CCP 219 Single and Multi System Trauma π©Έ Flashcards
American College of Surgeons Advanced Trauma Life Support (ATLS) hemorrhagic shock classification
links the amount of blood loss to expected physiologic responses in a healthy 70 kg patient
Class 1 hemorrhagic shock
- Volume loss up to 15% of total blood volume, approximately 750 mL
- Heart rate is minimally elevated or normal.
- Typically, there is no change in blood pressure, pulse pressure, or respiratory rate.
Class 2 hemorrhagic shock
- Volume loss from 15% to 30% of total blood volume, from 750 mL to 1500 mL.
- Heart rate and respiratory rate become elevated (100 BPM to 120 BPM, 20 RR to 24 RR).
- Pulse pressure begins to narrow, but systolic blood pressure may be unchanged to slightly decreased.
Class 3 hemorrhagic shock
- Volume loss from 30% to 40% of total blood volume, from 1500 mL to 2000 mL.
- A significant drop in blood pressure and changes in mental status occur.
- Heart rate and respiratory rate are significantly elevated (more than 120 BPM).
- Urine output declines. Capillary refill is delayed.
Class 4 hemorrhagic shock
- Volume loss over 40% of total blood volume
- Hypotension with narrow pulse pressure (less than 25 mmHg).
- Tachycardia becomes more pronounced (more than 120 BPM), and mental status becomes increasingly altered.
- Urine output is minimal or absent. Capillary refill is delayed.
Hemoglobin and hematocrit in acute hypovolemic shock
- Normal
- Hemoglobin and hematocrit values remain unchanged from baseline immediately after acute blood loss
- During the course of resuscitation, the hematocrit may fall secondary to crystalloid infusion and re-equilibration of extracellular fluid into the intravascular space.
- βIf you throw out half a pitcher of Kool-aid, it still tastes just as sweet.β
What trauma interventions target the βcoagulopathyβ portion of the trauma triad
π΅π΅π΅π΅ MONEY SLIDE π΅π΅π΅π΅
- Avoid dilutional fluid resuscitation with crystalloids
- Early/preferential blood product resuscitation with either fresh whole blood or a 1:1:1 ratio (PRBC:plasma:platelet)
- Allow permissive hypotension
- Prevent hypothermia
- TXA
What factors of shock physiology contribute to worsening coagulopathy?
- Consumption of clotting factors
- Hypothermia
- systemic Acidosis
- Third spacing dilution
- Shock liver (decreased production of clotting factors)
- Fibrinolysis
Discuss βpermissive hypotensionβ in trauma cases with TBI as a competing interest
- Target the brain first. Maintain MAP >80 to ensure cerebral perfusion to prevent secondary brain injury, regardless of bleeding status
Considerations for electrolytes when transfusing large volumes of PRBCs?
- Replenish calcium (due to citrate in RBCs) targeting serum ionized Ca++ >1
- watch out for hyperkalemia d/t possible blood product cell lysis during storage
Emergency reversal of anticoagulation from warfarin for life-threatening hemorrhage in adults
In descending order of preference
- 4-factor PCC + Vitamin K
- 3-factor PCC + Factor VIIA + Vitamin K
- 3-factor PCC + FFP + Vitamin K
- FFP + Vitamin K
Assessment of Blood Consumption (ABC) score for MTP
- Penetrating mechanism of injury
- Positive FAST (Focused Assessment with Sonography in Trauma) examination (ie, evidence of hemorrhage)
- SBP of 90 mmHg or less
- Heart rate of 120 beats per minute (bpm) or greater
- Each positive parameter receives a score of one.
- A score of 2 or more predicts the need for massive transfusion with a sensitivity of 75 percent and a specificity of 86 percent.
Which coagulation factors are dependent upon vitamin K for synthesis?
X-IX-VII-II (prothrombin group)
10-9-7-2
Coagulation cascade intrinsic pathway
- initiated by exposure of collagen in the vascular wall following trauma
- This exposure of collagen appears to directly activate Factor XII (Hageman Factor)
- Factor XII sets off the subsequent cascade
- Factor XII -> Factor XI -> Factor IX -> Factor VIII -> Factor X
Coagulation cascade extrinsic pathway
- triggered by the presence of Tissue Factor that is released from injured vasculature
- Tissue Factor in combination with Factor VII activates Factor X
- Factor X converts prothrombin to activated thrombin.
Coagulation cascade final common pathway
- Intrinsic and Extrinsic arms converge upon activation of Factor X
- Once activated, Factor X converts Prothrombin to Thrombin
- Activated thrombin converts fibrinogen to fibrin
the three stages of hemostasis
- vascular phase
- platelet phase
- coagulation phase
Primary haemostasis
the formation of a platelet plug
secondary hemostasis
the activation of the clotting cascade which results in deposition of fibrin to strengthen the platelet plug
Coagulation cascade intrinsic pathway
- Begins in blood stream
- activated when blood is exposed to collagen (damaged vessel)
- Factor XII activated to XIIa by exposed collagen
- XIIa activates XI to XIa
- XIa combines with calcium, activates IX to IXa
- simultaneously, VIII activated to VIIIa
- IXa will join with VIIIa and form factor X activating factor
- Factor X activated
Coagulation cascade extrinsic pathway
- Begins in vessel wall
- Damaged endothelial cells release factor III (tissue factor)
- factor III (tissue factor) combines with calcium, activates factor VII (hageman factor) and turns it into factor VIIa
- VIIa activates Factor X
targets for correcting anticoagulation in traumatic brain injury
- Platelets >100
- INR <1.5 (If supratherapeutic INR consider octaplex)
- Target PTT <40 (If PTT too high, consider FFP)
- If patient is heparinized consider protamine sulphate
- Fibrinogen >1 (if fibrinogen <1 consider cryoprecipitate)
- Target Hgb >90 (transfuse PRBC if necessary)
- Consider TXA in low pressure bleed (such as SDH)
antithrombin III
- Antithrombin is a protein
- functions as a naturally occurring mild blood thinner
- blocks clotting by inactivating thrombin
- heparin combines with antithrombin-III increasing the effectiveness of antithrombin-III by over 1000x
Coagulation cascade final common pathway
- factor Xa is activated
- Factor Xa cleaves prothrombin to its active form, thrombin
- Thrombin cleaves fibrinogen into its active form fibrin
- Fibrin strands will begin to join together, and with the help of XIIIa this will cause the cross-linking of fibrin strands