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CCP 219 Single and Multi System Trauma 🩸 Flashcards

1
Q

American College of Surgeons Advanced Trauma Life Support (ATLS) hemorrhagic shock classification

A

links the amount of blood loss to expected physiologic responses in a healthy 70 kg patient

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2
Q

Class 1 hemorrhagic shock

A
  1. Volume loss up to 15% of total blood volume, approximately 750 mL
  2. Heart rate is minimally elevated or normal.
  3. Typically, there is no change in blood pressure, pulse pressure, or respiratory rate.
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3
Q

Class 2 hemorrhagic shock

A
  1. Volume loss from 15% to 30% of total blood volume, from 750 mL to 1500 mL.
  2. Heart rate and respiratory rate become elevated (100 BPM to 120 BPM, 20 RR to 24 RR).
  3. Pulse pressure begins to narrow, but systolic blood pressure may be unchanged to slightly decreased.
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4
Q

Class 3 hemorrhagic shock

A
  1. Volume loss from 30% to 40% of total blood volume, from 1500 mL to 2000 mL.
  2. A significant drop in blood pressure and changes in mental status occur.
  3. Heart rate and respiratory rate are significantly elevated (more than 120 BPM).
  4. Urine output declines. Capillary refill is delayed.
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5
Q

Class 4 hemorrhagic shock

A
  1. Volume loss over 40% of total blood volume
  2. Hypotension with narrow pulse pressure (less than 25 mmHg).
  3. Tachycardia becomes more pronounced (more than 120 BPM), and mental status becomes increasingly altered.
  4. Urine output is minimal or absent. Capillary refill is delayed.
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6
Q

Hemoglobin and hematocrit in acute hypovolemic shock

A
  1. Normal
  2. Hemoglobin and hematocrit values remain unchanged from baseline immediately after acute blood loss
  3. During the course of resuscitation, the hematocrit may fall secondary to crystalloid infusion and re-equilibration of extracellular fluid into the intravascular space.
  4. β€œIf you throw out half a pitcher of Kool-aid, it still tastes just as sweet.”
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7
Q

What trauma interventions target the β€œcoagulopathy” portion of the trauma triad

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Avoid dilutional fluid resuscitation with crystalloids
  2. Early/preferential blood product resuscitation with either fresh whole blood or a 1:1:1 ratio (PRBC:plasma:platelet)
  3. Allow permissive hypotension
  4. Prevent hypothermia
  5. TXA
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8
Q

What factors of shock physiology contribute to worsening coagulopathy?

A
  1. Consumption of clotting factors
  2. Hypothermia
  3. systemic Acidosis
  4. Third spacing dilution
  5. Shock liver (decreased production of clotting factors)
  6. Fibrinolysis
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9
Q

Discuss β€œpermissive hypotension” in trauma cases with TBI as a competing interest

A
  1. Target the brain first. Maintain MAP >80 to ensure cerebral perfusion to prevent secondary brain injury, regardless of bleeding status
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10
Q

Considerations for electrolytes when transfusing large volumes of PRBCs?

A
  1. Replenish calcium (due to citrate in RBCs) targeting serum ionized Ca++ >1
  2. watch out for hyperkalemia d/t possible blood product cell lysis during storage
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11
Q

Emergency reversal of anticoagulation from warfarin for life-threatening hemorrhage in adults

A

In descending order of preference

  1. 4-factor PCC + Vitamin K
  2. 3-factor PCC + Factor VIIA + Vitamin K
  3. 3-factor PCC + FFP + Vitamin K
  4. FFP + Vitamin K
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12
Q

Assessment of Blood Consumption (ABC) score for MTP

A
  1. Penetrating mechanism of injury
  2. Positive FAST (Focused Assessment with Sonography in Trauma) examination (ie, evidence of hemorrhage)
  3. SBP of 90 mmHg or less
  4. 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.
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13
Q

Which coagulation factors are dependent upon vitamin K for synthesis?

