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Frostbites

Frostbites. Localized damage due to freezing of the tissues following a more or less prolonged exposure to temperatures below 0 ° C Clinical appearance close to the burn but different pathophysiology and therapeutic approach. No actual randomized treatment with proven efficacy

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Frostbites

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  1. Frostbites Localized damage due to freezing of the tissues following a more or less prolonged exposure to temperatures below 0 ° C Clinical appearance close to the burn but different pathophysiology and therapeutic approach. No actual randomized treatment with proven efficacy Bone vitality allows prognosis. 1

  2. People at risk Sportsmen (mountain and polar regions) Mainlyat Mont Blanc hospitals Frostbite 80 / year 20 severe cases (> stage 2) 2

  3. People atrisk Urban population: Homeless Tramp Suicide attempt 3

  4. People at risk Urban population Car failure Alcohol 4

  5. Pathophysiology / Clinical features Four phases 5

  6. Opening arteriovenous shunts

  7. Primary phase Cooling and frost action Peripheral vasoconstriction Closure of precapillary sphincters and opening arteriovenous shunts (wrists and ankles) in response to the decline in core temperature Cell death by mechanical damage (recrystallization) and cellular dehydration Physiopathologie

  8. Secondary phase (1h): warming Coagulation phase resulting in few hours to a more or less complete shutdown of the microcirculation. Crucial phase that allows the assessment of severity Initial lesion Grey appearance or cyanotic Hypo-or anesthesia Centripetal Unmoved Pulp temperature - Doppler - pathophysiology

  9. Secondary phase (24h): warming and progressive necrosis Ischemia-reperfusion syndrome [3] characterized by the release of vasoactive substances with progressive tissue necrosis upstream and endothelial permeability disorder causing some impressive blisters Appearance of blisters Hematic serum or hemorrhagic large compressive Physiopathology

  10. Rabbitear Priority: "fight against the progressive phase of necrosis! "

  11. Late phase: permanent damage Slow and gradual phase, may take several weeks (J7-J45), slowly devitalization and evolution toward irreversible dry gangrene. Physiopathology

  12. Aspirin, NSAIDs, calcium-blockers, vasodilators (buflomedil, pentoxifylline), anticoagulant, anti-plateletaggregation, dextran, acupuncture, ... Spinal block, or plexus nerve block ... sympatheticblockadeisregularlyadvocated and criticized. Hyperbaricoxygentherapy has been usedextensively in the late 1960s withoutevidence of itseffectiveness. The neurospinal stimulation isrecommended by the Zaragoza team. Itsmechanismisrelated to the autonomicvasodilation and prostacyclin production stimulation (R Arregui, 1989). Therapy 13

  13. Thrombolytic: r-tPA alteplase Thrombolytic activate the conversion of plasminogen to plasmin, which has a proteolytic action on fibrin clots but also the circulating fibrinogen. The desired effect is the lysis of fibrin pathological thrombus at the cost of bleeding risk fibrinolysis of hemostatic plug. Tissue plasminogen activator (tPA) or alteplase (Actilyse) lysing the clot faster than thrombolytic first generation. Prostacyclin analogue: iloprost antiplatelet Vasodilation of arterioles and venules Increased pressure of the capillary network Activation of fibrinolysis Inhibition of leukocyte adhesion Decreased release of free radicals Therapy 14

  14. Initial management Rapid warming protocol (30’ at 38°C) Infusion of 400 mg of buflomedil Aspirin 250 mg IV bolus Evaluation of extension level stage 1 stage 2 stage 3 stage 4

  15. Cauchy et al “New classification” in Wilderness Environ Med 2001 Winter; 12 (4) : 248-55. 16

  16. Dr Emmanuel Cauchy 17

  17. Hospital 8 days: 47 patients Treatment A (n: 15, 106 fingers / toes) Aspirin: 250mg IV / day buflomedil: 400mg IV / day Treatment B (n: 16, 142 fingers / toes) Aspirin: 250mg IV / day iloprost: 0.5 to 2 ng / kg / min / IV 5 hours / day Treatment C (n: 16, 164 fingers / toes) Aspirin: 250mg/jour r-PA: 100mg IV first day only (<24h) iloprost: 0.5 to 2 ng / kg / min / IV 5 hours / day 18

  18. Bone scintigraphy with Tc-99m Only further examination validated on a large series Non invasive Prognosis J2 Forensic Journal of Hand Surgery American (Sept 2000) European Journal of Nuclear Medicine (Mai 2000)

  19. 20

  20. 21

  21. Etude randomisée de 47 patients Risque d’amputation par stade de gravité en fonction du traitement 22

  22. Protocol NOT randomised 23

  23. Treatment A [42 patients] • Rapid rewarming protocol + aspirin+ vasodilator (buflomedil) • Treatment B [57 patients] • Rapid rewarming protocol + aspirin + prostacycline • Treatment C [18 patients] • Rapid rewarming protocol + aspirin + prostacycline + fribrinolysis • Treatment D [9 patients]High altitude rewarming and delayed treatment Treatement (1) 24

  24. Amputation if unsuccess of therapie 25

  25. % fingers amputated * * Only 2 patients were included in that group 26

  26. % of amputation of fingers n: 459 Amputation of fingers 27

  27. …few cases in pictures

  28. BBriancon, mountaineer Images transmitted via the Internet Aspegic + Iloprostriançon, alpinisteImages transmises par InternetAspegic + Iloprost

  29. D8 treatement with aspirine et iloprost 30

  30. AosteYoung Swedish drunk Teleconsultation by Iphone

  31. After 15 days

  32. Swedish St Jean de Maurienne28 years 33

  33. After 4 days with aspégic iloprost 34

  34. Frostbites and emergency Stage 1 and 2: Aspégic 250 mg / day (outpatient) Stage 3: 250 + Aspégic Iloprost PSE - 8 days Stage 4: Thrombolysis + Iloprost PSE - 8 days (?) J3 scintigraphyafterremoval blisters Europeanregister of frostbite 35

  35. THANK YOU Zanardi Fabio MD Hospital of Aosta ( Italy)

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