Fluid Resuscitation: Tintinalli Flashcards

1
Q

Most common causes of coagulopathy in trauma

A
Massive hemmorrhage
Hypothermia
Consumption of clotting factors
Consumption of platelets
Dilution of clotting factors/platelets
Trauma-induced fibrinolysis
Massive blood transfusions
Hypocalcemia
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2
Q

What is the “lethal triad?”

A

Coagulopathy
Hypothermia
Acidosis

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3
Q

Hemorrhage Class I

A

Blood loss ≤ 15% (750 mL)
Minimal or no tachycardia
No change in BP in healthy pt
Treatment: Fluid replacement may not be needed if bleeding stops

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4
Q

Hemorrhage Class II

A
Blood loss 15-30% (750-1500mL)
Tachycardia w/ narrow pulse pressure
Mild to moderate hypotension
Compensatory peripheral vasoconstriction
Possible mild mental status change
Treatment: Restore fluid volume. If red cell volume normal before insult & volume restored, RBC generally not needed
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5
Q

Hemorrhage Class III

A
Blood loss 30-40% (1500-2000mL)
Worsening hypotension
Worsening tachycardia
Peripheral hypoperfusion
Mental status change
Treatment: restore both fluid & RBC volume
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6
Q

Hemorrhage Class IV

A

Blood loss > 40% ( >2000mL)
This person probably looks pretty close to dead
Treatment: This is the limit of decompensation without aggressive intervention. Throw it all at them.

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7
Q

What are the preferred fluids for resuscitation in the US?

A

Isotonic crystalloids: normal saline or lactated Ringer’s

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8
Q

What is the 3:1 rule for isotonic crystalloid fluid replacement?

A

For every amount of blood lost, 3 times that much fluid is needed for replacement.

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9
Q

What’s the physiologic basis for the 3:1 rule of fluid resuscitation?

A

At best, 30% of infused fluid stays in the intravascular compartment.

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10
Q

What is the generally accepted rule for RBC transfusion during fluid resuscitation?

A

A patient in shock who demonstrates minimal to modest hemodynamic improvement after 2-3L bolus of crystalloid needs to be gettin’ some RBCs.

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11
Q

The American Society of Anesthesiologists has a hemoglobin level trigger for transfusing. What is it?

A

Tranfuse a healthy, young individual when hemoglobin drops < 6 gram/dL (Hct 18%). Transfusion is not recommended in any patient with Hgb > 10 or Hct > 30%.

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12
Q

What type of blood transfusion is best? Next best? Last resort?

A
  1. Typed & cross matched.
  2. Type-specific.
  3. O-negative.
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13
Q

Is there a clear basis for use of colloid products over crystalloid?

A

Nope. They cost a LOT more, & there are no clear benefits after several trials & systematic reviews.

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14
Q

What is the current conclusion regarding hypertonic solutions in fluid resuscitation?

A

Kinda like everything else: more studies are needed!

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15
Q

What’s the potential of hypertonic solution in fluid resuscitation?

A

Expands intravascular volume & promotes fluid shift into INTRAVASCULAR space instead of extravascular space. This could be a pretty good deal in head trauma patients (limiting cerebral edema) & pulmonary edema patients (limiting pulmonary edema). BUT WE’RE NOT SURE YET.

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16
Q

What is the theory behind “permissive hypotension?”

A

Usually, we can’t control the hemorrhage before we start the fluid resuscitation. There’s concern that resuscitating to a normal BP might be harmful by exacerbating the hemorrhage, because it can harm fragile clot formation at the injury site (i.e. we’re blowing the freaking clots out).

17
Q

Do we have good evidence for “permissive hypotension”? Why or why not?

A

Nope. Surprise surprise: we don’t have enough data from randomized trials to clearly demonstrate improved survival.

18
Q

What’s the goal of “permissive hypotension”?

A

Provide sufficient fluid resuscitation to maintain vital organ perfusion & avoid cardiovascular collapse (yeah, that would be an important goal I think) WHILE keeping the arterial BP relatively low (like systolic of 90-100 or a MAP of 60-70). This would go on until we could get the damn bleeding stopped, then we could get to the serious business type resuscitation.

19
Q

What about administering no fluid at all?

A

One randomized study of hypotensive patients with penetrating torso injuries found that survival rates improved if they delayed fluid resuscitation until surgical hemostasis. THIS HAS NOT BEEN ADEQUATELY EVALUATED, so maybe we are not gonna do this unless we find ourselves on an actual battlefield. (Probably hard to justify this in a real clinical setting. Don’t get sued, ladies.)

20
Q

What defines “massive transfusion?”

A

Requirement for >10 units of blood within the first 24 hours

21
Q

If a patient has been massively transfused with RBCs, what do we need to think about in further fluid resuscitation?

A

Dilutional coagulopathy! Might need to be thinking about adding some FFPs & some platelets. HOWEVER, as with just about everything, “randomized clinical trials are lacking to clearly make sweeping recommendations for a change in approach”. Just be thinking about it.

22
Q

What’s the major limitation of resuscitation fluids?

A

They don’t carry oxygen, just increase circulating volume.

23
Q

What two classes of agents are under development to help restore oxygen-carrying capacity? What would be their benefit?

A

Hemoglobin-based oxygen carriers
Fluorocarbon-based oxygen carriers

To restore oxygen-carrying capacity of lost RBCs without the ridiculously short shelf life & storage requirements of packed RBCs (storage temp, prep requirements). Also preferably it would have no side effects, while we’re shooting for the moon.

24
Q

So do we have an approved oxygen carrier fluid for use in the US?

A

Nope. Get to work on that.

25
Q

What’s one of the major limitations in assessing response to fluid resuscitation?

A

There is no one adequate, easily measurable parameter that can reliably reflex the patient status prior to & during resuscitation.

26
Q

CVP response to fluid administration is useful for…

A

…assessing volume status.

27
Q

How do we use CVP to assess volume status, anyway?

A

If the CVP doesn’t rise after infusion of a certain quantity, then we can conclude the vascular system is still compliant & it ain’t full yet. If it DOES rise ( >5-7mm Hg) after an infusion, then it’s reached the stretch limits & is full.

28
Q

ScvO2: why is it a useful measurement tool for fluid resuscitation/global hypoperfusion?

A

It correlates with pulmonary artery mixed venous O2 sat. Also, a CVL is way more feasible in the ED than a pulmonary artery cath. As a resuscitation marker, low ScvO2 (<70%) indicates global hypoperfusion (because it means the tissue is grabbing more O2 than usual out of the blood bc of low O2 delivery).

29
Q

ScvO2: what is the drawback as a measurement tool for global hypoperfusion?

A

May not be sensitive enough to identify regional hypoperfusion (like splanchnic, which is super common in shock) unless the hypoperfusion is severe or widespread.

30
Q

What are some other measurement tools for assessing a patient during fluid resuscitation?

A
  1. Simultaneous arterial & central venous blood gases: elevated O2 extraction ratio is consistent with hypoperfusion
  2. Arterial line catheter: allows continuous monitoring of cardiac output
  3. Pulmonary end-tidal CO2: predictive of eventual outcome in severely hypoperfused trauma patients, but not clear use in lesser degrees of hypoperfusion
  4. Serial assessment of metabolic labs: lactate & base deficit