Plaies

Question 1

Nommer 8 facteurs de risque d’infection de plaie

Answer 1

1.

Location: Leg and thigh, then arms, then feet, then chest, then back, then face, then scalp

2.

Contamination with devitalized tissue, foreign matter, saliva, or stool

3.

Blunt (crush) mechanism

4.

Presence of subcutaneous sutures

5.

Type of repair: Risk greatest with sutures > staples > tape

6.

Anesthesia with epinephrine

7.

High-velocity missile injuries

8.

Diabetes

Question 2

Dose sécuritaire de LET gel selon poids

Answer 2

0,175mL/kg

Question 3

Quel est l’agent de conservation dans les anesthésiques locaux?

Answer 3

Méthylparaben

Question 4

Comment irriguer de facon adéquate une plaie

Answer 4

7-8 psi avec aiguille 18 et seringue 35 mL

Question 5

Indications d’antibioprophylaxie pour les plaies

Answer 5

Plaies contaminées/tissu dévitalisé/crush injuries

Fractures ouvertes

Morsures de chats

Morsures de chiens si: mains, profondes, pts agés/immunosupprimés

Plaies a/n mains (MCP)

Lacération through-through orale ( vs juste à haut risque): PNC 5 jours

Plaies ponctiformes des pieds (couvrir pseudo avec cipro si doute pseudo avec ponction à travers une semelle)

+/- pts à risque (obésité, db, immunosupprimé)

Question 6

Comment retirer un corps étranger en utilisant l’irrigation

Answer 6

Seringue de 20mL avec cathéter 16

Question 7

Nommer les 3 zones de rétrécissement oesophagiens où se logent les CE

Answer 7

Esophageal constriction locations, where foreign objects tend to lodge, are (1) the proximal esophagus at the level of the cricopharyngeus muscle and thoracic inlet or, radiographically, the clavicular level; (2) the midesophagus at the level of the aortic arch and carina; and (3) the distal esophagus just proximal to the esophagogastric junction or, radiographically, a level two to four vertebral bodies cephalad to the gastric bubble

Question 8

Options médicamenteuses pour obstruction oesophagienne avec aliments

Answer 8

Glucagon

Liquides pétillants

Nitroglycérine

Adalat

Endoscopie

Question 9

Grosseur de CE gastrique qui ne passera pas le pylore/duodénum

Answer 9

2 cm de large, 5-6 cm de long

Question 10

Quand réparer ou non une morsure?

Answer 10

Question 11

Nommer 10 facteurs de risque d’infection de plaies par morsures

Answer 11

Question 12

Nommer les choix de traitement antibio des morsures selon l’espèce

Answer 12

Question 13

Indications d’hospit pour patients avec morsures

Answer 13

Structural

Injury to deep structures (bones, joints, tendons, arteries, or nerves)

Injuries requiring reconstructive surgery

Injuries requiring general anesthesia for appropriate wound care

Infectious

Rapidly spreading cellulitis

Significant lymphangitis or lymphadenitis

Evidence of sepsis

Infection in patients at high risk for complications (see Table 54.2)

Infections involving bones, joints, tendons

Infection with failed outpatient therapy

Question 14

Nommer l’agent responsable de la majorité des infections liées à une morsure de singe et sa présentation clinique

Answer 14

Virus B (hespes simiae, herpesvirus B…)

Vésicules au site de morsure, paresthésie et faiblesse du membre, AEC, paralysie NC, coma, ataxie, insuffisance respiratoire

3 présentations:

• Vesicular or ulcerative lesions, tingling, pain, or itching at the site of exposure, and local lymphadenopathy [29].

●Influenza-like illness with fever and myalgias. Later symptoms may include numbness or paresthesias near the site of exposure, fever, conjunctivitis, abdominal pain, hepatitis, or pneumonitis followed by central nervous system (CNS) symptoms.

●Nausea and vomiting and CNS symptoms including headache that may progress to meningismus, cranial nerve deficits, dysarthria, dysphagia, seizures, paralysis, respiratory failure, and coma.