A

X-IX-VII-II (prothrombin group)

10-9-7-2

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14
Q

Coagulation cascade intrinsic pathway

A
  1. initiated by exposure of collagen in the vascular wall following trauma
  2. This exposure of collagen appears to directly activate Factor XII (Hageman Factor)
  3. Factor XII sets off the subsequent cascade
  4. Factor XII -> Factor XI -> Factor IX -> Factor VIII -> Factor X
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15
Q

Coagulation cascade extrinsic pathway

A
  1. triggered by the presence of Tissue Factor that is released from injured vasculature
  2. Tissue Factor in combination with Factor VII activates Factor X
  3. Factor X converts prothrombin to activated thrombin.
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16
Q

Coagulation cascade final common pathway

A
  1. Intrinsic and Extrinsic arms converge upon activation of Factor X
  2. Once activated, Factor X converts Prothrombin to Thrombin
  3. Activated thrombin converts fibrinogen to fibrin
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17
Q

the three stages of hemostasis

A
  1. vascular phase
  2. platelet phase
  3. coagulation phase
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18
Q

Primary haemostasis

A

the formation of a platelet plug

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19
Q

secondary hemostasis

A

the activation of the clotting cascade which results in deposition of fibrin to strengthen the platelet plug

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20
Q

Coagulation cascade intrinsic pathway

A
  1. Begins in blood stream
  2. activated when blood is exposed to collagen (damaged vessel)
  3. Factor XII activated to XIIa by exposed collagen
  4. XIIa activates XI to XIa
  5. XIa combines with calcium, activates IX to IXa
  6. simultaneously, VIII activated to VIIIa
  7. IXa will join with VIIIa and form factor X activating factor
  8. Factor X activated
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21
Q

Coagulation cascade extrinsic pathway

A
  1. Begins in vessel wall
  2. Damaged endothelial cells release factor III (tissue factor)
  3. factor III (tissue factor) combines with calcium, activates factor VII (hageman factor) and turns it into factor VIIa
  4. VIIa activates Factor X
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22
Q

targets for correcting anticoagulation in traumatic brain injury

A
  1. Platelets >100
  2. INR <1.5 (If supratherapeutic INR consider octaplex)
  3. Target PTT <40 (If PTT too high, consider FFP)
  4. If patient is heparinized consider protamine sulphate
  5. Fibrinogen >1 (if fibrinogen <1 consider cryoprecipitate)
  6. Target Hgb >90 (transfuse PRBC if necessary)
  7. Consider TXA in low pressure bleed (such as SDH)
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23
Q

antithrombin III

A
  1. Antithrombin is a protein
  2. functions as a naturally occurring mild blood thinner
  3. blocks clotting by inactivating thrombin
  4. heparin combines with antithrombin-III increasing the effectiveness of antithrombin-III by over 1000x
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24
Q

Coagulation cascade final common pathway

A
  1. factor Xa is activated
  2. Factor Xa cleaves prothrombin to its active form, thrombin
  3. Thrombin cleaves fibrinogen into its active form fibrin
  4. Fibrin strands will begin to join together, and with the help of XIIIa this will cause the cross-linking of fibrin strands
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25
Q

LMWH (dalteparin, enoxaparin) moa

A
  1. binds to anti-thrombin III
  2. LMWH is less effective at inhibiting factor IIa (acting mostly via inhibition of Xa).
  3. Enhances AT effects more selectively on Factor Xa than on thrombin.
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26
Q

UFH moa

A
  1. binds to anti-thrombin III (AT-III)
  2. this enhances antithrombin’s inhibition of several coagulation factors – especially factor Xa and factor IIa (thrombin).
  3. Enhances AT effects on Factor Xa and thrombin.
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27
Q

Fondaparinux moa

A
  1. Binds and enhances the anti-Xa activity
    of ATIII by 300-fold
  2. Enhances anti-Xa activity of ATIII
  3. Specificity for AT β†’ no binding to other plasma proteins
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28
Q

UFH vs. LMWH

A
  1. LMWH is easier to give logistically (doesn’t require IV infusion or monitoring).
  2. LMWH has a decreased risk of heparin induced thrombocytopenia with thrombosis (HIT).
  3. Studies comparing UFH and LMWH generally show that LMWH is more effective and causes less bleeding.
  4. LMWH cannot be used in Renal failure (GFR < 30 ml/min).
  5. LMWH cannot be used in situations where the Need to rapidly stop anticoagulation (e.g., in a patient at risk for bleeding, or pending a procedure)
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29
Q

fibrinolysis pathway definition

A
  1. Process of degrading the fibrin clot when it is no longer needed
  2. prevents extension of clot beyond site of injury
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30
Q

fibrinolysis pathway

A
  1. Fibrinolysis initiated by endogenous tPA or uPA (urokinase-like plasminogen activator)
  2. tPA or uPA convert plasminogen to plasmin in the presence of fibrin
  3. Plasmin degrades the fibrin clot
  4. Plasmin also inactivates factors Va and VIIIa
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31
Q

