Choc hémorragique – Damage control...Damage control Keeping afloat a badly damaged ship by...
Transcript of Choc hémorragique – Damage control...Damage control Keeping afloat a badly damaged ship by...
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Choc hémorragique – Damage control
Pr Philippe VignonRéanimation Polyvalente
CIC U0802
CHU Limoges
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Plan
1. Rappels de physiologie
2. Choc hémorragique traumatique
3. Damage control
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1. Rappels de physiologie
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Répartition du volume sanguin total
~ 65 % de la volémie est contenue dans le système veineux (rôle de stockage)
Volémie : volume sanguin total de l’organisme
65 à 75 mL/kg : ~ 5 L adulte
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Reservoirveineux(65%)
Coeur droit(3%)
Poumons(9%)
Coeurgauche (3%)
Arteres(13%)
Arterioles+
Capillaires(7%)
Volumecontraint
VolumeNon
contraint
Régulation du système cardiovasculaire
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Perfusion des tissus
DEBIT régional PRESSION de perfusion d’organe
PERFUSION DES ORGANESPERFUSION DES ORGANES(adéquation besoins / apport en nutriments)(adéquation besoins / apport en nutriments)
Débit Débit cardiaquecardiaque
Pression Pression artérielleartérielle
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Pression artérielle (PA)
PA (mmHg) = DC (L/min) x RAS (UI)
DC DC
Maintien d’un niveau de PA adéquat
Maintien d’un niveau de PA adéquat
DC : débit cardiaque ; RAS : résistances artérielles systémiques
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Régulation : système nerveux autonome
PARASYMPATHIQUESYMPATHIQUE
Sympathique : + lent mais + puissant que le parasympatique
• ↑ fréquence cardiaque
• ↑ débit cardiaque
• ↑ vaso-constriction(pression artérielle)
• ↓ fréquence cardiaque
• ↓ débit cardiaque
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Stimulation du sympathique
Vasoconstriction : veines + artères
↑ débit cardiaque
veines
↑ pression artérielleartères
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Transport artériel en oxygène (TO2)
TO2 = DC x CaO2
VES x FC
DC : débit cardiaqueVES : volume d ’éjection systoliqueFC : fréquence cardiaque
(Hb • SaO2) + (PaO2)
CaO2 : contenu artériel en O2Hb : hémoglobinémieSaO2 : saturation artérielle en O2PaO2 : pression en O2 du sang artériel.
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JAMA 1998 ; 279 : 217JAMA 1998 ; 279 : 217--221221
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Le transport en O2 diminue pour une Hb < 6 g/dL chez un sujet normal au repos
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Vatner S. NEJM 1975; 293, 293:970Vatner S. NEJM 1975; 293, 293:970--976.976.
0 5 10 15 20 25
-10
-20
-30
-40
-50
∆∆ PAM (%)PAM (%)0
EveillEveillééEveillEveilléé et barodenervet barodenervééPentobarbitalPentobarbital
Hémorragie (mL/kg)
-60
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2. Choc hémorragique traumatique
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Choc hémorragique traumatique
• Polytraumatisme : 1ère cause de décès chez < 44 ans
• 30 à 50 % de décès précoces par hémorragie non contrôlée
• 50 % de décès sur les lieux de l’accidents
• 30% de décès dans les 24 h
• 20% de décès tardifs (défaillance polyviscérale)
Kauvar DS Crit Care 2005 ; 9 : S1-S9
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Conduite à tenir
1. Identifier l’état de choc hémorragique
2. Localiser le saignement actif
3. Maintenir une oxygénation tissulaire adéquate
4. Eviter de péréniser le saignement.
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Choc hémorragique
> 140> 120> 100< 100FC (bpm)
< 55 - 1520 - 30> 30Diurèse (ml/h)
effondréediminuéenormalenormalePA (mmHg)
comaconfusionagitationanxiétéNiveau de conscience
> 20001500-2000800-1500750Vol. pertes (ml)
> 40 %30 – 40 %15 – 30 %< 15 %% volémie perdue
MassiveImportanteModéréeMinime
Hypotension artérielle : > 1,5 L de sang perdu….
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Anémie aiguë : perte et hémodilution
L’hématocrite reste initialement normale
(perte proportionnelle de GR et eau plasmatique)
L’anémie est aggravée par les perfusions
(hémodilution) nécessaire pour le maintien du débit
cardiaque et de la pression artérielle
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Conduite à tenir
1. Identifier l’état de choc hémorragique
2. Localiser le saignement actif
3. Maintenir une oxygénation tissulaire adéquate
4. Eviter de péréniser le saignement
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Polytraumatisé & choc hémorragique
Brancard : +
Stable Instable
Bloc / embolisation
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Hémorragie extériorisée : geste d’hémostase
• Compression directe d’une lésion vasculaire
• Suture plaie scalp (attention âges extrêmes)
• Immobilisation foyer fracture
• Tamponnement épistaxis (trauma facial).