Prophylaxie post-exposition: valtrex 1 g q 8hr

Maladie : acyclovir IV

Question 15

Nommer des situations où la prophylaxie pour virus B est recommandée/considérer ou non recommandée

Answer 15

Prophylaxie avec valtrex 1 g PO TID 14 jours

Traitement avec acyclovir IV

Question 16

Qu’est-ce que le rat bite fever?

Answer 16

Rat bite fever is a disease syndrome caused by Streptobacillus moniliformis or Spirillum minus, both found in the nasopharyngeal flora of healthy rats.

Fièvre suivie de polyarthralgie migratrices avec rash maculopapulaire/purpurique

tx PNC ou tetracycline/streptomycine si allergie

Question 17

Nommer 5 maladies transmises par les rats

Answer 17

Rat bite fever

Leptospirose

Tularémie

Sporotrichose

Peste

Typhus murin (Rickettsia typhi)

.

Question 18

Mammifères à risque de transmission rage

Answer 18

Chauves souris

Coyotes

Ratons laveurs

Renards

Mouffettes

Chiens errants

Question 19

Comment différencier un serpent venimeux d’un non venimeux?

Answer 19

Question 20

Nommer des facteurs qui influencent la sévérité d’un morsure de serpent venimeux

Answer 20

Serpent: âge, santé et taille

Toxicité du venin

Condition des crocs

Si serpent s’est nourri ou est malade

Victime: taille, age, santé

Localisation morsure

Question 21

Décrire un empoisonnement par une vipère

Answer 21

Au site de morsure: dlr et engourdissement, oedème sous cutané qui progresse, risque de compartiment

Nécrose cutanée locale, ecchymose, pétéchies/bulles hémorragiques

Engourdissement/picottement péri-buccal, goût métallique, no/vo/faiblesse, fasciculations, hypotension

MOF 2nd CIVD et atteinte perméabilité capillaire

Question 22

Décrire l’empoisonnement aux coral snake

Answer 22

Many of these species’ venoms contain compounds that block neuromuscular transmission at acetylcholine receptor sites and have direct inhibitory effects on cardiac and skeletal muscle. Ptosis is common and often the first outward sign of envenomation. Other signs and symptoms include vertigo, paresthesias, fasciculations, slurred speech, drowsiness, dysphagia, restlessness, increased salivation, nausea, and proximal muscle weakness. The usual cause of death is respiratory failure.

Question 23

Prise en charge d’une morsure de serpent

Answer 23

1. Dégager la victime du serpent et transport rapide vers un hôpital
2. Calmer la victime, immobiliser le membre, NPO
3. Bandage constrictif pour limiter dispersion du venin
4. Glace localement pour diminuer douleur
5. Identification du serpent/prise de photo
6. Analgésie, soluté
7. Histoire au DU: Specific historical information includes time elapsed since the bite, the number of bites, whether first aid was administered and what type, location of the bite, and symptoms (eg, pain, numbness, nausea, tingling around the mouth, metallic taste in the mouth, muscle cramps, dyspnea, and dizziness).
8. Risque d’allergie à l’anti-venin: An allergy history with emphasis on symptoms after exposure to horse or sheep products, previous injection of horse or sheep serum, and a history of asthma, hay fever, urticaria, or allergy to wool, papain, chymopapain, papaya, or pineapple should be obtained if antivenom treatment is being considered.
9. Anti-venin
10. vérifier immunisation tétanos, antibio si surinfection (clavulin)
11. Nettoyage plaie avec eau + savon

