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EPA Addressed:
#8 Perioperative care of the critically ill surgery patient.
#18: Evaluation and initial management of a patient presenting with blunt or penetrating trauma.
Goals and Objectives
Goals and Objectives
Understand the clotting cascade and the fibrinolytic system
Understand the differences between ROTEM, TEG, and standard coagulopathy labs
Understand how to interpret and treat abnormalities in TEG and ROTEM results
Clinical Scenarios
Clinical Scenarios
Scenario 1
Scenario 1
A young adult presents after blunt trauma with ongoing hemorrhage and hypotension. Initial labs show elevated INR and low platelets. TEG is performed on arrival, revealing prolonged reaction time (R) and decreased maximum amplitude (MA).
Note: The American Association for the Surgery of Trauma recommends TEG-guided resuscitation as an adjunct to conventional damage control resuscitation, noting that TEG can reduce unnecessary transfusions and may improve outcomes in trauma patients, although recent multicenter data show no difference in major outcomes compared to conventional testing.
Scenario 2
Scenario 2
A young adult presents after blunt trauma with ongoing hemorrhage and hypotension. Initial labs show elevated INR and low platelets. TEG is performed on arrival, revealing prolonged reaction time (R) and decreased maximum amplitude (MA).
Note: The American Association for the Study of Liver Diseases and the American Gastroenterological Association both highlight that TEG provides a more accurate assessment of bleeding risk in cirrhosis than INR or platelet count, and TEG-guided transfusion strategies significantly reduce blood product use without increasing bleeding risk.
Scenario 3
Scenario 3
A postoperative patient develops bleeding after receiving a bolus of unfractionated heparin for a DVT. A standard TEG reveals a significantly prolonged R time, and a heparinase-modified TEG shows a normal R time.
Regarding TEGs:
The viscosity of the sample does not change during the initial phases of clotting cascade activation, as no platelets have been cross-linked with fibrin yet. This is why the R time (reaction time) is stable and normalized to a baseline amplitude.
The R time (time to get through the clotting cascade) is dependent on how many factors are around to go through the cascade.
Two pathways exist for triggering the coagulation cascade: the intrinsic (contact) pathway and the extrinsic (tissue factor/thrombomodulin) pathway.
Both pathways converge and activate factor X, which in turn activates factor II (Prothrombin) into Thrombin.
Warfarin inhibits vitamin K activation which inhibits factor II, VII, IX, X, protein S, and protein C synthesis in the liver. Warfarin effects are monitored with INR.
Four factor PCC (Prothrombin Complex Concentrate) causes rapid correction of factor-based deficiencies (e.g., Warfarin) to begin a thrombin burst.
Liver disease decreases production of prothrombotic (Factors II, VII, IX, and X) and antithrombotic (plasminogen, protein C and S) factors. As such, INR is not a reliable measure of actual coagulation in cirrhosis patients. A functional test such as TEG/ROTEM should be used to assess the coagulation profile in liver patients.
Heparins bind to and activate antithrombin III. AT3 inactivates thrombin and factor Xa preventing clot formation. Heparin effects are measured with aPTT or anti-Xa levels.
Protamine is the reversal agent for unfractionated heparin.
Xa inhibitors, such as apixaban (Eliquis) and rivaroxaban (Xarelto), directly inhibit Xa.
These are reversed with PCC, as the specific reversal agent, andexanet alfa, was removed from the market.
Direct thrombin inhibitors bind to thrombin, inactivating coagulation.
Idarucizumab (Praxbind) or dialysis remove dabigatran.
Bivalirudin and Argatroban are often used as first line agents in HITT before eventually being converted to Xa inhibitors for outpatient management. Bivalirudin has no specific reversal agent, but it has a short half-life with effects gone withing 4 hours in patients with normal renal function.
Regarding TEGs:
Once platelets begin to cross-link via fibrin, the viscosity of the blood sample begins to change. This manifests as an increase in the maximum amplitude (MA) of the plot. The rate of cross-linking is related to the amount/abundance of fibrinogen available.
Once the platelet plug as reached maximum platelet activation and aggregation, the viscosity of the sample reaches a plateau/maximum as well. This is measured on the TEG as the maximum amplitude and serves as a marker for platelet count AND platelet activity.
Exposed collagen binds GP VI and von Willebrand Factor, which in turn binds GP Ib, to bind platelets to the site of injury.
