Radiofrequency tumor ablation: principles and techniques

Abstract

Radiofrequency (RF) tumor ablation has been demonstrated as a reliable method for creating thermally induced coagulation necrosis using either a percutaneous approach with image-guidance or direct surgical placement of thin electrodes into tissues to be treated. Early clinical trials with this technology have studied the treatment of hepatic, cerebral, and bony malignancies. However, more recently this technology has been used to treat a host of malignant processes throughout the body. This article will discuss the principles and technical considerations of RF ablation with the goal of defining optimal parameters for the therapy of focal lesions. This includes technologic innovations that permit large volume tumor ablation (i.e., hooked and internally cooled electrodes), as well as methods and adjuvant therapies that can modulate tumor biophysiology to permit improved tumor destruction (i.e, altered tissue conductivity and blood flow). Potential biophysical limitations to RF induced coagulation, such as perfusion mediated tissue cooling (vascular flow) will likewise be discussed. Lastly, the principles governing safe usage of the system, such as proper grounding pad placement, will be adressed.

Introduction

The purpose of this article is to review the basic principles of radiofrequency (RF) thermal ablation with the goal of providing insights into achieving optimal results (i.e. reproducible large volume tissue coagulation) in the safest possible manner. This article will attempt to provide a better understanding of radiofrequency ablation that can hopefully be applied to clinical practice with favorable results. Overviews of potential clinical applications (Gazelle et al., 2000, McGahan and Dodd, 2001), and specific clinical application in the liver (Solbiati et al., 1997a, Solbiati et al., 1997b, Rossi et al., 1998, Curley et al., 1999, Livraghi et al., 1999, Livraghi et al., 2000) and other organs (Anzai et al., 1995, Zlotta et al., 1997, Birdwell et al., 1998, Lewin et al., 1998, Rosenthal et al., 1998, McGovern et al., 1999, Dupuy et al., 2000a, Dupuy et al., 2000b); and comparison to other thermal ablative therapies (Dodd et al., 2000, Goldberg et al., 2000a) can be found elsewhere.

Preparatory to RF heat ablation of a tumor, thin (usually 21–14 gauge) needle-like electrodes are placed directly into the tumor using US, CT, or MR imaging guidance. The RF electrode typically comprises a metal shaft, which is insulated except for an exposed conductive tip that is in direct electrical contact with the targeted tissue volume (Fig. 1a). The RF generator supplies RF power to the tissue through the electrode. It is connected both to the shaft(s) of the RF electrode (and thus the exposed RF electrode tip) and a reference electrode, usually a large area conductive pad contacting the patient's skin in an area of relatively good electrical and thermal conductivity. The RF generator produces a RF voltage between the active RF electrode and the reference electrode, thereby establishing lines of electric field within the patient's body between the two electrodes. At the low RF frequencies used for this procedure (<1 MHz), the electric field pattern is governed essentially by electrostatic equations (Organ, 1976, Cosman et al., 1984). Essentially, the electric field oscillates with the RF frequency, which causes oscillatory movement of ions in the tissue with a velocity that is proportional to the field intensity. The mechanism of tissue heating with RF ablation is frictional (or resistive) energy loss associated with this ionic current.

The main aim of thermal tumor ablation therapy is to destroy an entire tumor using heat to kill the malignant cells in a minimally invasive fashion without damaging adjacent vital structures (Dodd et al., 2000, Gazelle et al., 2000, Goldberg et al., 2000a, McGahan and Dodd, 2001). This often includes the treatment of a 0.5–1 cm margin of apparently normal tissue adjacent to the lesion (i.e., a ‘surgical’ margin) in order to eliminate microscopic foci of disease and the uncertainty which often exists regarding the precise location of actual tumor margins (Dodd et al., 2000, Goldberg et al., 2000a). The parameter governing tissue destruction is temperature. Thus, it is necessary to understand how heat interacts with tissue to induce cell death.

Essentially, it is the generation of the tissue heating that induces cellular death occurs via thermal coagulation necrosis (Cosman et al., 1984, Goldberg et al., 2000b). The volume of RF heat ablation is therefore governed by the temperature distribution within the tissue. The thermal distribution in a targeted lesion can be modeled by the ‘Bio-heat’ equation as previously described by Pennes (1948). We have previously described a simplified framework of viewing thermal ablation along the lines of this equation reduced to a first approximation as ‘Coagulation necrosis=energy deposited×local tissue interactions-heat lost’ (Goldberg et al., 2000a).

Cellular homeostasis can be maintained with mild elevation of temperature to approx. 40°C. When temperatures are increased to 42–45°C (hyperthermia), cells become more susceptible to damage by other agents such as chemotherapy and radiation (Seegenschmiedt et al., 1990, Trembley et al., 1992). However, even prolonged heating at these temperatures will not kill all cells within a given volume, as continued cellular functioning and tumor growth can be observed following relatively long exposure to these temperatures. When temperatures are increased to 46° C for 60 min, irreversible cellular damage occurs (Larson et al., 1996). Increasing the temperature only several degrees to 50–52°C markedly shortens the time necessary to induce cytotoxicity (4–6 min) (Goldberg et al., 1996a). Between 60–100°C, there is near instantaneous induction of protein coagulation which irreversibly damages key cytosolic and mitochondrial enzymes, as well as nucleic acid–histone protein complexes (Zevas and Kuwayama, 1972, Thomsen, 1991, Goldberg et al., 2000b). Cells experiencing this extent of thermal damage most often, but not always, undergo coagulative necrosis over the course of several days. The term ‘coagulation necrosis’ has therefore been used to denote irreversible thermal damage to cells whether or not the ultimate manifestations of cell death fulfill the strict histologic criteria of coagulative necrosis. This last point has significant implications, as it has limited the use of percutaneous biopsy and histologic interpretation as a reliable method for documenting adequate ablation of a tumor. Temperatures greater than 105°C result in tissue boiling, vaporization, and carbonization. These processes usually retard optimal ablation due to a resultant decrease in energy transmission (Goldberg et al., 1996a). Thus, a key aim for ablative therapies is achieving and maintaining a 50–100°C temperature range throughout the entire target volume.