Question 24

Décrire les différents stade d’empoisonnement aux serpents

Answer 24

• Grade 0 (minimal): There is no evidence of envenomation, but snakebite is suspected. A fang wound may be present. Pain is minimal, with less than 1 inch of surrounding edema and erythema. No systemic manifestations are present during the first 12 hours after the bite. No laboratory changes occur.
• Grade I (minimal): There is minimal envenomation, and snakebite is suspected. A fang wound is usually present. Pain is moderate or throbbing and localized to the fang wound, surrounded by 1 to 5 inches of edema and erythema. No evidence of systemic involvement is present after 12 hours of observation. No laboratory changes occur.
• Grade II (moderate): There is moderate envenomation, more severe and widely distributed pain, edema spreading toward the trunk, and petechiae and ecchymoses limited to the area of edema. Nausea, vomiting, and a mild elevation in temperature are usually present.
• Grade III (severe): The envenomation is severe. The case may initially resemble a grade I or II envenomation, but the course is rapidly progressive. Within 12 hours, edema spreads up the extremity and may involve part of the trunk. Petechiae and ecchymoses may be generalized. Systemic manifestations may include tachycardia and hypotension. Laboratory abnormalities may include an elevated white blood cell count, creatine phosphokinase, prothrombin time, and partial thromboplastin time, as well as elevated fibrin degradation products and D-dimer. Decreased platelets and fibrinogen are common. Hematuria, myoglobinuria, increased bleeding time, and renal or hepatic abnormalities may also occur.
• Grade IV (very severe): The envenomation is very severe and is seen most frequently after the bite of a large rattlesnake. It is characterized by sudden pain, rapidly progressive swelling that may reach and involve the trunk within a few hours, ecchymoses, bleb formation, and necrosis. Systemic manifestations, often commencing within 15 minutes of the bite, usually include weakness, nausea, vomiting, vertigo, and numbness or tingling of the lips or face. Muscle fasciculations, painful muscular cramping, pallor, sweating, cold and clammy skin, rapid and weak pulse, incontinence, convulsions, and coma may also be observed. An intravenous bite may result in cardiopulmonary arrest soon after the bite.

Question 25

Décrire l’administration d’un anti-venin

Answer 25

Anti-venin: use of antigen-binding fragments (Fabs) of sheep (ovine) immunized against four species of venomous snake found in the United States.

1. être prêt en cas de réaction anaphylactique à l’anti-venin
2. Grossesse n’est pas une CI
3. Administration IV (pas près de la morsure)
4. Chez les patients ayant reçu de hautes doses d’anti-venin, risque de développer maladie sérique dans les semaines suivantes.

Question 26

Décrire les sx d’une piqûre par fire ant

Answer 26

The sting usually produces a sterile pustule within 24 hours. Le venin induit une destruction tissulaire et une hémolyse. Other symptoms include local burning, redness, and itching. With multiple stings and in sensitive individuals, urticaria, angioedema, dyspnea, nausea, vomiting, wheezing, dizziness, and respiratory arrest may occur.

Question 27

Décrire les ss/sx d’une morsure par veuve noire

Answer 27

Dlr lors de la morsure, puis oedème et rougeur

Associated symptoms include dizziness, restlessness, ptosis, nausea, vomiting, headache, pruritus, dyspnea, conjunctivitis, facial swelling, sweating, weakness, difficulty speaking, anxiety, and cramping pain in all muscle groups. Priapism has been reported in children. The patient is usually hypertensive, and cerebrospinal fluid pressure is sometimes elevated.

(The ingredient most toxic to humans is thought to be a neurotoxin. This toxin destabilizes neuronal membranes by opening ionic channels, causing depletion of acetylcholine from presynaptic nerve terminals and increasing the frequency of spontaneous miniature endplate potentials at neuromuscular junctions)

Question 28

Traitement morsure veuve noire

Answer 28

Inspecter la plaie à la recherche lacérations 2nd crocs

Laver avec eau + savon

Vérifier tétanos

Analgésie

Tx spasmes musculaires avec benzo

Candidates for antivenom include patients with severe envenomation manifesting as seizures, respiratory failure, or uncontrolled hypertension, and patients not responding to other therapy. The dose of the antivenom is one vial diluted in 50 mL of normal saline and administered intravenously over a period of 15 minutes.