Platelets can be activated by collagen, adenosine diphosphate, thrombin, and thromboxane.
Activated platelets are cross linked by GPIIb/IIIa and Fibrin (Ia) to form a platelet plug.
Aspirin is a COX inhibitor and thereby prevents platelet production of thromboxane A2 and subsequent activation and aggregation.
The effect on a TEG with platelet mapping is measured as a percent of arachadonic acid inhibition.
Clopidogrel, and other P2Y12 antagonists such as ticagrelor, bind to the P2Y12 ADP receptor and thereby inhibit platelet activation and aggregation.
The effect on a TEG with platelet mapping is measured as a percent of ADP inhibition.
Antiplatelet agents have no true reversal agents.
Platelet goals include:
>100,000 for neurosurgery
>50,000 for major surgery, endoscopic procedures, or DVT prophylaxis (though this is controversial)
>20,000 for bronchoscopy or central line placement
>10,000 to prevent spontaneous bleeding
Regarding TEGs:
The fibrinolysis pathway will break down the platelet plug and decrease the viscosity of the sample over time. This is measured via the lysis at 30 minutes (LY30) percentage.
Rapid fibrinolysis will drop the viscosity more than 3% at 30 minutes.
The fibrinolysis pathway depends on plasminogen, which is synthesized in the liver, and tPA, which is synthesized in the endothelium.
tPA release from the endothelium activates plasminogen to plasmin, which in turn begins to break down fibrin into fibrin degradation products.
Hyperfibrinolysis can lead to excessive bleeding and clot instability, and treatment requires Tranexamic Acid (TXA) administration to bind to plasminogen and prevent tPA activation.
Hyperfibrinolysis occurs in around 10% of trauma patients and increases mortality. This is mediated by massive endothelial tPA release from a post-traumatic catecholamine surge from sympathoadrenal activation, tissue hypoperfusion and shock activation of protein c, and inflammatory cytokine production from injury.
Rotem System
Rotem System
Here is a video on the Werfen ROTEM system. It demonstrates why the ROTEM (and similarly TEG) graphs look the way they do: increasing viscosity in the blood sample as it clots causes increased rotational deflection of the pin.
A video of the old TEG 5000 can be found here for comparison: TEG 5000 Simulation Video (cld.bz)
Think of a TEG as a graph where the blood sample's viscosity is measured on the Y-axis and time is measured on the X-axis.
A standard TEG 5000 (the older TEG) reports R times, K times (and angles), MA, and LY30.
The Reaction time (R time) represents the progression through the clotting cascade. As this represents enzyme interactions and zero platelet adhesion, there is no significant increase in viscosity.
A long R time indicates there are very few factors around to interact and progress through the coagulation cascade. Treatment requires factor replacement through FFP or PCC.
The Kinetics time (K time) represents the rate at which platelets are being crosslinked via fibrinogen/fibrin.
A long K time indicates there is a paucity of fibrinogen around to interact with and cross link platelets. Treatment requires fibrinogen replacement through Cryoprecipitate.
The angle is another way to evaluate the Kinetics time as they are related entities. A long K time results in a low angle, and a short K time results in a high angle.
The Maximum Amplitude (MA) represents the maximum platelet plug able to be formed.
A low MA represents few functional platelets around to form a platelet plug and increase the sample's viscosity. This can be from thrombocytopenia OR platelet inhibition. Treatment requires platelet transfusion.
The Lysis at 30 minutes (LY30) represents how quickly the plasmin is breaking down the clot.
High LY30s represent fibrinolysis. Excess fibrinolysis is treated with Tranexamic Acid (TXA), which binds to plasminogen preventing conversion to plasmin and subsequent fibrin breakdown.
A TEG 6s global hemostasis with lysis (the main order we use in the trauma bay) runs several samples at once to tease out how heparin, fibrin, and platelets all contribute to the plot.
It reports an R time from the citrated kaolin sample.
It reports an MA from the Citrated Rapid TEG-MA (CRT). This CRT-MA represents the greatest viscosity change caused by the platelet-fibrin plug. This represents platelet aggregation AND fibrin-fibrin interactions.
Whereas the old TEG 5000 graphs attributed the entire MA to just platelet function, the reality is that the MA is a summation of the viscosity changes from platelet crosslinking and fibrin clot as well.
