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Burst Mode Blood Transfusion in Acute GI Hemorrhage Victor Tseng, MD Internal Medicine Emory University School of Medicine Coached by Roshan Patel, MD

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Page 1: The Zen of Blood Attacking the Immunologic Roots of Sepsisteasnag.org/wp-content/uploads/2015/04/GI-Bleeding-BST.pdf · Burst Mode Blood Transfusion in Acute GI Hemorrhage Victor

Burst ModeBlood Transfusion in Acute GI Hemorrhage

Victor Tseng, MDInternal Medicine

Emory University School of Medicine

Coached by Roshan Patel, MD

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WHAT’S SPECIAL ABOUT ACUTE GI BLEEDING?

• It’s the bleeding that our specialty (IM) takes care of!

• Other considerations

• Mucosa are uniquely susceptible to platelet and coagulation dysfunction• No tamponade effect within hollow lumen• Only vague estimation of bleeding rate is possible• 10% coincidence with acute thrombotic disease (DVT, ACS) • 10% chance of obscure bleeding

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YOU SHOULD KNOW

1. Is acute isovolemic (aka hemodilutional) anemia dangerous to my actively bleeding patient?

2. What is the hemoglobin target, and does it matter?

3. What’s the deal with “large bore” IVs?

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51 F – Grady, March 2015• Essential Hypertension + LVH, Peripheral Atherosclerotic Disease with Chronic

Claudication, Alcoholism complicated by Hepatic Steatosis and Accelerated Osteopenia

• In the ER with melena and maroon stools x 8 episodes over 2 days. Called by floor team after active witnessed melena. She is otherwise asymptomatic.

• Medications: ASA 81, Naproxen PRN, Lipitor 40, Norvasc 10, Chlorthalidone 25, Ca/D2

• VS: T 35.8, P 112 sinus, BP 112/54, R 22 manual, SpO2 = 99% ambient

• Exam: thin female, AO x 4, psychomotor slowing, pallid face and palpebrae, cool and clammy skin, icy cold distal extremities, hyperdynamic precordium, JVP supraclavicular, normal radial pulses, right femoral bruit, clear lungs, soft and nontender abdomen with hyperactive bowel sounds, DRE melanic stool

• Labs: Hb 6.8 (10.2 in Feb), creatinine 1.4, BUN 42, protime 19 (INR 1.5), platelet 236, lactate 1.6

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RBCs typed and cross-matched. They will be ready in around 90 minutes. IV access = 20 g x 3. Intravenous PPI infusion is begun.

• Intern: “We need to prioritize the circulation. Let’s give a bolus of 2 liters crystalloid (plasma-lyte A) while waiting for the blood”

• Student 1: “No, we can’t risk the hemodilution. She could become unstable from the anemia”

• Student 2: “Let’s get GI to scope her right now so we can get hemostasis while waiting for blood”

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Delivery of O2 (DO2)

CO x [1.39 · Hb · SpO2 + 0.003 · PaO2]

Oxyhemoglobin Gas (Dissolved)

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Effects of Acute Isovolemic Anemia

No change in preload (volume) statusCVP and PCWP remain constant

Increase in Cardiac Output by 2-foldThis is mediated by equally tachycardia (HR) and stroke volume index (SVI)

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Effects of Acute Isovolemic Anemia

At Hg < 7, a net decrease in DO2 by 25%This is due to overwhelming dependence of oxygen transport on oxyhemoglobin

Delivery

Mixed Venous O2

… but no deleterious physiologic effects

• ST depression in 2/32 patient• No lactic academia• No chance in anaerobic threshold, VO2

Even when DO2 reduced even further by addition of esmolol and diltiazem!

Consumption

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Is hemodilution dangerous to my actively bleeding patient?i.e. can I resuscitate acutely with RBC-free IVFs?

• Exception: some patient are dependent on DO2 (sepsis, cellular respiratory chain poisoning – CN, salicylates)

Hb ≥ 7 Hb < 7

No acute ischemia No issues Fluids reduce DO2

but well-tolerated physiologically

Acute ischemia present (e.g. primary ΔST,

oliguria, lactic acidosis)

IVF will help DO2 Wait for blood

Start vasopressors/inotropes for shock and maximize PaO2 in this situation

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MANIFESTATION If UGIB (mL/hr) If LGIB

Coffee-Ground Emesis (CGE) 10 None

Blood-Streaked Browns None 10

Melena 25 Rare (Cecal)

Maroonic Stool 45 25

Hematochezia (BRBPR) > 200 Anything > 5

Frank Hematemesis Anything > 20 None

Estimating Bleed Rate

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Barcelona UGIB Transfusion Trial of 7 vs 9 – NEJM 2013

• Hb goal > 7 associated with survival benefit

• Driven largely by reduced rebleeding risk in class B cirrhotic patients

• Patients with recently symptomatic arterial ischemia were excluded

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TANK UPDeficit from Target Ongoing Bleeding

RBC x 1 per 400 mL Melena300 mL Hematochezia200 mL Hematemesis

+ CATCH UP

Hb ≥ 7 General goalIncluding NDHF, sepsis, ICU

Hb ≥ 8

Compensated chronic ischemia orUrgent non-cardiac surgery

Hb ≥ 10 Acute ischemia (TIA, ACS)

Hb ≥ ? Hemorrhagic shockOngoing Exsaguination

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What is the hemoglobin target, and does it matter?

• Goal Hb ≥ 7 generally and especially in portal hypertensive bleeding

• Goal Hb ≥ 10 for acute cardiac or cerebral ischemia. Hemorrhage-induced ischemia has never been studied in a randomized fashion

• 400 mL melena = 1 unit RBC transited through GI tract over 8 hours

• All ongoing GI bleeding requires admission to ICU

• Numeric thresholds are irrelevant in a rapidly exsanguinating patient.