Question 29

Nommer ss/sx morsure par brown recluse

Answer 29

brûlure lors morsure

Zone blanchâtre due vasoconstriction intense

Bulle se forme qui devient hémorragique (aspect bull’s eye)

Nécrose cutanée

fever, chills, rash, petechiae, nausea, vomiting, malaise, and weakness. Hemolysis, thrombocytopenia, shock, jaundice, renal failure, hemorrhage, and pulmonary edema are the usual signs of severe envenomation

Question 30

Tx brown recluse

Answer 30

Anti-venin, non disponible aux USA

Tx support - analgésie, échanges plasmatiques, hémofiltration

Antibio si surinfection

Tx HBO PRN

Dapsone ( peu recommandé)

Question 31

Sx et tx d’une morsure de scorpion

Answer 31

the victim may have heightened sensitivity to touch in the area of the sting along with local numbness and weakness. The diagnosis is often made by tapping on the site of the sting and causing an increase in pain at the site. Systemic symptoms may then develop, including anxiety, restlessness, muscle spasms, nausea, vomiting, excessive salivation, sweating, itching of the nose and throat, hyperthermia, blurred vision, roving eye movement or nystagmus, myoclonus, priapism, hypertension, hemiplegia, syncope, cardiac dysrhythmias, and respiratory arrest

Tx: anti venin si sx sévères, analgésie, benzo pour spasmes

Question 32

Sx d’une piqûre de raie

Answer 32

The victim experiences an immediate, intense pain in the area of the wound, which may spread to the entire extremity. Systemic symptoms include salivation, nausea, vomiting, diarrhea, syncope, muscle cramps, fasciculations, dyspnea, cardiac dysrhythmias, and convulsions.

Question 33

Traitement des marine stings

Answer 33

Immersion dans l’eau chaude pour diminuer la douleur, vinaigre sur nematocystes ou vinaigre chaud

Analgésie

Antibio prophylaxie si doute CE (cipro)

Anti-venin pour certaines espèces

Tétanos

Question 34

Décrire les stades de brûlures

Answer 34

Question 35

Quel est le score de Baux?

Answer 35

The Baux score is the sum of the patient’s age and the percentage of TBSA burned.18 In the original article, the Baux score that predicted 100% mortality was 100. A more recent study found that a Baux score of 160 predicted 100% mortality, and a Baux score of 109.6 predicted 50% mortality (95% confidence interval), which is a testament to improved therapy and outcomes.

Question 36

Nommer les stades de sévérité de brûlures

Answer 36

Question 37

PRise en charge d’un brûlé

Answer 37

• Monitoring cardiovasculaire / monitorer température
• Refroidir brûlure avec eau froide
• Signes de brûlures des voies aériennes: facial burns, hoarseness, drooling, carbonaceous sputum, and singed nasal hairs
• Éviter ISR sauf si aucun
• Remplissage volémique
• R/O CO, cyanure
• tétanos

Question 38

Critères de transfert en centre de grands brûlés

Answer 38

Partial thickness burns greater than 10% TBSA

Burns that involve the face, hands, genitalia, perineum, or major joints

Third degree burns in any age group

Electrical burns, including lightning injury (see Chapter 134)

Chemical burns

Inhalation injury

Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality

Any patient with burns and concomitant trauma (such as, fractures) in which the burn injury poses the greatest risk of morbidity or mortality

Burned children in hospitals without qualified personnel or equipment for the care of children

Burn injury in patients who will require special social, emotional, or rehabilitative intervention

Question 39

Décrire la classification des brûlures de l’oeil

Answer 39

Question 40

Décrire la toxicité du HF

Answer 40

Induit nécrose de liquéfaction (malgré qu’il soit acide)

L’ion libre fluor lie le Ca et Mg, induisant hypocalcémie et hypomagnésémie, inhibe pompe NaKATPase et cycle Krebs, hyperkaliémie (2nd destruction cellulaire + inhibition NaKATPase)

Inhalation: oedème pulmonaire, pneumonite, ARDS, +/- décès

GI: rare, no/vo/dlr abdo +/- toxicité systémique au fluor

Oeil: irrigation

Peau: + fréquent, cause une destruction tissulaire, peut progresser ad brûlures 3e degré

Traitement: irrigation 15-30 min, débrider phlyctènes

topique: gel 2.5% gluconate de calcium (3.5g gluconate Ca dans 150 mL lubrifiant à base d’eau

