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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5524_Библиотеки_им_академика_М_И_Перельмана.pdf
388 E. Gonzalez and E. E. Moore
Fig. 4. Current understanding of the pathophysiology of trauma induced coagulopathy.
APC: activated protein-C, PAI-1: plasminogen activator inhibitor, tPA: tissue plasminogen activator, DAMPs: damage-associated molecular pattern molecules TLR-4: toll-like
receptor 4.
Fig. 5. Thrombelastography (TEG) tracing (see Table 1 for description of variables).
Diagnosis and Management of Coagulopathy 389
Fig. 6. Denver Health Medical Center massive transfusion protocol (MTP).
390 E. Gonzalez and E. E. Moore
Fig. 7. Pediatric massive transfusion protocol (MTP).
Table 1. Thrombelastography (TEG) parameters.
TEG Parameter Significance Unit of Measure Normal Range
Diagnosis and Management of Coagulopathy 391
R-time Time elapsed from the initiation of the test until the point where the
onset of clotting provides enough resistance to produce a 2-mm
amplitude reading on the TEG tracing.
ACT Used as a surrogate of R-time in the rapid-TEG assay which uses
tissue factor to obtain a quicker reading.
K-time Time interval from the R time to the point where fibrin cross-linking
provides enough clot resistance to produce a 20-mm amplitude
reading. Reflects potentiation of enzymatic factors yielding clot
strengthening mostly derived from fibrin.
alpha-angle Angle of a tangent line between the initial split point of the tracing and
the growing curve. Reflects potentiation phase of enzymatic factors
yielding clot strengthening mostly derived from fibrin.
MA Point at which clot strength reaches its maximum measure in
millimeters on the TEG tracing. Reflects the end result of maximal
platelet-fibrin interactions.
G Overall total clot strength resulting from all coagulation interactions,
calculated from MA; G=(5000*MA)/(100-MA).
LY-30 Percentage of clot strength loss 30 minutes after reaching maximal
amplitude. Reflects amount of fibrinolysis.
R-time: reaction time; K-time: coagulation time; MA: maximum amplitude; G: total clot strength; LY-30: lysis at 30 minutes.
minutes kaolin-TEG: 3.8–9.8
seconds rapid-TEG: 78–110
minutes rapid-TEG: 0.5–2.0
kaolin-TEG: 0.5–3.5
degrees rapid-TEG: 66–82
kaolin-TEG: 47–77
millimeters rapid-TEG and
kaolin-TEG: 50–72
dynes/cm2 rapid-TEG and
kaolin-TEG: 5.3–12.4
percent rapid-TEG and
kaolin-TEG: <3.0%
Table 2. Blood products.
Product Volume Per Unit Content** Details
RBC 200–350 mL 1 unit RBC: Hct of 60% Transfused RBC have a half-life of 30 days in the absence of bleeding
or hemolysis. 1 unit increases Hgb by 1g/dL and Hct by 3%, in the
absence of ongoing bleeding or hemolysis. In neonates and children
transfusion dose is 10–15 mL/kg with an expected 2–3 g/dLHgb rise.
Plasma 200–350 mL 1 unit plasma: 600 mg of
fibrinogen, 1 IU/mL
of all coagulation
FFP*: frozen within 8h of collection (contains functional quantities of
all coagulation factors). F24*: frozen within 24h of collection (may
contain variably reduced levels of factor VIII, 40–80% of normal)
factors and coagulation
inhibitors.
Cryoprecipitate 15 mL 1 unit of cryoprecipitate:
200 mg of fibrinogen,
100 IU of factor VIII,
100 IU of vWF, and
75 IU of factor XIII.
Platelets 300 mL (SDP)
60 mL (RDP)
1 unit SDP: 3.5 × 10
platelets
1 unit RDP: 5.5 × 10
platelets
RBC: red blood cells, IU: international units, vWF: von-Willebrand factor, SDP: single-donor platelets, RDP: random-donor platelets.
* depends on local blood banking practices; DHMC products: plasma F24, cryoprecipitate “10-packs,” SDP apheresis platelets.
** the average of the accepted range value is used.
†
at 1h post-transfusion, accounts for estimated 30% splenic secuestration, and assumes no platelet destruction or ongoing bleeding.
