Management of Massive Intraoperative Bleeding

Defining and Understanding Massive Intraoperative Bleeding

How is massive intraoperative bleeding defined?

It is defined as a blood loss of more than one circulating volume within 24 hours,
or more than 50% of blood volume within 3 hours.
It can also be defined as a loss of more than 150 to 200 ml per minute,
or if the patient needs a transfusion of four or more units of PRBCs within 1 hour.
Any blood loss that compromises the patient's hemodynamic stability and requires immediate intervention is also considered massive bleeding.

What factors, besides the speed and volume of loss, can threaten a surgical patient with massive bleeding?

Other threatening factors include ischemic co-morbidity, preceding anemia,
delay of blood transfusion, and delay of blood supply.

What are the main causes of massive intraoperative bleeding?

The causes can be categorized into three main areas:

Surgical causes: These depend on the complexity of the procedure, technical difficulties, and the approach to hemostasis. Examples include vascular injuries, organ laceration, neoplasm resections, and anatomical variances of the surgical patient.
Coagulopathic causes: These could be pre-existing coagulopathy, patients on anti-coagulant therapy, or the development of dilutional coagulopathy leading to loss of clotting factors or DIC.
latrogenic causes: These include anesthetic factors like hypotension during surgery, surgical techniques, or equipment failure.

What are the two types of bleeding observed in the operating room?

Bleeding can be of two types:

Surgical bleeding: This is confined to the operative site and can be minimized by meticulous surgical technique and good patient selection.
Microvascular or coagulopathic bleeding: This is due to abnormal hemostatic mechanisms. It presents as generalized bleeding from the operative site, as well as from percutaneous cannulation sites, urinary catheters, and the nasogastric tube.

How does bleeding paradoxically evolve into a thrombotic process?

Bleeding can paradoxically lead to thrombosis due to:

Overzealous replacement of deficient procoagulant factors.
Inattention to deficient anti-coagulant factors.
A reluctance to initiate needed anti-coagulant agents for venous thromboembolic prophylaxis after a recent bleed.

Pre-operative Assessment and Optimization

What does the pre-operative assessment for managing severe perioperative bleeding involve?

It involves a comprehensive history and physical examination to identify patients who need to be optimized before surgery.
This includes patients with preoperative anemia, those on anti-thrombotic drugs,
patients with comorbidities involving impaired hemostasis, patients on chronic medications that can impair hemostasis,
patients with inherited bleeding disorders, and now also COVID-19 coagulopathy patients.

Why is pre-operative anemia a concern for bleeding, and how should it be managed?

Anemia itself is associated with prolonged bleeding times.
This is because the rheology of red blood cells permits the margination of platelets to the endothelial wall, which is crucial for coagulation.
Additionally, the surface of hemoglobin has a procoagulant effect.
Management involves screening for anemia, identifying and treating the underlying cause,
giving oral or IV iron for iron deficiency anemia (even one dose of IV iron prior to surgery in malignancy patients helps),
and using erythropoietin stimulating agents for anemia of chronic disease.
Pre-operative RBC transfusion is indicated only if it cannot be corrected by comprehensive hematological therapy.

How should anti-thrombotic drugs be managed perioperatively?

Aspirin: Usually not withdrawn unless the risk of bleeding exceeds the thrombotic risk from withholding it.
P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel): Clopidogrel and ticagrelor should be stopped 5 days prior to surgery, and prasugrel 7 days prior. They should be resumed as soon as possible postoperatively. If bleeding occurs, platelet transfusion can be given.
Anticoagulants (heparin, fondaparinux, vitamin K antagonists, DOACs): For low-risk surgeries, they continue until the day prior to surgery and resume within 6 hours. For intermediate and high-risk surgeries, DOACs are stopped 3 to 5 days prior depending on creatinine clearance and resumed within 72 hours. Bleeding in patients on heparin may be treated with protamine.

How should patients with chronic liver disease be assessed for bleeding risk?

Mild to moderate prolongation of PT and INR and moderate thrombocytopenia do not predict bleeding in patients with chronic liver disease.
Therefore, a viscoelastic hemostatic assay is better for predicting bleeding risk.
In patients with acute liver disease, routine prophylactic correction of standard lab tests is not recommended.
If the patient bleeds, first correct platelets, then correct fibrinogen, and then correct prolonged PT.

What other patient factors and medications can increase bleeding risk?