Normal range for platelets

A

150–400 Γ— 10⁹/L

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32
Q

Normal range for INR (non anti-coagulated blood)

A

0.9–1.2

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33
Q

Normal range for Prothrombin time (PT)

A

10–14 seconds

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34
Q

Normal range for aPTT (non anti-coagulated blood)

A

22-30 seconds

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35
Q

Normal range for fibrinogen

A

2.0 to 4.0 g/L

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36
Q

Normal range for hemoglobin

A

Male 125–170 g/L

Female 115–155 g/L

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37
Q

warfarin reversal

A
  1. The goal of warfarin reversal is to increase the available amount of Vitamin–K dependent clotting factors, which will lead to a decrease in INR
  2. Warfarin is a vitamin-K dependent clotting factor inhibitor, specifically Factors 10-9-7-2
  3. treatment options include withholding warfarin, administering oral or intravenous vitamin K, fresh frozen plasma (FFP), and prothrombin complex concentrate (PCC)
  4. Rapid reversal is 4F-PCC + Vitamin K. If no 4F-PCC use FFP + Vitamin K
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38
Q

explain the role of prothrombin complex concentrate’s (PCC) in reversal of anticoagulation

A
  1. PCCs are β€œpooled plasma products”
  2. PCC’s contain factors 10-9-2 with variable amounts of factor 7 in a concentrated form
  3. they are virally inactivated and can be given in a small volume without the need to thaw the product first
  4. All PCCs contain factors 10-9-2 but some products contain no or very little factor 7
  5. PCCs with normal amounts of F7 are known as 4-factor PCCs whilst the products without F7 are 3-factor PCCs
  6. Octaplex is a pooled plasma coagulation factor concentrate. Each vial contains coagulation factors 10-9-7-2. It also contains protein C, protein S, albumin, heparin and sodium citrate.
  7. PCC (Octaplex) provides a more rapid and effective reversal of Warfarin than FFP, and uses less volume too (less chance of volume overloading your patient)
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39
Q

explain the role of FFP in reversal of anticoagulation

A
  1. FFP comes in approx ~250cc bags and contains all the clotting factors
  2. It is type specific (must be ABO compatible)
  3. FFP contains all coagulation factors present in whole blood
  4. One unit of FFP corrects clotting factors by 2.5-5% in a 70 kg person
  5. Going by current dosing, to achieve the equivalent amount of factor in 8 vials of 4F-PCC, it would take 4 liters, thatΚΌs 16 bags, of FFP.
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40
Q

reversal of heparin/LMWH

A
  1. Protamine sulfate
  2. Protamine sulfate binds to either heparin or LMWH to form a stable ion pair, which does not have anticoagulant activity
  3. Provides rapid reversal of anticoagulation d/t heparin or LMWH
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41
Q

ATLS trauma assessment

A
  1. Airway
  2. Breathing
  3. Circulation (carotid, femoral, pelvis, FAST)
  4. Disability (pupils, GCS, collar)
  5. Exposure, environment
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42
Q

Hemostatic goals in MTP

A
  1. Hgb > 70
  2. Platelets > 100
  3. INR < 1.8
  4. Temp > 36
  5. Fibrinogen > 1.5
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43
Q

cornerstone principles of damage control resuscitation

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Permissive hypotension
  2. Balanced haemostatic resuscitation
  3. Early Damage control surgery
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44
Q

cornerstone principles of balanced hemostatic resuscitation

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Minimal administration of crystalloid
  2. Prevention of acidemia
  3. Reduce coagulopathy of trauma
  4. prevent hypothermia
  5. Early transfusion of blood
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45
Q

benefits of permissive hypotension in trauma

A

Decreased:

  1. Decreased blood loss
  2. Decreased Intra-abdominal hypertension
  3. Decreased Academia
  4. Decreased Haemodilution
  5. Decreased Thrombocytopenia
  6. Decreased Coagulopathy
  7. Decreased Apoptotic cell death
  8. Decreased Tissue injury
  9. Decreased Sepsis
  10. Decreased Mortality
  11. Decreased volumes of crystalloid administration needed
  12. Decreased blood product utilisation
  13. Decreased postoperative recovery time

Improved:

  1. Improved organ perfusion and survival
  2. Improved recovery times post injury
46
Q

What are the principles of hemostatic resuscitation in trauma?