Each unit or “bag” of cryo is obtained from precipitation of one unit
of plasma. In most centers it is delivered as pre-pooled “10-packs” *
(10 units or “bags,” 150 mL), “5-packs,” or as individual units*.
A “10-pack” will increase the recipient's fibrinogen by 70–100 mg/
dL. Neonates and children dose: 1–2 “bags” or units/10 kg.
11
SDP* are obtained by apheresis of a single donor (also called “apheresis
platelets”). RDP* are obtained by centrifugation, 4–6 units from
10
different donors are then pooled. 1 unit of SDP is equivalent to 6 RDP
units. 1 SDP unit (or 6 RDP units) increases the recipient's platelet
count by 50,000/mcl.
†
392 E. Gonzalez and E. E. Moore
Mechanism
Drug
Warfarin Vitamin K
of action
epoxide
reductase
inhibition
Table 3. Anticogulants.
Indications
(FDA Approved) Dose Route Half-life Metaboilism Excretion
— Post-VTE risk
reduction (acute
management of DVT
or PE should be done
with an agent of fast
therapeutic onset).
2–10 mg/d.
See table # for dosing
adjustments.
oral 36 h
(very variable,
range 20–60h)
(peak plasma
levels reached
72–96 h)
hepatic
(CYP–2C9)
biliary INR CYP450: 1A2,
Detection
of anti-
coagula-
tion
Drug
interactions
2C9, 3A4
inhibitors and
inducers
†
Unique Issues
— 2C9 and
VKORC1 genetic
variations influence
dose response and
impact bleeding
risk.
— 99% bound to
plasma albumin.
— No hepatic dose
adjustment needed
(however, marked
dose response in
liver desease).
— No renal dose
adjustment needed.
(Continued )
Diagnosis and Management of Coagulopathy 393
i.v. infusion.
Drug
Heparin
(unfractionated)
Mechanism
of action
Thrombin
and
factor Xa
inhibition
(anti Xa/
thrombin
ratio: 1.0)
Table 3 (Continued)
Indications (FDA
approved) Dose Route Half-life Metaboilism Excretion
— VTE prophylaxis.
— DVT and PE tx
(only for acute management, transition to
warfarin for post-VTE
risk reduction).
— NSTEMI or unstable angina.
— STEMI.
— VTE prophylaxis:
5,000 units q 8–12 h
subq (recommended
dose is 5000 units q8h;
5000 units q12h can be
used to minimize
bleeding risk, but efficacy is comparable to
placebo in high VTE
risk patients).
— DVT and PE tx
(only for acute management, transition to
warfarin for post-VTE
risk reduction): 80
units/kg bolus i.v., then
18 units/kg/h continuous i.v. infusion.
— NSTEMI or unstable angina: 60 units/kg
bolus i.v., then 12
units/kg/h continuous
i.v. infusion.
— STEMI: adjunct to
fibrinolysis; 60 units/
kg bolus i.v., then 12
units/kg/h continuous
parenteral
(intravenous and
sub-cutaneous)
— i.v. infusion:1.5 h
(increased with
renal
impairment).
— i.v. bolus
(dose dependent):
25 units/kg =
30 min, 100
units/kg = 60
min.— subq:
1.5–3.0 h.
hepatic mostly
renal
Detection
of anti-
coagula-
tion
PTT No significant
Drug
interactions
interactions
†
Unique issues
— No hepatic dose
adjustment needed.
— No renal dose
adjustment needed.
— VTE prophylaxis
for BMI ≥ 40: 7500
units subcutaneous
q8h.
— Anti-Xa prophylactic goal
(measured 4 h after
dose): 0.1–0.4.
— Anti-Xa therapeutic goal
(measured 4h after
dose): 0.3–0.7.
— Relationship
between anti-Xa
and PTT is variable
by institution, however usually the
therapeutic PTT is
2.0–2.5 times the
control PTT.
394 E. Gonzalez and E. E. Moore
Diagnosis and Management of Coagulopathy 395
Enoxaparin
(LMWH)
Thrombin
and factor Xa
inhibition
(anti Xa/
thrombin
ratio: 3.3)
— VTE prophylaxis.
— DVT and PE tx
(only for acute management, transition to
warfarin for post-VTE
risk reduction).
— NSTEMI or
unstable angina.
— STEMI.
— VTE prophylaxis:
40 mg/d (for ICUtrauma, post-op hip
and knee replacement,
hip and pelvic fracture
patients: 30 mg q12 h).