If you have ever used Vistaseal or Tisseel, you have probably noted that the hemostatic products are viscous when activated. These are fibrin/thrombin sealants, and there are no platelets in them. This shows that a component of the maximum viscosity of a blood sample on a TEG is actually part fibrin clot AND part platelet plug.
A separate sample inhibits all of the platelets in the sample and produces a Citrated Functional Fibrinogen (CFF). This shows the viscosity change purely associated with fibrin networking without any platelet effects.
A low CRT-MA may be from low fibrinogen OR low/inhibited platelets. You have to look at the CFF (fibrin clot) and the difference between the CRT and CFF (platelet contribution) to determine which product to needed to fix a low CRT.
A logical progression is the check the CFF-MA first. If this is low, it means that fibrin (thus fibrinogen) is low, and this should be treated with Cryoprecipitate. If the CFF-MA is normal but the CRT-MA is low, this suggests that platelet contribution is insufficient and this should be treated with platelet transfusion.
Finally, it reports a LY30 just like the old TEG machines.
TEG 6s with platelet mapping is used to determine if a patient has any Aspirin or Plavix platelet inhibition. It does not report an R time or an LY30, so it is not a replacement for the TEG 6s global hemostasis with lysis in a trauma patient. It is an additional order in select patients.
Platelet transfusion may be helpful in bleeding patients if ADP% inhibition exceeds 60% or AA% inhibition exceeds 50%.
TEG/ROTEM in Trauma
TEG/ROTEM in Trauma
Here is a lecture on how TEG/ROTEM is used in trauma.
Learn how to read and interpret the graphs! Values are illustrative and not meant for medical decision making. Made by Eric Petersen
Transfusion
Transfusion
During hemorrhage, it is important to ensure adequate access for blood administration. The rate of fluid administration through a line is governed by Poiseuille's Law, which means that wide and short access lines produce the least flow resistance and allow more rapid blood administration.
Average volumes and responses for various blood products are as follows:
Whole blood ~ 500 cc.
Packed RBCs ~ 400 cc. This should increase the hgb concentration ~ 1 g/dL per unit administered.
FFP ~ 250 cc. A dose of 20cc/kg will raise factors ~20-30% in an adult, which is around 4 units in the "standard" 70kg adult.
Platelets ~ 200 cc. 1 bag is actually 6 apheresis packs together and should raise the platelet count ~50k in the "standard" 70kg adult.
Cryoprecipitate ~ 100 cc. 1 bag is actually 5 units. Each unit raises fibrinogen ~ 50mg/dL in the "standard" 70kg adult.
Viral transmission risk is low in the modern age. The risk of HIV transmission is about 1 in 500,000, the risk of Hepatitis B transmission is about 1 in 1,000,000, and the risk of hepatitis C transmission is about 1 in 1,500,000.
Bacterial contamination is higher risk than viral, with platelets (1 in 2000 patients) higher risk than pRBCs or FFP (1 in 50,000 patients) since platelets are stored at room temperature. Certain transplant protocols require bacterial coverage if there are high transfusion requirements during the operation.
Transfusion reactions are rare:
Acute (ABO incompatibility) and Delayed (antigen incompatibility) hemolytic reactions require stopping the transfusion and supportive care.
Febrile nonhemolytic reactions (cytokines) require antipyretics and may be able to continue the transfusion if other acute reactions are ruled out.
Allergic and anaphylactic reactions (histamine release generally 4 hours after transfusion) require cessation of the transfusion and antihistamines or epinephrine if anaphylactic.
Transfusion-related acute lung injury (TRALI) generally requires support care and lung protective mechanical ventilatory support.
Learn which access you need in an emergency and why! Values are illustrative and not meant for medical decision making. Made by Eric Petersen
When do we transfuse in non-hemorrhagic patients?
When do we transfuse in non-hemorrhagic patients?
TRICC Trial (1999):
The Transfusion Requirements in Critical Care (TRICC) trial was the landmark study that established restrictive transfusion practice. This RCT enrolled 838 euvolemic critically ill patients, comparing a restrictive strategy (transfuse if Hb <7 g/dL, maintain 7–9 g/dL) versus a liberal strategy (transfuse if Hb <10 g/dL, maintain 10–12 g/dL). Overall 30-day mortality was similar (18.7% vs. 23.3%; p = 0.11), but rates were significantly lower with the restrictive strategy among patients with APACHE II ≤20 (8.7% vs. 16.1%; p = 0.03) and patients <55 years (5.7% vs. 13.0%; p = 0.02). Hospital mortality was significantly lower in the restrictive group (22.3% vs. 28.1%; p = 0.05).