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Minimize crystalloid use
  2. Prevent acidemia
  3. Reduce coagulopathy
  4. Keep warm
  5. Give early blood
47
Q

main causes of secondary neuronal injury in TBI

A
  1. Hypoxia

2. Hypotension

48
Q

describe diffuse axonal injury

A
  1. occurs as the result of shearing forces from rotational acceleration or deceleration
  2. shearing has a predilection for axons and the grayβˆ’white junction due to different specific gravities of gray and white matter
  3. Cells are damaged β†’ edema
49
Q

describe Intraparenchymal hemorrhage

A
  1. the accumulation of blood in the parenchyma of the brain

2. caused by disruption of small intraparenchymal vessels

50
Q

describe Traumatic SAH

A

the accumulation of blood between the pia mater and the arachnoid membrane.

potential causes include:

  1. direct extravasation of blood from an adjacent cerebral contusion
  2. arterial dissection
  3. direct damage to smaller veins or arteries
  4. sudden increase in intravascular pressure leading to rupture
51
Q

describe subdural haemorrhage

A
  1. the accumulation of blood immediately outside the arachnoid membrane of the brain underneath the dura mater membrane
  2. caused by tearing of small bridging veins
52
Q

describe epidural hematoma

A
  1. the accumulation of blood outside the brain, between the inner surface of the skull and the dura mater
  2. caused by laceration of an artery (most commonly the MMA)
53
Q

hallmark signs of concussion (mTBI)

A
  1. confusion

2. amnesia (involves loss of memory of the traumatic event)

54
Q

bleeding reversal for direct thrombin inhibitors (dabigatran)

A
  1. Idarucizumab
  2. TXA
  3. 4F-PCC
55
Q

bleeding reversal for factor Xa inhibitors (Rivaroxaban, apixaban)

A
  1. 4F-PCC

2. TXA

56
Q

bleeding reversal for warfarin

A
  1. Vitamin K
  2. 4F-PCC
  3. FFP
57
Q

bleeding reversal for UFH

A
  1. Protamine sulfate
58
Q

bleeding reversal for fibrinolytic agents

A
  1. Cryoprecipitate
  2. TXA
  3. FFP
59
Q

bleeding reversal for anti platelet agents

A
  1. DDAVP

2. platelets

60
Q

bleeding reversal for LMWH

A
  1. Protamine sulfate
61
Q

L πŸ”₯ T fluid airway intubation algorithm

A
  1. 45Β° upright positioning
  2. Suction-Assisted Laryngoscopy Airway Decontamination (SALAD)
  3. seldinger intubation with a large-bore suction device (bougie through the DuCanto)
  4. esophageal diversion using an endotracheal tube with meconium aspirator attached
  5. scalpel-finger-bougie cricothyrotomy rescue
62
Q

initial ventilator settings for post drowning

A

initial settings per ARDS protocol

  1. Tidal volume 6-8 mL/kg
  2. Plateau pressure <30 mmHg
  3. PaO2 80-100 mmHg
  4. escalating PEEP
  5. gastric tube to decompress stomach and increase lung ventilation
63
Q

define β€œdrowning” (2002 Ustein-Style World Congress on Drowning)

A
  1. An air/liquid interface present at the entrance to a victim’s airway, preventing the victim from breathing air.
64
Q

describe the pathophysiology of the drowning process

A
  1. drowning person has reflex inspiratory effort occurs after breath holding, gasping, or unconsciousness
  2. aspiration results in laryngospasm and the ingestion of liquid
  3. Hypoxia leads to unconsciousness
  4. tachycardia β†’ bradycardia β†’ PEA β†’ asystole β†’ death.
65
Q

pulmonary manifestations of drowning

A
  1. Saltwater vs freshwater drowning doesn’t matter (in retrospective reviews of drowning victims they found that the actual amount/volume of fluid introduced into the lungs is typically quite negligible)
  2. aspirated water reaches the capillary space β†’ surfactant destruction β†’ disruption of the alveolar-capillary membrane β†’ subsequent fluid shift into the alveolar space
  3. results in pulmonary edema and poor gas exchange β†’ decreased lung compliance β†’ increased right-to-left shunting, atelectasis, alveolitis, and ARDS
66
Q

most important predictor of drowning outcome

A

time interval or duration that the victim was underwater

67
Q

CaO2 equation

A

CaO2 = (1.34 X Hgb X SaO2) + (0.003 X PaO2)

