Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Thermal applicators
Reexamination Certificate
2002-04-24
2004-04-27
Gibson, Roy D. (Department: 3739)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Thermal applicators
C607S104000, C606S022000, C606S023000
Reexamination Certificate
active
06726709
ABSTRACT:
BACKGROUND
Field of Invention
This invention relates to a method and device for inducing localized hypothermia in tissue, specifically brain tissue that is at risk of necrosis due to stroke.
BACKGROUND
Description of Prior Art
Stroke is a leading cause of death and disability. It is estimated that over 725,000 people suffer a major stroke in the United States each year, and that over 100,000 of these people die. There are two main categories of stroke: ischemic and hemorrhagic. A blockage in an artery in the brain causes ischemic stroke, and a rupture in an artery in the brain causes hemorrhagic stroke. There are approximately 600,000 ischemic stokes, and 125,000 hemorrhagic strokes in the United States each year.
Within the last decade there has been a marked increase in understanding why and how brain cells die from ischemic stroke. Cells within an infarction zone have dramatically reduced blood flow of 20% of normal or less. Cells within this infarction zone will be irreversibly damaged within a few minutes. Surrounding the infarcted zone is a volume of tissue called the “ischemic penumbra” or “transitional zone” in which blood flow is between 20% and 50% of normal. Cells in this area are endangered, but not irreversibly damaged. Ischemia in the infarction zone, and in the ischemic penumbra causes the ischemic cells to release excitatory proteins which migrate into surrounding tissues triggering a hyper metabolic response that leads to cell death beyond the infarction zone and the ischemic penumbra. This hyper metabolic response triggers inflammation, edema, local and global pyrexia, cerebral hypertension, apoptosis, and an increase in intra-cranial pressure causing a cascade of cell injury and death. This cascade of cell injury and death is referred to as secondary ischemic injury in the literature. Nowhere in the art is a mechanism described to that can effectively prevent or limit the migration of excitatory proteins from ischemic tissue, to surrounding normal tissue in the brain.
There is a growing body of research that shows that hypothermia is neuroprotective, however, the exact mechanisms are not fully understood. Schwab et al recently demonstrated that inducing systemic hypothermia following severe ischemic stroke provides a significant improvement in clinical outcome. Schwab treated 25 patients suffering from hemispheric stroke as a result of infarction of the middle cerebral artery with systemic hypothermia at 33 degrees centigrade for 48 to 72 hours. All patients were under full anesthesia during the period of hypothermia. The survival rate, and the clinical outcome of the survivors was significantly better than would otherwise have been expected. Schwab also demonstrated that critical elevations in intra-cranial pressure could be effectively reduced by systemic hypothermia following ischemic stroke.
However, there was a significant complication rate, unrelated to the stroke, but due to the depth and duration of systemic hypothermia Also, it took 3.5 to 6.2 hours for the body core temperature to reach the target therapeutic temperature of 33 degrees centigrade, and it took an average of 18 hours for the body temperature to return to normal after systemic cooling was withdrawn. All of the patients that died in this study did so as a result of a terminal rise in intra-cranial pressure during the rewarming period. Schwab notes, “Rewarming has to be considered the critical phase of hypothermia therapy”.
Kammersgaard et al recently reported treating 17 patients suffering ischemic stroke with systemic hypothermia for 6 hours upon admission of the patient to the hospital. Unlike in the Schwab study, there was no body core temperature target; the patient was cooled by “forced cold air method” for 6 hours and the core body temperature was monitored. At six hours the average core body temperature was 36.5 degrees centigrade. Kammersgaard reported that the hypothermia therapy was well tolerated by the patients, and did not require anesthesia. Also, there were no complications encountered due to the hypothermia therapy. However, the clinical outcome of patients studied showed no statically significant improvement in outcome over the historical controls used in this study.
Systemic hypothermia has historically been accomplished by immersion of the patient's body in a cool bath. Today there are several commercial systemic hypothermia systems available. They consist of blankets or pads where cooled water is circulated through channels in the walls of the blanket or pad, and the patient's body is maintained in intimate contact. Medivan Corp. manufactures an example of a modern hypothermia system under the trade name Arctic Sun Cooling System.
Systemic hypothermia has been demonstrated to be effective in improving the outcome of ischemic stroke, however, there are several drawbacks to this approach: 1) It takes several hours to lower a patient's body to therapeutic temperatures. This delay in achieving therapeutic temperatures allows for the progression of irreversible injury to the brain. 2) The practical therapeutic hypothermic temperature and duration is limited by the ability of the patient to tolerate, or survive the therapy. 3) The side effects of systemic hypothermia are frequent and can be life threatening, especially in frail patients. Side effects include shivering, cardiac arrhythmia and arrest, pneumonia, infections, and coagulation disorders. 4) The target of hypothermia therapy is the zone around the cerebral infarction, therefore inducing hypothermia systemically places the patient at undue risk. 5) During the “critical phase” (rewarming period) of hypothermia treatment, there is no effective way to manage a sudden and critical increase in intra-cranial pressure, since re-cooling the body to reverse the increase in intra-cranial pressure takes several hours. 6) Brain tissue in a zone of infarction, and in the transitional zone surrounding the infarction have substantially reduced blood perfusion rates, and brain tissues in a zone of infarction, and in the transitional zone surrounding the infarction are in a hyper-metabolic state, therefore heat generated by the hyper-metabolic processes inside the zone of infarction, and inside the transitional zone cannot be effectively dissipated by blood perfusion. This results in a temperature differential between the infarcted and transitional zone, and the surrounding normal tissue, where tissues in the infarcted and transitional zone are at a higher temperature than the surrounding normal tissue. Systemic hypothermia cools a zone of infarction and surrounding transitional zone from without, and therefore cannot eliminate this temperature differential.
There are several examples in the art where catheters are constructed with a cooling means which is placed into the carotid artery to cool the blood entering the head. This offers an advantage over systemic hypothermia, since it provides a means to cool the head to lower temperatures than the rest of the body, but it still results in systemic hypothermia. Also, since the scientific evidence suggests that hypothermia must be maintained for extended periods of time, there is a great risk that clots will form on the catheters and migrate into the brain leading to further episodes of stroke. The mechanism of cooling a zone of infarction in the brain, or the surrounding transitional zone with this approach is the same as with systemic hypothermia, and does not overcome the significant limitations as described above.
There are numerous examples of interstitial cooling probes in the art. Nowhere in the art is it suggested that interstitial cooling probes may be used to treat stroke, and nowhere in the art is there an example of a cooling probe that may be practically fixated to the head and left indwelling in the brain for the extended periods of time required for effective hypothermia treatment of stroke.
SUMMARY
Therefore, it is an object of this invention to provide a method and apparatus for treating stroke. Another object of this invention is to provide a method
Chapin, Esq. Barry W.
Chappin & Huang, L.L.C.
Gibson Roy D.
MedCool, Inc.
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