TRISS Trial (2014):
The Transfusion Requirements in Septic Shock (TRISS) trial addressed transfusion thresholds of 7 g/dL versus 9 g/dL in 1,000 septic shock patients, showing similar 90-day mortality, ischemic events, and use of life support, with fewer transfusions in the lower-threshold group.
Cochrane Systematic Review (2025):
The most recent Cochrane review (61 trials, 27,639 adult participants) confirmed that restrictive transfusion strategies reduced the risk of receiving at least one RBC transfusion by 42% (RR 0.58, 95% CI 0.52–0.65) without modifying 30-day mortality (RR 1.01, 95% CI 0.90–1.14; high-certainty evidence). Two notable exceptions emerged: in gastrointestinal bleeding, mortality was lower with restrictive strategies (RR 0.63, 95% CI 0.42–0.95), while in critically ill patients with brain injury, unfavorable neurological outcome was lower with liberal strategies (RR 1.14, 95% CI 1.05–1.22).
Building on the findings that TBI may benefit from more liberal transfusion strategies:
TRAIN Trial (Taccone et al., JAMA 2024):
This is the most impactful study and was named JAMA's "Research of the Year" for 2025. This was a multicenter, phase 3, open-label, parallel-group RCT across 72 ICUs in 22 countries. Enrolled 850 patients with acute brain injury (TBI, aneurysmal SAH, or ICH) who had Hb <9 g/dL within 10 days of injury and expected ICU stay ≥72 hours. The intervention was to compare a liberal (transfuse at Hb <9 g/dL) vs. restrictive (transfuse at Hb <7 g/dL) over 28 days. The primary outcome was unfavorable neurological outcome (GOS-E 1–5) at 180 days. Unfavorable outcome occurred in 62.6% (liberal) vs. 72.6% (restrictive), an absolute difference of −10.0% (aRR 0.86, P = .002). Cerebral ischemic events were also lower in the liberal group (8.8% vs. 13.5%). Limitations included: open-label design, pre-randomization transfusions were not tracked, heterogeneous population (TBI, SAH, ICH combined), non-standardized neuroprognostication, cerebral ischemia assessment was not protocolized, GOS-E dichotomization at 1–5 vs. 6–8 was more conservative than other trials (which used 1–4 vs. 5–8) contributing to higher rates of "unfavorable" outcomes overall, and no standardized VTE screening which potentially underestimated thromboembolic events.
HEMOTION Trial (Turgeon et al., NEJM 2024):
This was a multicenter RCT enrolling 742 adults with moderate-to-severe TBI and anemia across multiple countries. The intervention was comparing liberal (transfuse at Hb ≤10 g/dL) vs. restrictive (transfuse at Hb ≤7 g/dL). The primary outcome was unfavorable GOS-E at 6 months using a sliding dichotomy based on baseline prognosis. Unfavorable outcome occured in 68.4% (liberal) vs. 73.5% (restrictive) which was a nonsignificant 5.4 percentage-point absolute difference (95% CI, −2.9 to 13.7). Among survivors, the liberal strategy was associated with better scores on some (but not all) functional independence and quality-of-life measures. Limitations included potentially being underpowered for the observed effect size, a higher liberal threshold (10 g/dL) compared to TRAIN (9 g/dL) which may have introduced more transfusion-related complications (e.g., ARDS was 3.3% vs. 0.8% in liberal vs. restrictive groups) without proportionally greater benefit, and the TBI-only population limits generalizability to other acute brain injuries.
Why do we do "balanced" 1:1:1 resuscitations?
Why do we do "balanced" 1:1:1 resuscitations?
Early Military Studies:
Borgman et al. (2007) published the seminal retrospective study from the US military hospital in Baghdad analyzing combat casualties requiring massive transfusion (≥10 U RBC/24 h), finding that higher FFP:RBC ratios were associated with improved survival. Multiple military follow-up studies reinforced this finding. The critical limitation of all early studies was survival bias, as the patients who died early were categorized in the low-ratio group because plasma administration typically started later than RBCs. A Monte Carlo simulation demonstrated that survival bias alone could produce a relative risk of 0.33–0.56 favoring high ratios even when the true effect was null.