68
Q

Do2 equation

A

DO2 = CaO2 x CO

69
Q

CO equation

A

CO = HR Γ— SV

70
Q

define oxygen consumption (VO2)

A

total amount of oxygen removed from the blood due to tissue aerobic metabolism per minute

71
Q

normal VO2 in a 75 kg adult undertaking routine activities

A

approximately 250 ml/min

72
Q

define global oxygen delivery (DO2)

A

the total amount of oxygen delivered to the tissues per minute

73
Q

define the Oxygen extraction ratio (O2ER)

A

the ratio of oxygen consumption (VO2) to oxygen delivery (DO2)

74
Q

O2ER equation

A

O2ER = VO2/DO2

75
Q

causes of increased oxygen consumption (VO2)

A
  1. fever and inflammatory states (e.g. sepsis, burns, trauma, surgery)
  2. ↑ metabolic rate (e.g. hyperthyroidism, adrenergic drugs, hyperthermia)
  3. ↑ muscular activity (e.g exercise, shivering, seizures, agitation/anxiety/pain, ↑ respiratory effort)
76
Q

what is the purpose of a β€œtrauma score” within the context of a trauma system

A
  1. trauma scores provide an accurate, reliable and reproducible description of injuries and prediction of morbidity and mortality outcomes
  2. outcome predictions are based on anatomical injury + physiological injury + patient’s reserve
77
Q

describe the β€œRevised Trauma Score”

A
  1. Quantifies severity of trauma injuries based on GCS, blood pressure, and respiratory rate
  2. Higher score associated with higher survival. Consider trauma center for Trauma Score <4
78
Q

Describe the β€œAbbreviated Injury Scale”

A
  1. an anatomically based severity scoring system that classifies an individual injury by body region according to its relative severity on a 6 point scale
  2. AIS is the system used to determine the Injury Severity Score (ISS) of the multiple injury patient
79
Q

describe the β€œInjury Severity Score (ISS)”

A
  1. Standardizes severity of traumatic injury based on worst injury of 6 body systems
  2. The ISS is a score that attempts to standardize the severity of injuries sustained during a trauma
  3. Rate only the most severe injury from each body system
80
Q

define β€œMassive transfusion”

A
  1. the replacement of β‰₯10 units PRBC (1x total adult blood volume) in 24hr or;
  2. β‰₯4 units PRBCs (Β½ total adult blood volume) in 4-6hrs
  3. β‰₯4 units PRBC in one hour
81
Q

what are the primary goals of treatment in transfusion of the trauma patient?

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. maintaining cardiac output
  2. maintaining oxygen carrying capacity
  3. maintaining hemostatic potential
82
Q

define Trauma-induced coagulopathy (TIC)

A
  1. an impairment of hemostasis and activation of fibrinolysis that occurs in response to severe injury
  2. independent of significant acidosis, hypothermia, or hemodilution
  3. mediated primarily by activation of the thrombomodulin-protein C system
  4. In trauma patients without preexisting coagulation defects, a prolonged PT and/or aPTT greater than 1.5 times normal on admission defines the presence of TIC
83
Q

how much does one unit of PRBC raises the hemoglobin level by?

A

approx 10 g/L

84
Q

how much does one unit of aphaeresis platelets (6-pack) raises the platelet count by?

A

approx 50k

85
Q

what clotting factors are replaced with cryoprecipitate?

A
  1. fibrinogen
  2. factor VIII
  3. von Willebrand factor
86
Q

thresholds for anemia in different patient population groups (per WHO guidelines)

A
  1. Pregnant females: <110 g/L
  2. Non-pregnant females: <120 g/L
  3. Males: <130 g/L
87
Q

define anemia

A
  1. Anemia is a reduced concentration of RBCs, resulting in an inadequate oxygen supply to the tissues
88
Q

normal circulating blood volume in an adult

A
  1. 75-80 mL/kg body weight

2. 5-5.5 L in a 70-kg adult

89
Q

what is the effect on body temperature of transfusion of un-warmed blood

A

Each unit of blood reduces the core temperature by 0.25Β°C

90
Q

why is it important to monitor calcium levels during transfusion?