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Conduite à tenir
1. Identifier l’état de choc hémorragique
2. Localiser le saignement actif
3. Maintenir une oxygénation tissulaire adéquate
4. Eviter de péréniser le saignement.
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Remplissage vasculaire
Vasopresseur - Norepinephrine0,5 mg/h ou 0,1 g/kg/min
Choc hémorragiquePAS < 90 mmHg, PAM < 60 mmHg
Hémostase chirugicaleou artérioembolisation
1000 - 1500 mL
PA
80 ≤ PAS ≤ 90 mmHg
Transfusion produitsdérivés du sang
PAS < 80 mmHg PAM < 60 mmHg
Hb 7-9 g.dL-1
TP > 40%Plaquettes ≥ 50.109 L-1
Pas de trauma crânien
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Remplissage vasculaire
Vasopresseur - Norepinephrine0,5 mg/h ou 0,1 g/kg/min
Choc hémorragiquePAS < 90 mmHg, PAM < 60 mmHg
Hémostase chirugicaleou artérioembolisation
1000 - 1500 mL
PA
PAS ≥ 120 mmHg
Transfusion produitsdérivés du sang
PAS < 120 mmHg PAM < 90 mmHg
Hb 10 g.dL-1
TP > 50%Plaquettes ≥ 80-100.109 L-1
Trauma crânienGlasgow ≤ 8
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Conduite à tenir
1. Identifier l’état de choc hémorragique
2. Localiser le saignement actif
3. Maintenir une oxygénation tissulaire adéquate
4. Eviter de péréniser le saignement.
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Eviter d’aggraver le saignement
• Cible de PA adaptée (systolique entre 80 et 90 mmHg
en l’absence de trauma crânien sévère)
• Introduction précoce des vasopresseurs (éviter
hémodilution par remplissage excessif)
• Apport précoce de GR et produits de coagulation (PFC,
plaquettes et fibrinogène)
• Prévention de l’hypothermie
• Prévention de l’acidose
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Triade de la mort
Coagulopathie
HypothermieAcidose
métabolique
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Coagulopathie induite : aggravation du saignement
Saignement
Traitement (perfusions)
Hémodilution + hypothermie
Coagulopathie
Il faut réchauffer et transfuser précocement le (poly)traumatisé
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Rossaint R et al. Shock 2006;26:322-331
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Iraq : 246 patients avec transfusions massives (≥ 10 CG ou sang total)
Borgman MA et al., J Trauma. 2007;63:805–813
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3. Damage control
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Damage controlKeeping afloat a badly damaged ship by procedures to limit flooding, stabilize the vessel, isolate fires and explosions and avoid their spreading
Part de la réanimation dans laquelle il y a un contrôle chirurgical de l’hémorragie et de la contamination (digestive) suivie par une fermeture rapide permettant une correction
des désordres physiologiquesMoore EE. World J Surg. 1998; 1184-1191
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Lésion hémorragique identifiée
Contrôle du saignement lors d’une chirurgie brève
Correction de la triade mortelle
Chirurgie définitive ultérieure
Prévenir le syndrome du compartiment abdominal
Damage control : les étapes
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The “bloody vicious cycle”
Damage Control is…Damage control resuscitation
andstaged surgery
Damage Control is…Damage control resuscitation
andstaged surgery
1
Selection
2
Resuscitativelaparotomy
3
Restorationof
physiology
5
Abdominal wall
reconstruction
ED / OR OR ICU OR OR / ICU
4
Definitivesurgery
K Boffard
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1. Sélection des blessés
• Facteurs principaux : la triade mortelle
– Coagulopathie
– Hypothermie : Tº < 34º C
– Acidose métabolique sévère : pH < 7,2 ; lactates > 5 mmol/L
• Facteurs secondaires :
– Polytraumatisme sévère
– Temps opératoire > 90 min.
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2. Contrôle de l’hémorragie
• Compression manuelle
• Packing
• Clampage
Ecourter au maximum la durée de l’intervention
Limiter la contamination
Eviter le syndrome du compartiment abdominal
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3. Réanimation : correction triade
• Optimisation hémodynamique (correction acidose
lactique)
• Réchauffement
• Correction de la coagulopathie
• Optimisation de la ventilation
• Identification lésions traumatiques associées.
Attention piège : syndrome du compartiment abdominal !!
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4. Retour au BO pour complément chirurgical
• Identifier le bon moment
• Patient stabilisé (plus de saignement actif)
• Triade corrigée
• Hyperpression intra-abdominale débutante ?
• Risque infectieux ?
Geste chirurgical définitif ou non
Pb paroi abdominal ?
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0%10%20%30%40%50%60%70%80%90%
100%
damage control procédureconventionnelle
35%
93%
Taux de décès selon la technique chirurgicale
Étude prospective n = 17Stone et als Ann Surg 1983
Survie des patients en choc hémorragique grave non contrôlé
Etude prospective n = 102Burch Ann Surg 1993
67%
87%
Damage control et pronostic
Décrit initialement pour l’abdomen mais applicable à la chirurgie thoracique, orthopédique, vasculaire, neurochir…
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Facteur VIIa ?
• Conditions d’utilisation strictes (pour qu’il puisse agir) :– Ht > 24 %
– Plaquettes > 50000/mm3
– Fibrinogène > 0,5 à 1 g /L
– pH > 7,20
– Température > 32°C
– Calcium inonisé > 1,8 mmol/L
• Information des proches
• Avis médical consensuel
Vincent JL et al. Critical Care 2006; 10:R120
Attention : pas d’AMM officielle dans cette indication
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Conclusion
• Hypotension artérielle tardive dans le choc hémorragique
• Hémogramme initial trompeur : anémie sous-estimée
• Maintenir une bonne oxygénation tissulaire
• Triade mortelle : coagulopathie, hypothermie, acidose
métabolique (lactique)
• Vasopresseurs et produits sanguins précocement
• Damage control : stratégie chirurgicale en plusieurs
temps pour permettre la réanimation.