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Bleeding Complications

Anthony H. Guarino MD and Neill Wright MD

Creve Coeur, Missouri, USA

Introduction

At every critical juncture in patient care, a healthcare practitioner needs to apply judgment in deciding what is the best option for their patient in the presenting clinical setting. This is apropos the situation when one decides to offer a pain management intervention and needs to determine whether the patient will be put at any risk for pressure injury from a blood clot with a planned procedure.

We have a natural clotting event in and out of our blood vessels. In this chapter, the author will discuss the overview of the event as well as recommendations for temporarily ceasing a medication use for an intervention.

Many patients are taking medications that affect their clotting mechanism. These are usually intended to prevent a problem that occurs when clotting may manifest in a dangerous way: heart attacks, strokes, and other end-organ ischemic pathologic events.

One needs to decide whether the risk of stopping an anticoagulant outweighs the benefit of the proposed procedure. There have been many studies that can help inform our decisions as well as guidelines presented by various organizations to help us determine what may be the best therapeutic approach.

When a clot forms in the epidural space, a potentially dangerous morbid and mortal event may be occurring. This chapter will also discuss how to identify the problem as well as how to address it.

Coagulation

The blood clotting and bleeding balance represents a complex interaction between many molecules from the coagulation and fibrinolytic system. Usually, there is more inhibition of clotting than clot formation [1]. If one of the molecules involved in one of the processes is malfunctioning, the balance can be tipped toward more clotting or clot lysis [1].

Factors in the vessel wall that can be thrombogenic include the following: exposed endothelium, tissue factor, and collagen [1]. Factors in the circulation that may be thrombogenic include the following: platelets, platelet activating factor, clotting factor, prothrombin, fibrinogen, and the Von Willerband factor [1]. Components in the body that oppose clotting include the following: heparin, thrombomodulin, tissue plasminogen activator, protein C, protein S, and plasminogen [1].

The balance can be disturbed by an interventional pain management procedure. Other contributing factors include cytokines and infectious agents as well as hypoxia, hypercarbia, and metabolic acidosis [1].

Primary Hemostasis

Clotting results from a complex interaction between platelets, the vessel wall and adhesive proteins. Endothelial cells exhibit antithrombotic properties via negatively charged glycosaminoglycans, neutral phospholipids, synthesis, and secretion of platelet inhibitors, coagulation inhibitors as well as fibrinolysis activators [1]. The subendothelial layer is highly thrombogenic and contains collagen, Von Willebrand factor, and other proteins like laminin, thrombospondin, and vitronectin that are involved in platelet adhesion [1]. Acute vascular insults result in arteriolar vasospasm mediated by reflex neurogenic mechanisms and release of local mediators such as endothelin and platelet-derived thromboxane A2 [2–4].

Platelets form the initial hemostatic plug that provides a surface for the assembly of activated coagulation factors leading to the formation of fibrin stabilized platelet aggregates and subsequent clot retraction. Platelets do not adhere to intact vascular endothelium. When there is a vascular insult, platelets adhere to collagen and von Willebrand factor in the subendothelial tissue and undergo a morphologic change by assuming an irregular surface, forming numerous pseudopods [5].

When platelets aggregate, there is a temporary seal to the vascular injury. A chemical reaction causes the deposition of fibrinogen. Thrombin generation also leads to further buildup of fibrin which also adds to the stability of the platelet plug [6]. This is secondary hemostasis.

Clotting

Coagulation proteins are the core components of coagulation that lead to a complex interplay of reactions resulting in the conversion of soluble fibrinogen to insoluble fibrin strands. The majority of clotting factors are precursors of proteolytic enzymes that circulate in an inactive form. They are primarily produced in the liver. Anticoagulant effects in the blood regulate the procoagulant activity in blood thus limiting the thrombus formation [1].

Performing Pain Management Procedures on Patients Taking Medications that Effect Coagulation

There are many guidelines published around the world but in the US, the main ones are published by ASIPP [7, 8] and ASRA [9]. They give recommendations but ultimately recommend that changing or altering a patient’s use of medication should be done in consultation with the clinician who prescribed the medicine to effect coagulation. There is a risk of a thromboembolic phenomenon if a medication is stopped and one must question if the benefit of a procedure outweighs the risk.

Neither the ASIPP nor ASRA recommend stopping NSAIDs including low-dose baby aspirin prior to performing a pain management procedure. However, both organizations recommend considering cessation of high-dose aspirin for one week prior to any procedure.

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