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anesthesia for fetoscopy

Anesthesia for Fetoscopy

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Ø Anaesthesia for Fetoscopy

Ø By: Dr. Nesrine El-Refai

Ø Professor of Anesthesia

Ø Cairo University

Ø Objectives

Ø Introduction.

Ø Techniques of fetal intervention.

Ø General idea about Fetoscopy.

Ø Anesthetic considerations.

Ø Future of fetoscopy.

Ø Anesthetic complications.

Ø Kasr-Aini  experience.

Ø Introduction

Ø Anesthesia for fetal surgery involves coordination between the surgical and anesthetic teams.

Ø It is important to understand the maternal, fetal and placental issues to tailor the anesthetic to the surgical plan.

Ø Anesthetic risks for the parturient during nonobstetric surgery include fetal asphyxia , fetal and maternal cardiovascular depression from anesthetics and uterocaval compression, and potential teratogenicity of anesthetic drugs and preterm labor/delivery .

Ø However, fetal surgery also involves repair of the fetal or placental anomaly, and the fetus is usually critically ill, such that survival without the surgery is unlikely.

Ø Factors influencing anesthetic management for fetoscopic surgery include fetal cardiovascular status, history of uterine activity, and location of the placenta relative to the amniotic membranes and umbilical cord.

Ø Cordocentesis and IUT - History

Ø 1963 - First intraperitoneal transfusion (Liley)

Ø 1974 - Fetoscopy to obtain fetal samples (Hobbins,       et al)

Ø 1981 - Fetoscopic transfusion (Rodeck, et al)

Ø 1982 - First ultrasound guided IUT (Bang, Bock &                Troll)

Ø 1983 - First large study of IUT - 66 cases (Daffos, et     al)

Ø

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DISORDERS OF HEMOSTASIS

DISORDERS OF HEMOSTASIS

Normal Hemostasis

Any disruption of vascular endothelium is a potent stimulus to clot formation. As a localized process, clotting acts to seal the break in vascular continuity, limit blood loss, and begin the process of wound healing. Prevention of an exuberant response that would result in pathologic thrombosis involves several counterbalancing mechanisms, including anticoagulant properties of intact endothelial cells, circulating inhibitors of activated coagulation factors, and localized fibrinolytic enzymes. Most abnormalities in hemostasis involve a defect in one or more of the integrated steps in this coagulation process. It is important, therefore, to understand the physiology of hemostasis.

Fifty years ago, two groups simultaneously described the “waterfall” or “cascade” model of soluble coagulation. The cascade model dovetailed well with the clotting assays that were developed at that time to guide warfarin and heparin dosing, and these tests came to be the gold standard for measuring soluble coagulation. Although this cascade model continues to be useful for interpretation of laboratory clotting tests, it does not accurately represent in vivo clotting.

In vivo coagulation follows exposure of the blood to a source of tissue factor (TF), typically on subendothelial cells following damage to a blood vessel. The intrinsic, or contact, pathway of coagulation has no role in these earliest clotting events. TF-initiated coagulation has two phases, one an initiation phase and a second, the propagation phase. The initiation phase begins as exposed TF binds to factor VIIa, picomolar amounts of which are present in the circulation. This VIIa-TF complex catalyzes the conversion of small amounts of factor X to Xa, which in turn generates similarly small amounts of thrombin.

The seemingly trivial amount of thrombin formed during the initiation phase triggers the propagation phase, which fosters explosive thrombin generation in abundance. Thrombin ramps up its own formation by activating platelets and factors (FV, FVIII), setting the stage for formation of the FVIIIa–IXa complex, a pivotal point in the propagation phase. Formation of this FVIIIa–IXa complex allows FXa generation to switch from a TF-VIIa complex–catalyzed reaction to one produced by the intrinsic Xase pathway. This switch is of enormous kinetic advantage, with the intrinsic Xase complex exhibiting 50-fold higher efficiency at Xa generation. The bleeding diathesis associated with hemophilia, with its intact initiation phase and absent propagation phase, is testament to the hemostatic importance of the propagation phase.

The commonly used laboratory tests of soluble coagulation only measure the kinetics of the initiation phase. The prothrombin time (PT) and activated partial thromboplastin time (aPTT) both have as endpoints the first appearance of fibrin gel, which occurs after completion of less than 5% of the total reaction. These tests are sensitive at detecting severe deficiencies in clotting factors, for example, hemophilia, and in guiding warfarin/heparin therapy; however, they do not model the sequence of events necessary for hemostasis and do not necessarily predict the risk of intraoperative bleeding.

In the venous circulation, the kinetic advantage of coagulation cascade assembly on the platelet surface is readily apparent; however, relatively small numbers of platelets are needed to fulfill this function. To increase the risk of venous bleeding, the platelet count must decrease to very low levels, that is, less than 10,000/μL. This contrasts sharply with the arterial circulation, in which the minimum platelet count needed to ensure hemostasis for operative procedures is at least five times that number (see “Arterial Coagulation” below).

Coagulation Abnormalities Made Easy

 Coagulation Abnormalities Made Easy
Linda L. Liu, M.D. San Francisco, California

Back decades ago, the coagulation cascade was taught in terms of 2 pathways, the intrinsic versus the extrinsic.

Figure 1 shows a very simplified version of the proposed waterfall/ cascade model of the coagulation system.
Unfortunately, as we started to understand more about the coagulation system, it became more and more complex.
Many of the enzymes were found to be cofactors or were precursors to the active form. We also found that the 2
pathways were not completely separate in function. They appeared to be an intertwined system where modulation
of one arm may or may not affect the second arm. The modern view of coagulation is to actually look at the
coagulation system as a series of steps, 1) initiation, 2) amplification, and 3) propagation, as opposed to distinct
pathways, (1) but the old 2 pathway model is still beneficial in terms of helping us understand what abnormal
coagulation tests mean. This chapter will exam some causes of abnormal coagulation in the perioperative period and
discuss agents that are used to modulate the coagulation system.
Figure 1: Waterfall/ Cascade Model of the Coagulation System