— DVT and PE tx
(only for acute management, transition to
warfarin for post-VTE
risk reduction): 1mg/kg
q12 h or 1.5 mg q24h.
— NSTEMI or unstable angina: 1 mg/kg
q12 h with concurrent
aspirin tx.
— STEMI: 30 mg
bolus (i.v.), then 1 mg/kg
q12 h (subq) (>75 y.o.:
no bolus and
0.75 mg/kg q12h)
parenteral
(subcutaneous)
3.5 h (up to 8 h
in renal impairment)
hepatic mostly
renal
anti-Xa No significant
interactions
— VTE prophylaxis
for BMI 40–49:
40 mg q12h, BMI
≥50: 60 mg q12 h.
— No hepatic dose
adjustment needed.
— Avoid if Cr clearance <30mL/min.
— LMWH efficacy
reduced by vasopressor use.
— Anti-Xa
prophylactic goal
(measured 4h after
dose): 0.2–0.6
(q12h or q24 h
dosing).
— Anti-Xa therapeutic goal
(measured 4h after
dose): 0.6–1.0
(q12h dosing),
1.0–2.0 (q24 h
dosing).
(Continued )
Drug
Dalteparin
(LMWH)
Mechanism
of action
Thrombin
and factor Xa
inhibition
(anti Xa/
thrombin
ratio: 2.0)
Table 3 (Continued)
Indications (FDA
approved) Dose Route Half-life Metaboilism Excretion
— VTE prophylaxis.
— DVT and PE tx
(only for acute management, transition to
warfarin for post-VTE
risk reduction(except
cancer patients)).
— Post-VTE risk
reduction (cancer
patients only).
— MI (non-Q wave)
or unstable angina.
— VTE prophylaxis:
5000 units/d
— DVT and PE tx:
200 units/kg daily
(transition to warfarin
for post-VTE risk
reduction in
non-cancer patients).
— Post-VTE risk
reduction (cancer
patients only): 200
units/kg daily for 1
month, then 150 units/
kg daily for months
2–6.
— MI (non-Q wave)
or unstable angina:
120 units/kg Q12h
(max. dose: 10,000
units q12h) with concurrent aspirin tx.
parenteral
(subcutaneous)
4 h (up to 8 h in
renal impairment)
hepatic mostly
renal
Detection
of anti-
coagula-
tion
anti-Xa No significant
Drug
interactions
interactions
†
Unique issues
—VTE prophylaxis
for BMI ≥40:
6500 units/d.
— No hepatic dose
adjustment needed.
— Avoid if Cr
clearance
<30mL/min.
— LMWH efficacy
reduced by vasopressor use.
— Anti-Xa prophylactic goal
(measured 4 h after
dose): 0.2–0.5.
— Anti-Xa therapeutic goal
(measured 4 h after
dose): 0.5–1.5.
396 E. Gonzalez and E. E. Moore
Diagnosis and Management of Coagulopathy 397
Bivalirudin Thrombin
inhibition
— HIT tx.
— PCI for ACS in
HITT or HITT-risk
patients.
— Cardiopulmonary
bypass in HIT
patients.
— HIT tx: 0.1–0.2 mg/
kg/hr continuous i.v.
infusion (goal PTT
2.0–2.5 times control)
(start warfarin once
therapeutic goal
reached and PLT count
9
≥150 × 10
, and continue bivalirudin until
INR within desired
range; stop bivalirudin
and check INR in 4h,
if INR is below desired
range then resume
bivalirudin and repeat
until desired INR is
reached on warfarin
alone).
— PCI for ACS in
HIT: 0.75 mg/kg bolus
i.v.,1.75 mg/kg/hour
for the duration of procedure and up to 4h
post-procedure.
parenteral
(intravenous)
25 min (up to
3h with renal
insufficiency)
blood
proteases
20% renal,
proteolysis
PTT No significant
interactions
— Transition to
warfarin may be
delayed based on
bleeding risk and
need for interventional procedures.
— Critically ill
patients require
lower doses.
— No hepatic dose
adjustment needed.
— Renal dose
adjustment
required: CrCL
30–60 mL/min =
0.08–0.1 mg/kg/
hour; CrCL
<30 mL/min =
0.04–0.05 mg/kg/
hour.
— Hemodialysis
removes 25%.
(Continued )