmonary circulation Seizure disorder (not taking medication) (altitude diminue le seuil convulsif. acetazolamide a un effet anti convulsif) Radial keratotomy **Haut risque - CI** Sickle cell anemia (with history of crises) Severe COPD Symptomatic pulmonary hypertension Uncompensated CHF

Answer 31

Syncope lors d'immersion dans l'eau d'au moins 5deg inf à la température corporelle. Réaction vagale entrainant asystolie, FV 2nd prolongement du QT par libération catécholamines.

Answer 32

Diving reflex, ## Footnote L'immersion du visage dans l'eau induit une redistribution du débit sanguin vers le coeur et le cerveau (apnée et brady 2nd) et permet de prolonger la durée d'immersion sans séquelles neurologiques

Answer 33

Rayons gamma émis par le noyau alors que les rayons X sont émis par le déplacement des électrons autour du noyau.

Answer 34

The major sources of background radiation are radon and thoron (37%), cosmic radiation (5%), naturally occurring internal radioisotopes (eg, potassium-40 [5%]), and terrestrial background (3% Radon is a naturally occurring radioactive gas that is formed from the radioactive decay of uranium dirty bomb are cesium-137, cobalt-60, or strontium-90 Ionizing radiation includes particles and photons that have sufficient energy to produce ionization of the atoms that they encounter. (gamma rays, x-rays, and far ultraviolet). Induit effet direct (atteinte ADN) vs indirect (création de radicaux libres avec atteinte cellulaire 2nd). Cellules les plus radiosensibles sont les cellules non différenciées, qui se répliquent beaucoup et qui ont un métabolisme élevé. (marrow stem cells, lymphocytes, spermatogonia, intestinal crypt cells, and epidermal basal cells) Radiation induit un effet deterministic (sévérité de l'atteinte est dose dépendante) ou stochastic. (probabilité de l'atteinte est dose dépendante ex néo) Exposition interne: Demi-vie efficace d'un isotope est dépendant de sa demi-vie radioactive et de sa demi-vie biologique

Answer 35

Irradiation: exposition à une source radioactive. L'objet ou la personne ne devient pas radioactive (sauf s'il y a activation des neutrons) Incorporation: lorsque la substance radioactive est incorporée par un tissu/organe ou cellule. Contamination: exposition à une matière radioactive (particules alpha et beta). Contamination peut être interne ou externe

Answer 36

3 phases: Prodrome: non spécifique, no/vo, fatigue, diarrhée Latence: amélioration temporaire des sx Manifeste: trois syndromes - atteinte principalement a/n hématopoiétique et gastrointestinal Hématopoiétique: aplasie médullaire, lymphopénie est la première atteinte Gastrointestinal (1sem post): no/vo, sgmt GI 2nd destruction de la muqueuse intestinale, thrombocytopénie et immunosuppression de l'aplasie médullaire prédispose aux infections/thromboses Neuro, habituellement mortel; irritability, altered mental status, seizures, prostration, ataxia, and hypotension. Coma and death usually occur within a few hours.

Answer 37

La lymphopénie à 48 heures prédit la sévérité de l'atteinte. Mesure les lymphocytes à l'arrivée puis q 6heures. Si à 48hrs, sup 1200 - atteinte lég à mod probable. Si entre 100-500, atteinte très sévère

Answer 38

Moelle: G-CSF - neupogène pour exposition greater than 2 Gy dose, decrease in lymphocyte count, and if leukopenia is expected to last more than 7 days. It should be started within 24 hours of exposure and continued until the absolute lymphocyte count is above 1000 cells/µL. Bone marrow transplant should be considered for patients who continue to have prolonged leukopenia (2 to 3 weeks) in spite of cytokine treatment; however, the patients must not have other significant organ involvement.19 Prophylactic antibiotics should also be given in accordance with the Infectious Disease Society of America recommendations for neutropenia Treatment for the gastrointestinal sub-syndrome is largely supportive with antiemetics (preferably serotonin receptor antagonists), antidiarrheals, fluid resuscitation, antibiotics, and monitoring for signs of gastrointestinal perforation.