A
  1. Plasma contains citrate, which chelates calcium.

2. Frequently check ionized calcium levels and replenish calcium as necessary.

91
Q

VGH ICU fluid resuscitation formula for burn patients in the first 24 hours

AKA β€œModified Parkland”

A
  1. 3mL/kg LR or Plasmalyte-A x BSA % burned

2. Run the first half of the volume in over 8 hours and the rest over the remaining 16 hours.

92
Q

VGH/BC Burn Network burn resuscitation guidelines 2020

A
  1. fluid resuscitation for major burns should start at 3cc/kg/%TBSA.
  2. Perform hourly calculation of β€œins” and β€œouts”. Titrate fluid resuscitation hour-by-hour, especially in the early phase of major burns trauma. Clinical endpoints include responses in blood pressure, heart rate, and lactate clearance.
  3. Titrate urine output to 30-50cc/hr for major burns (50-100cc/hr in electrical burns to facilitate clearance of myoglobin and decrease the risk of acute kidney injury).
  4. Use warmed, balanced crystalloids (Ringer’s Lactate or Plasmalyte-A) in major burns
  5. Keep the patient warm
93
Q

indications to suspect cyanide toxicity in a burn patient

A
  1. enclosed-space fire and presence of inhalation injury with altered level of consciousness (GCS < 13)
  2. profound shock (SBP < 90mmHg)
  3. high serum lactic acid (lactate > 10mmol/L)
  4. narrow arterio-venous gradient (PaO2 on an arterial blood gas is similar to the PaO2 on a venous blood gas).
94
Q

VGH/BC Burn Network burn referral guidelines 2020 (AKA when to transport to a burn center)

A
  1. Partial thickness burns >20% TBSA in 10 – 50yo
  2. Partial thickness burns >10% TBSA in <10 or >50yo
  3. Full-thickness burns >5% TBSA any age
  4. partial or full-thickness burns of the hands, feet, face, eyes, ears, perineum, and/or major joints any age
  5. high-voltage electrical injuries, including lightning injuries any age
  6. significant burns from caustic chemicals any age
  7. burns complicated by major trauma in which the burn injury poses the greatest risk of morbidity or mortality. if the trauma is main problem, transport to trauma centre with later referral
  8. burns who suffer inhalation injury (critical airway/unsecured to nearest ER)
  9. comorbidities that could complicate management, prolong recovery, or affect mortality
  10. Hospitals without qualified personnel or equipment for the care of children should transfer children with burns to a burn center with these capabilities (aka VGH versus BCCH)
  11. Burn Injury in patients who will require special social/emotional and /or long-term rehabilitative support, including cases involving suspected child abuse, substance abuse, etc
95
Q

define β€œmassive hemothorax”

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Immediate return of blood of β‰₯1500mL when the chest tube is thrown in
  2. Other indicator is β‰₯200mL/hr for 2-4 hours
  3. Rapid accumulation of β‰₯1500mL blood in chest or β‰₯1/3 of patients blood volume in chest
  4. Indicates need for urgent thoracotomy
96
Q

six leading causes of death associated to chest trauma

A
  1. Tension PTX
  2. Massive HTX
  3. Open PTX
  4. Cardiac tamponade
  5. Airway obstruction
  6. Flail chest
97
Q

Populations that hide shock well

A
  1. Obstetrics (changes to HR, circulating volume)
  2. Pediatrics (compensate compensate crash)
  3. Rate controlled (mask the tachycardia)
  4. Geriatric (baseline HTN, relative hypovolemia)
98
Q

What are the three highest yield data points for shock state differentiation?

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

1) Skin (Distributive vs ALL)
2) JVP (Hypovolemic/distributive vs cardiogenic/obstructive)
3) U/S (Cardiogenic vs obstructive)