PROMMTT Study (2013):
The PRospective Observational Multicenter Major Trauma Transfusion (PROMMTT) study was a landmark prospective observational study at 10 US Level I trauma centers enrolling 1,245 adult trauma patients. Its key innovation was using time-dependent proportional hazards models to address survival bias. In multivariable time-dependent Cox models, increased plasma:RBC ratio was independently associated with decreased 6-hour mortality (adjusted HR 0.31; 95% CI 0.16–0.58), and increased platelet:RBC ratio was similarly protective (adjusted HR 0.55; 95% CI 0.31–0.98). Patients with ratios <1:2 were 3–4 times more likely to die in the first 6 hours. Critically, after 24 hours, ratios were not associated with mortality, when competing risks from nonhemorrhagic causes prevailed. Limitations: Observational design precluding causal inference; ratios were not randomized; residual confounding despite time-varying analysis. PROMMTT formed the direct "biological basis" for the PROPPR trial.
PROPPR Trial (2015):
The Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) trial was the definitive phase 3, multicenter RCT at 12 Level I trauma centers in North America, enrolling 680 severely injured patients (median ISS 26; 48.5% penetrating injury) predicted to require massive transfusion. Patients were randomized to 1:1:1 (plasma:platelets:RBC) versus 1:1:2. Primary outcomes were not statistically significant: 24-hour mortality was 12.7% (1:1:1) vs. 17.0% (1:1:2) (difference −4.2%; 95% CI −9.6% to 1.1%; p = 0.12); 30-day mortality was 22.4% vs. 26.1% (p = 0.26). However, death from exsanguination at 24 hours was significantly reduced in the 1:1:1 group: 9.2% vs. 14.6% (difference −5.4%; 95% CI −10.4% to −0.5%; p = 0.03), and more patients achieved hemostasis (86% vs. 78%; p = 0.006). No differences were observed in any of 23 prespecified complications including ARDS, MOF, VTE, or transfusion-related complications. Limitations: The trial was underpowered for the observed effect size; the comparator was 1:1:2 (already a relatively balanced ratio), not a truly unbalanced approach; after the randomized ratio-driven phase ended, clinicians in the 1:1:2 group used laboratory-guided "catching up" toward 1:1:1 cumulative ratios; and the independent effects of plasma vs. platelets could not be separated.
How to do this at BUMCP?
When activating MTP, blood comes in "buckets". Each bucket contains 6 pRBCs, 6 FFP, and 1 bag of Platelets (6 pooled platelets). As most people are not anaerobic until extremely low hemoglobin levels, consider hanging the platelets first followed by 1 FFP and then 1 pRBC. Then alternate 1 FFP and 1 pRBC until the bucket is empty. Do not forget to replace Calcium during a massive transfusion. Generally you need 1 gram of Calcium Chloride (central line or IO) or 3 grams of Calcium Carbonate (peripheral IV) per MTP bucket to maintain ionized calcium levels required for cardiac inotropy and as a cofactor in coagulation.
Why do we allow for permissive hypotension in hemorrhagic shock/trauma?
Why do we allow for permissive hypotension in hemorrhagic shock/trauma?
Bickell et al. (1994):
The foundational study by Bickell et al. randomized 598 patients with penetrating torso injuries to immediate versus delayed fluid resuscitation (until operative intervention). Delayed resuscitation was associated with improved survival (70% vs. 62%; p = 0.04) and fewer complications. This study validated Walter Cannon's century-old dictum that uncontrolled hemorrhage should not be treated with intravenous fluids until surgical control.
Schreiber et al. (2015):
This multicenter pilot RCT (19 EMS systems, n = 192) compared controlled resuscitation (SBP target ≥70 mmHg, 250 mL boluses) versus standard resuscitation (2 L initial, SBP target ≥110 mmHg). The controlled resuscitation group received 1.0 L less crystalloid; 24-hour mortality was 5% vs. 15% (adjusted OR 0.39, 95% CI 0.12–1.26). In the blunt trauma subgroup, 24-hour mortality was 3% vs. 18% (adjusted OR 0.17, 95% CI 0.03–0.92).