Pas gluconate de calcium a/n yeux

Infiltration sous-cutanée: gluconate de calcium 5% avec 1:1 salin 0.9%, 0,5mL/cm 2 en sous-cutané. Souffrant, penser bloc nerveux

Perfusion intra-artérielle: The extremity is elevated for 1 minute, and a double-cuffed tourniquet is inflated to 40 kPa. An elastic bandage is then placed at 8 kPa. Subsequently, 10 ml of a 10% solution of calcium gluconate in 30-40 ml of normal saline solution was infused over 2 minutes. The tourniquet is then deflated over 20 minutes.12 Another approach involves the administration of a mixture of 10 mL of solution of 10% calcium gluconate in 40 to 50 mL of normal saline infused over 4 hours

Perfusion de calcium IV

Question 41

Acide formique

Answer 41

nécrose coagulation

Acidose métabolique, saignement GI, perforation intestinale, hémolyse par induction stress oxydant

Tx de support, acide folinique pour intox sévère, hémodialyse

Question 42

Ammoniac

Answer 42

Stocké à -30 degré, donc exposition au liquide induit nécrose et engelures.

Exposition gazeuse induit une nécrose de liquéfaction avec destruction tissulaire, très soluble donc lésions proximales a/n muqueuses

Tx support

Question 43

Ciment

Answer 43

Oxyde de calcium se combine à l’eau pour former de l’hydroxyde de calcium

Brûlures liées à la chaleur, abrasion ou blast

Tx support

Question 44

Phénol

Answer 44

Induit nécrose de coagulation.

Plus la substance est concentrée, plus la coagulation se développe rapidement et entraîne moins de dommage qu’une substance moins concentrée

a/n systémique: altération SNC (coma, convulsions, léthargie), troubles de conduction cardiaque (tachy/brady), hypothermie, acidose métabolique

Tx avec PEG lyte ou alcool isopropylique

Traitement de support pour toxicité systémique, xylo pour arythmies ventriculaires

Question 45

phosphore

Answer 45

The autoignition temperature (the temperature at which spontaneous combustion can occur) is 30°C (86°F). When white phosphorus comes in contact with air at temperatures above the autoignition point, the phosphorus spontaneously oxidizes, forming phosphorus pentoxide. Phosphorus pentoxide can combine with small amounts of moisture in the air, forming phosphoric acid

Acide phosphorique cause une brûlure thermique

After oral ingestion of white phosphorus, three stages of toxicity are described, although it is uncommon that all three stages occur. The first stage, which can last 8 to 24 hours, is characterized by gastrointestinal tract irritation, including vomiting, abdominal pain, diarrhea, and gastrointestinal bleeding. The stool is occasionally described as being luminescent or “smoking.” Hypovolemic shock can result. Up to one third of patients who ingest significant quantities of white phosphorus will die during this stage. The second stage is a latent phase. During this period, which can last 1 to 3 days, symptoms appear to be improving. However, the third stage is characterized by multisystem organ failure, including hepatic failure, renal failure, and CNS depression. Renal failure is usually present at days 1 to 4, whereas jaundice typically manifests at days 3 to 5.

Metabolic derangements can also occur after white phosphorus exposure, including hypocalcemia and hyperphosphatemia. Conduction system disturbances, including bradycardia, QT prolongation, and ST and T wave abnormalities,

Tx: décontamination, immersion dans l’eau froide en préhospitalier, irrigation avec salin 09% à l’urgence

Tx support

Question 46

Nitrates et nitrites

Answer 46

Induction de méthémoglobinémie

Étourdissement, céphalée, dyspnée, arythmies, acidose, confusion, léthargiescoma, convulsions

Tx: 1-2 mg/kg de bleu de méthylène

Si inefficace ou déficit G6PD, échanges transfusionnels

Question 47

Chlorine, chloramine, phosgène

Answer 47

Nébulisation bicarbonate de Na 4% pour chlorine, chloramine

Nébulisation n-acétylcystéine pour phosgène

Question 48

Décrire les 4 types de gaz utilisés comme agents de terrorisme

Answer 48