99
Q

Key questions to ask when presented with a patient in shock

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Is the patient in shock?
  2. What type of shock is it?
  3. How do I reverse this kind of shock?
100
Q

describe TEG for hemostatic evaluation

A
  1. TEG is a whole-blood measure of the clotting cascade. 2. TEG measures clot stiffness from the point of primary hemostasis through stabilization and subsequent fibrinolysis
  2. because TEG uses whole blood, the device analyzes all components of the hemostatic system
  3. TEG is the best clinically available test of the coagulation profile in cirrhotic patients
  4. The R-time reflects both pro- and anticoagulant factors, allowing the technique to measure the β€œbalanced hemostasis.”
101
Q

optimal transfusion ratio in trauma

A
  1. Haemostatic resuscitation involves resuscitation with blood components resembling whole blood
  2. aims to avoid or ameliorate acute coagulopathy of trauma and the complications of aggressive crystalloid fluid resuscitation while maintaining circulating volume
  3. Involves blood component ratios of 1 unit PRBCs : 1 FFP : 1 unit platelets
102
Q

goals of hemostatic resuscitation approach

A
  1. maintain circulating volume
  2. limit ongoing bleeding
  3. prevent the lethal trial of hypothermia, acidosis and acute coagulopathy of trauma
103
Q

effects of hypothermia on trauma patients

A
  1. Decreases platelet responsiveness
  2. Increases platelet sequestration in liver and spleen
  3. Reduces clotting Factor function (Factors XI and XII)
  4. Leads to fibrinolysis
104
Q

effects of acidosis on trauma patients

πŸ₯ΌπŸ₯ΌπŸ₯Ό PIMPABLE πŸ₯ΌπŸ₯ΌπŸ₯Ό

A
  1. pH strongly decreases activity of clotting Factors V, VIIa and X
  2. Acidosis inhibits thrombin generation
  3. Cardiovascular effects of acidosis (pH <7.2) – decreased contractility and CO, vasodilatation and hypotension, bradycardia and increased dysrhythmias
105
Q

what are the problems associated with Large volume crystalloid resuscitation in trauma

A
  1. Large volume crystalloids can β†’ dilutional coagulopathy and exacerbate bleeding
  2. Crystalloids have no O2 carrying capacity and do little to correct the anaerobic metabolism and O2 debt associated with shock
  3. large volume crystalloid resuscitations β†’ tissue and organ edema β†’ organ failure (eg pulmonary oedema, abdominal compartment syndrome)
106
Q

how does ARDS relate to trauma (how does trauma lead to ARDS)

A
  1. Severe trauma predisposes to ALI and ARDS
  2. development of ARDS may be related to mechanism of injury (eg, lung contusion, long bone fracture leading to fat embolism) or resuscitation (eg, transfusion)
  3. In a study that included 1762 patients with major traumatic injury, ARDS occurred in 24%
  4. Predictors of ARDS after trauma included increasing subject age; increasing APACHE II score; increasing injury severity score; and the presence of blunt injury, pulmonary contusion, massive transfusion, or flail chest.
107
Q

what are the 5 sites of clinically significant bleeding?

A
  1. external (eg slashed wrists)
  2. intrathoracic
  3. intraperitoneal
  4. retroperitoneal
  5. pelvic or long bone fractures
108
Q

Steps to diagnosing air leak in chest tube

A
  1. Persistent bubbling at the water seal indicates an air leak within the lung, tubing, or connections.
  2. If the leak is within lung and the patient is mechanically ventilated, look at the set Vt, compared with the exalted Vt, to determine how much mL of air you are losing.
  3. Clamp the chest tube near the chest wall. If this stops the leak, it is either a BPF or leakage from incision site. Seal up the incision site real good. Still leaking with clamp? BPF
  4. If leak does not stop with proximal clamping, your drainage system is fucked. Do sequential clamping down the hose away from the patient to find the spot. Check all connections
109
Q

minimum suction pressure needed to operate the chest drain system at -20 cmH20 (water seal system or dry system)

A
  1. To operate the chest drain at -20 cm H20, wall suction must have at least -80 mm Hg of vacuum.
110
Q

If a chest drainage unit is not connected to suction, how is it draining fluid from the chest cavity?

A

gravity draining

111
Q

explain chest tube tidaling

A
  1. With a chest tube in the pleural space, the water level should fluctuate in the water seal chamber (tidaling) corresponding with respiration
  2. When there is no air leak, the water level in the water seal chamber should rise and fall with the patient’s respiration
  3. During spontaneous respiration (negative pressure breathing), the water level will rise during inhalation and fall during exhalation
  4. during positive pressure ventilation (positive pressure breathing), the oscillation will be opposite. the water level will fall during inhalation and rise during exhalation
  5. If tidaling doesn’t occur, the tubing could be kinked or clamped, or CT/tubing section may have become clogged
112
Q

The management of Traumatic Brain Injury (TBI) is focused on the prevention of _______ injury

A

secondary

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