Tran et al. (2018):
This meta-analysis of 5 RCTs (n = 1,158) found a pooled OR of 0.70 (95% CI 0.53–0.92) favoring permissive hypotension, with reduced blood loss and product use, though studies were of poor-to-moderate quality and mostly underpowered.
Current guidelines recommend targeting SBP 80–90 mmHg until hemorrhage control, except in TBI where hypotension is associated with worse outcomes.
Is TXA beneficial in trauma?
Is TXA beneficial in trauma?
CRASH-2 Trial (2010):
The Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage (CRASH-2) trial remains the largest trauma resuscitation RCT ever conducted. It was a multinational, randomized, placebo-controlled trial across 274 hospitals in 40 countries enrolling 20,211 adult trauma patients with, or at risk of, significant bleeding within 8 hours of injury. TXA (1 g IV bolus over 10 min, then 1 g infusion over 8 hours) reduced 28-day all-cause mortality from 16.0% to 14.5% (RR 0.91, 95% CI 0.85–0.97; p = 0.0035) and death due to bleeding from 5.7% to 4.9% (RR 0.85, 95% CI 0.76–0.96; p = 0.0077). Notably, there was no increase in vascular occlusive events. The critical time-dependency analysis (2011) showed the effect on bleeding death varied dramatically by time from injury (interaction p < 0.0001): ≤1 hour RR 0.68 (p < 0.0001); 1–3 hours RR 0.79 (p = 0.03); >3 hours RR 1.44 (p = 0.004). This indicated potential harm if TXA was administered more than 3 hours after injury. Limitations: Predominantly enrolled in low- and middle-income countries; injury severity scores not reported; less than half required transfusion or surgery; no fibrinolytic assays measured; questions about applicability to severely injured patients in advanced trauma systems.
MATTERs Study (2012) and the MATTERs II (2013):
The Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) study was a retrospective cohort of 896 combat casualties at Camp Bastion, Afghanistan. All-cause mortality was 17.4% TXA vs. 23.9% no-TXA (absolute reduction 6.5%); in the massive transfusion subgroup, the reduction was 13.7% (14.4% vs. 28.1%). MATTERs II showed TXA and cryoprecipitate were each independently associated with reduced mortality (OR 0.61 for each); combined use had OR 0.34 (95% CI 0.20–0.58). Limitations: Retrospective, non-randomized; significant selection bias (TXA patients were more severely injured); single-center military setting; a subsequent larger military registry study (Howard et al., 2017; n = 3,773) found no statistically significant mortality association with TXA but raised concerns about increased PE (HR 2.82) and DVT (HR 2.00).
CRASH-3 Trial (2019):
Building on the subgroup that may have benefit most from the CRASH-2 trial, this trial enrolled 12,737 adults with TBI (GCS ≤12 or intracranial bleeding on CT) within 3 hours of injury across 175 hospitals in 29 countries. The primary outcome (head injury–related death within 28 days) was 18.5% TXA vs. 19.8% placebo (RR 0.94, 95% CI 0.86–1.02) which was not statistically significant. However, in the mild-to-moderate TBI subgroup, TXA significantly reduced mortality (RR 0.78, 95% CI 0.64–0.95), while severe TBI showed no benefit (RR 0.99). Excluding moribund patients, early deaths within 24 hours were significantly reduced (RR 0.74, 95% CI 0.58–0.94). Limitations: Primary outcome did not reach significance; wide confidence intervals; most participants from low/middle-income countries; no data on intracranial hemorrhage progression.
STAAMP Trial (2020):
The Study of Tranexamic Acid during Air Medical Prehospital Transport (STAAMP) was a phase 3, multicenter, double-blind, placebo-controlled RCT at 4 US Level I trauma centers enrolling 903 patients at risk for hemorrhage. The primary outcome (30-day mortality) was 8.1% TXA vs. 9.9% placebo (HR 0.81, 95% CI 0.59–1.11; p = 0.17) which was not statistically significant. Post hoc subgroup analyses showed significant benefit when TXA was given within 1 hour (4.6% vs. 7.6%) and in severe shock (SBP ≤70: 18.5% vs. 35.5%). Limitations: Stopped early at 93% enrollment; underpowered (powered for 7% absolute difference, observed 1.8%); broad inclusion criteria captured many patients with low injury severity (median ISS 12); subgroup findings are post hoc.