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3 units RBC are now at bedside. Patient’s hemodynamics have deteriorated: P 130 and BP 92/55. Another episode of maroon stool occurs. The ED resident has just placed a subclavian central venous triple lumen line due to hypotension. Lactated Ringers’ (LR) is being infused through one PIV.

• Intern 1: “Alright, we need to give the blood through the central line right away”• No. Blood cannot be transfused rapidly through a central line.

• Intern 2: “The patient is shocky. Let’s give three units simultaneously through each PIV’• No. Units must be given sequentially per RN and hospital protocol.

• Student: “Yeah, they are crashing. We need to pressure-bag the blood, one unit througheach infusion port of the central line”• No. For the two reasons listed above.

BACK IN THE ED…

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ORANGE

GRAY/TLC

GREEN

PINK

BLUE

YELLOW

14

16

18

20

22

24

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π ΔP r4

8 L

· ·

· ·Flow =

rFlow

L

ΔP

• Cutting the radius by half is the same as multiplying the length by a factor of 16!

• It takes 16 times as much pressure to get the same flow through half the radius!

ηviscosity

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COLOR Gauge Maximum RBC Flow (mL/hr)

Hrs per RBC Unit Units/Hr

CORDIS ~ 10 3500 0.1 10

ORANGE 14 900 0.3 3

GRAY 16 500 0.5 2

GREEN 18 300 1 1

PINK 20 150 1.5 0.6

BLUE 22 100 3.5 0.3

YELLOW 24 50 ∞ Cannot Use

Larg

e B

ore

Smal

l Bo

re

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What’s the deal the ‘large bore’ IVs?

• IV access is the limiting factor in rapidly bleeding patients, not blood availability

• It takes 1 hour to transfuse 1 RBC unit with an 18-g PIV

• Units must be given sequentially, unless O-neg massive transfusion protocol

• Central line lumen is 16-g. Only indicated for pressor administration

• Pressurized blood can only be given through IV ≤ 16-g

• Place a cordis for brisk bleeding or hemorrhagic shock

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SUMMARY

1. Is acute isovolemic (hemodilutional) anemia dangerous to my actively bleeding patient?

• Only if Hb < 7 + active ischemia• Fluids reduce DO2 overall, but it is usually inconsequential• Wait for blood if ischemia is due to anemia

2. How much blood to give?

• Hb > 7 and INR ≤ 1.5 for endoscopy • Hb > 10 for cardiac ischemia• Use bleeding manifestation to ballpark ongoing loss• Excessive transfusion leads to increased mortality

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SUMMARY

3. What are the advantages of large bore PIVs?

• Faster flows under lower pressures → less hemolysis• Transfuse one unit at a time, unless activating MTP• A central venous line is ineffectual for rapid transfusion• IV access, not blood availability, is the limiting factor• 1 unit, 1 hour, 18 guage

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1. Weiskopf et al. Human cardiovascular and metabolic response to acute, severe isovolemic anemia. JAMA. 1998 Jan 21;279(3):217-21.

2. Leiberman et al. Critical oxygen delivery in conscious humans is less than … . Anesthesiology. 2000 Feb;92(2):407-13.

3. Villaneuva et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3;368(1):11-21

4. Cooper et al. Conservative versus liberal red cell transfusion in acute myocardial infarction (the CRIT Randomized Pilot Study). Am J Cardiol. 2011 Oct 15;108(8):1108-11

5. Carson et al. Liberal versus restrictive transfusion thresholds for patients with symptomatic coronary artery disease. Am Heart J. 2013 Jun;165(6):964-971

REFERENCES

“An environment that does not nurture

one's sense of purpose will only dull it over time.”– George Mathew, M.D.

1971 - 2014

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AppendixMassive Transfusion Protocol

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Threshold in Acute Coronary Syndrome: Unresolved

KEY POINT: Effect of active bleeding not studied. Are these data applicable to unstable coronary disease that is specifically provoked by GIB?

CRIT Trial – AJC 2011 New Brunswick Trial – AHJ 2013vs

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“Ooze”1 – 2 units per day

“Frank Non-Brisk”3 – 6 units per day

Brisk Hemorrhage> 3 units in 6 hours> 10 units per day

Stage 1Asymptomatic Anemia PIV + Sequential PIV + Sequential PIV or Cordis + MTP

Stage 2Tachycardia PIV + Sequential PIV + Sequential Cordis + MTP

Stage 3Acute Hypotension PIV + MTP Cordis + Sequential Cordis + MTP

Stage 4Acute Hypotension andOrgan Failure

Cordis + MTP Cordis + MTP Cordis +MTP

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• Dilutional Coagulopathy: At 8 units RBC, plasma coagulation factor content decreases to 25%

• Dilutional Thrombocytopenia: At 10 units RBC, platelet count decreases by half.

Products are given in ~ 1:1:1 ratioEach MTP cooler contains: 6 RBC: 4 FFP: 1 x 5 Platelet

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HOW TO ACTIVATE MASSIVE TRANSFUSION

1. Call the Blood Bank

1. Arrange ICU Transfer

2. Fill out “Emergent Blood Products” Consent for Uncrossed Units

3. Obtain Adequate IV Access• 20G x 3 • 18G x 2• Cordis + 20G

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• Coagulopathy and Thrombocytopenia

• Acute Pneumonitis (TRALI)

• Hydrostatic Pulmonary Edema (TACO)

• Hyperkalemia (+ 5 – 7 mEq per unit)

• Free Hypocalcemia and Tetany

• Hypothermia

• Acute Metabolic Alkalosis (citrate converted to 23 mEq HCO3 per unit)

Other complications of MTP (RBC > 10 units)