Plaies Flashcards
Nommer 8 facteurs de risque d’infection de plaie
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
Dose sécuritaire de LET gel selon poids
0,175mL/kg
Quel est l’agent de conservation dans les anesthésiques locaux?
Méthylparaben
Comment irriguer de facon adéquate une plaie
7-8 psi avec aiguille 18 et seringue 35 mL
Indications d’antibioprophylaxie pour les plaies
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)
Comment retirer un corps étranger en utilisant l’irrigation
Seringue de 20mL avec cathéter 16
Nommer les 3 zones de rétrécissement oesophagiens où se logent les CE
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
Options médicamenteuses pour obstruction oesophagienne avec aliments
Glucagon
Liquides pétillants
Nitroglycérine
Adalat
Endoscopie
Grosseur de CE gastrique qui ne passera pas le pylore/duodénum
2 cm de large, 5-6 cm de long
Quand réparer ou non une morsure?
Nommer 10 facteurs de risque d’infection de plaies par morsures
Nommer les choix de traitement antibio des morsures selon l’espèce
Indications d’hospit pour patients avec morsures
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
Nommer l’agent responsable de la majorité des infections liées à une morsure de singe et sa présentation clinique
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
Nommer des situations où la prophylaxie pour virus B est recommandée/considérer ou non recommandée
Prophylaxie avec valtrex 1 g PO TID 14 jours
Traitement avec acyclovir IV
Qu’est-ce que le rat bite fever?
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
Nommer 5 maladies transmises par les rats
Rat bite fever
Leptospirose
Tularémie
Sporotrichose
Peste
Typhus murin (Rickettsia typhi)
.
Mammifères à risque de transmission rage
Chauves souris
Coyotes
Ratons laveurs
Renards
Mouffettes
Chiens errants
Comment différencier un serpent venimeux d’un non venimeux?
Nommer des facteurs qui influencent la sévérité d’un morsure de serpent venimeux
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
Décrire un empoisonnement par une vipère
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
Décrire l’empoisonnement aux coral snake
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.
Prise en charge d’une morsure de serpent
- Dégager la victime du serpent et transport rapide vers un hôpital
- Calmer la victime, immobiliser le membre, NPO
- Bandage constrictif pour limiter dispersion du venin
- Glace localement pour diminuer douleur
- Identification du serpent/prise de photo
- Analgésie, soluté
- 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).
- 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.
- Anti-venin
- vérifier immunisation tétanos, antibio si surinfection (clavulin)
- Nettoyage plaie avec eau + savon
Décrire les différents stade d’empoisonnement aux serpents
- 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.
Décrire l’administration d’un anti-venin
Anti-venin: use of antigen-binding fragments (Fabs) of sheep (ovine) immunized against four species of venomous snake found in the United States.
- être prêt en cas de réaction anaphylactique à l’anti-venin
- Grossesse n’est pas une CI
- Administration IV (pas près de la morsure)
- Chez les patients ayant reçu de hautes doses d’anti-venin, risque de développer maladie sérique dans les semaines suivantes.
Décrire les sx d’une piqûre par fire ant
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.
Décrire les ss/sx d’une morsure par veuve noire
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)
Traitement morsure veuve noire
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.
Nommer ss/sx morsure par brown recluse
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
Tx brown recluse
Anti-venin, non disponible aux USA
Tx support - analgésie, échanges plasmatiques, hémofiltration
Antibio si surinfection
Tx HBO PRN
Dapsone ( peu recommandé)
Sx et tx d’une morsure de scorpion
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
Sx d’une piqûre de raie
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.
Traitement des marine stings
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
Décrire les stades de brûlures
Quel est le score de Baux?
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.
Nommer les stades de sévérité de brûlures
PRise en charge d’un brûlé
- 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
Critères de transfert en centre de grands brûlés
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
Décrire la classification des brûlures de l’oeil
Décrire la toxicité du HF
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
Acide formique
nécrose coagulation
Acidose métabolique, saignement GI, perforation intestinale, hémolyse par induction stress oxydant
Tx de support, acide folinique pour intox sévère, hémodialyse
Ammoniac
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
Ciment
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
Phénol
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
phosphore
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
Nitrates et nitrites
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
Chlorine, chloramine, phosgène
Nébulisation bicarbonate de Na 4% pour chlorine, chloramine
Nébulisation n-acétylcystéine pour phosgène
Décrire les 4 types de gaz utilisés comme agents de terrorisme