PATCH-Trauma Trial (2023):
The Pre-hospital Anti-fibrinolytics for Traumatic Coagulopathy and Haemorrhage (PATCH-Trauma) trial was a randomized, placebo-controlled trial in advanced trauma systems (Australia, New Zealand, Germany) enrolling 1,310 patients. The primary outcome, which was survival with favorable functional outcome at 6 months (GOS-E ≥5), showed no difference: 53.7% TXA vs. 53.5% placebo (RR 1.00, 95% CI 0.90–1.12; p = 0.95). However, 28-day mortality was significantly reduced (17.3% vs. 21.8%; RR 0.79, 95% CI 0.63–0.99), as was 24-hour mortality (9.7% vs. 14.1%; RR 0.69, 95% CI 0.51–0.94). The critical finding was that for every 100 patients treated, approximately 4 extra survived at 6 months but approximately 4 extra had severe disability.
EAST 2025 Practice Management Guideline:
A meta-analysis of 30 studies conditionally recommending routine TXA use in both prehospital and in-hospital settings, with statistically significant reductions in 24-hour and 30-day mortality and no increase in vaso-occlusive events.
Quiz Questions
Quiz Questions
In a standard TEG, what does the R time represent, and what does a prolonged R time suggest?
R time is the latency from test start until initial fibrin formation (clot amplitude of 2 mm). A prolonged R time suggests a deficiency in clotting factors or the presence of anticoagulants.
What does the K time measure in TEG, and what does a prolonged K time indicate?
K time is the time from clot amplitude of 2 mm to 20 mm, reflecting the speed of clot strengthening. A prolonged K time suggests low fibrinogen levels or impaired fibrin cross-linking.
In TEG, what does the α (alpha) angle represent?
The α angle reflects the rate of fibrin build-up and cross-linking, influenced by fibrinogen concentration and function. A low α angle suggests hypofibrinogenemia.
What does Maximum Amplitude (MA) measure, and what are the main contributors?
MA measures the maximum clot strength, determined by platelet function and fibrinogen. Low MA can be due to thrombocytopenia, platelet dysfunction, or low fibrinogen.
What does LY30 indicate in TEG?
LY30 is the percentage decrease in clot amplitude 30 minutes after MA, reflecting fibrinolysis. High LY30 suggests hyperfibrinolysis.
In TEG 6s Global Hemostasis with Lysis, what channels give R, CRT, and CFF respectively?
Citrated Kaolin (CK) — Gives R time
Citrated Rapid TEG (CRT) — Gives combined platelet + fibrin MA
Citrated Functional Fibrinogen (CFF) — platelet inhibited well that gives fibrin MA
How do you determine platelet contribution to clot strength in TEG 6s?
Subtract the CFF-MA (fibrin clot strength) from the CRT-MA (total clot strength). The difference represents platelet contribution.
If CRT-MA is low but CFF-MA is normal, what is the likely problem?
Platelet deficiency or dysfunction.
If both CRT-MA and CFF-MA are low, what is the likely problem?
Low fibrinogen levels.
What is the role of TEG 6s Platelet Mapping?
It assesses platelet inhibition from antiplatelet agents like aspirin or clopidogrel. It does not measure R time or LY30, so it’s not a replacement for Global Hemostasis in trauma.
Why might TEG/ROTEM be preferred over PT/INR in trauma resuscitation?
They provide a dynamic, real-time assessment of clot formation, strength, and breakdown, guiding targeted transfusion therapy more effectively than static coagulation labs.
What product would you give for:
Prolonged R time? A low α angle? A low MA with normal CFF-MA?A high LY30?
Prolonged R time → Fresh Frozen Plasma (FFP)
Low α angle or high K → Cryoprecipitate
Low MA with normal CFF-MA → Platelets
High LY30 → Antifibrinolytics (e.g., TXA)
Checklists
Checklists
Read through the provided resources and gain an understanding of the clotting cascade and the fibrinolytic system.
Understand the limitations of standard clotting labs such as PT/INR, especially in liver patients.
Watch the videos to understand physically how ROTEM and TEG systems work to better understand their outputs.
Use the simulators to better understand IV flow rates during emergency resuscitation as well as classical TEG and TEG 6s graph analysis.
Express an understanding of how to treat abnormalities in TEG and ROTEM results
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