Renal dysfunction: May be managed with DDAVP to improve platelet function; conjugated estrogens can also be given.
Overt hypothyroidism: May be associated with a bleeding tendency.
SSRIs: They reduce platelet function, increasing bleeding risk. If the patient is stable, it can be discontinued 2 weeks prior to surgery.
Valproic acid: May increase the risk of bleeding.
Inherited bleeding disorders.

Intraoperative Management and Monitoring

What is the initial response when massive intraoperative bleeding is encountered?

The initial response involves:

Coordinating with the surgical team.
Mobilizing resources and getting help.
Initiating hemostatic resuscitation (administering blood products, monitoring coagulation status).
Managing anesthesia to ensure hemodynamic stability, minimize cardiovascular depression, and closely monitor vital signs.
Focusing on human factors, clear communication, and teamwork with defined roles.
Preparing equipment like rapid infusers, ultrasound/TEE, and central venous and arterial access.

What are the three primary concerns during massive bleeding that guide management?

The three concerns are:

Loss of volume.
Loss of red cell mass.
Loss of coagulation factors.

Management must address all three, not just volume replacement or increasing hemoglobin.

What is the general approach to transfusion in massive intraoperative bleeding?

In the early phase, start with a massive transfusion protocol with a high plasma to RBC ratio.
Transition to a goal-directed therapy as soon as possible, based on hemoglobin thresholds, physiological triggers (organ ischemia, cardiopulmonary reserve), and coagulation support.
Always keep in mind the need to avoid over-transfusion.

What is the hemoglobin target and transfusion trigger?

A hemoglobin level around 7 to 9 g/dL is generally acceptable.
This usually balances oxygen delivery and transfusion risk.
You also need to consider patient co-morbidities and perfusion markers,
such as central venous oxygen saturation and AV oxygen difference, to assess the adequacy of oxygen delivery and extraction.

How should hemoglobin be monitored, and what is the role of non-invasive monitoring?

Pre-operative, intraoperative, and post-operative monitoring of hemoglobin should be done.
Non-invasive hemoglobin monitoring is worthwhile because it provides a continuous trend,
which is especially useful in situations where frequent sampling (e.g., every half hour) is difficult, such as in children.

How is tissue perfusion monitored during massive bleeding?

Tissue perfusion is monitored using:

Static monitors: Hemoglobin, hematocrit, lactic acid, and base deficit.
Dynamic monitors: Pulse pressure variation and stroke volume variation.

What is the role of crystalloids and colloids in fluid management during massive bleeding?

Crystalloids: Isotonic crystalloids should be given in a timely and protocol-based manner. More volume is generally required.
Colloids: They may provide faster hemodynamic stabilization, but the downside is they may increase the coagulopathic risk of the patient.

How is the coagulation status monitored, and how are defects corrected?

Coagulation status is monitored using standard lab tests (PT, INR, platelets) and viscoelastic assays.
Viscoelastic assays provide a good assessment of where the defect is, guiding the correction with coagulation factor concentrates, fibrinogen, prothrombin complex concentrates, and recombinant activated factor VII.

What other hemostatic agents can be used?

Tranexamic acid: An anti-fibrinolytic that inhibits plasminogen conversion to plasmin. Dose is 10-20 mg/kg, given intravenously, intraarticularly, orally, or locally.
Desmopressin (DDAVP): A V2 analog that releases von Willebrand factor from endothelial stores to facilitate platelet action. Dose is 0.3 microgram/kg infused over 15-30 minutes.

Key Takeaways and Summary

What are the key takeaways for managing massive intraoperative bleeding?

Start with a massive transfusion protocol (1:1 plasma to RBC ratio) and then individualize therapy.
Continuously monitor hemoglobin, prioritizing non-invasive tools for trending.
Correct post-operative anemia aggressively with IV iron and ESAs.
Avoid over-transfusion; go for single-unit strategies as far as possible.
Maintain the patient's body temperature, hemostasis, and tissue perfusion.

What are the risk factors associated with severe bleeding of more than 20% of blood volume?

Severe bleeding of more than 20% of blood volume is a risk factor for anemia, allogeneic blood transfusion, coagulopathy, and tissue hypoperfusion.

What is the recommended approach for managing high-bleeding-risk patients?

For high-bleeding-risk patients, management should be guided by blood gas analysis, global coagulation tests, and viscoelastic hemostatic assays.
It is worthwhile to have standard operating procedures in your hospital.
Surgical bleeding should be stopped by surgical measures, while acquired coagulopathic bleeding requires individualized correction of the actual pathomechanism using anti-fibrinolytics, procoagulant drugs, and coagulation factor concentrates.