A fiber optic probe for measurement of an autonomic dysreflexia event on SCI patients

ABSTRACT Autonomic Dysreflexia (AD) is an inappropriate response of the sympathetic nervous system that often occurs in individuals with spinal cord injury (SCI ) at or above the sixth thoracic vertebrae (T6) level when a noxius stimulus is applied below the level of injury. An AD event can be put into motion by something as simple as an ingrown toenail or a full bladder, with symptoms such as headache, elevated blood pressure, reduced heart rate, decreases in blood flow below the level of injury, and in extreme cases, stroke. We have developed a quantitative method of measuring skin oxygen levels during AD using a fiber optics based probe. Two such probes were located above and below the injury level (on the patient forearm and thigh respectively) and were connected to a dual channel spectrophotometer. Oxygen saturation was calculated using the reflectance spectra and an algorithm based on melanin and hemoglobin absorption. We found that during an AD event, the amount of oxygen in the skin below the injury level drops by as much as 40%, while above the injury level skin oxygenation remains constant. Additionally, we observed elevated persperation levels below the injury level. We hypothesize that the combination of AD-related ischemia with pressure related ischemia and increased perspiration places individuals with injury level at T6 or above at significant risk for developing a pressure sore below the injury site. Keywords: Autonomic Dysreflexia, oxygenation, fiber optics probe 1. INTRODUCTION Autonomic Dysreflexia (AD) is an inappropriate response of the sympathetic nervous system in individuals with spinal cord injuries at or above the sixth thoracic vertebrae. Some common symptoms of AD are excessive sweating, pilomotor erection, headache, hypertension, blurring of vision and more rarely convulsion, loss of consciousness, cerebral hemorrhage, and death [1]. An AD event is often induced by a noxious stimulus below the level of injury, such as a full bladder, an ingrown nail, or pressure sore. A noxious stimulus below T6 can cause a sympathetic response resulting in vasoconstriction, headaches, as well as pallor and chills below the injury level. Vasoconstriction produces a rise in blood pressure and consequent reflex bradycardia through the baror eceptor reflex [1,2]. An AD episode can be stopped quickly removing the painful stimulus that triggered it, however if no action is taken, the individual will experience elevating levels of discomfort. AD has been the focus of many studies for its cardiovascular effects however no studies to date have evaluated its effect on pressure sore formation. We believe that the circulatory dysfunction caused by AD (hypoxia and ischemia) can negatively impact the health of the skin contributing to the formation of skin ulcers. Stover et al. [3,4] have shown that AD is a possible cause of skin restructuring. Studying skin thickening in SCI patients with and without AD symptoms he showed that 80% of individuals with severe AD (grade 3) developed skin thickening compared to the 22% of patients without AD symptoms. The reduction of oxygenated flow coming from the femoral artery characteristic of autonomic dysreflexia is likely to exacerbate the ischemic hypoxia due to pressure. AD also causes increased perspiration that has been linked to skin ulcer formation [5]. The goal of this study was to characterize the events leading up to and during an episode of Autonomic Dysreflexia in an individual with spinal cord injury. Specifically, we were interested in quantifying blood flow rate, skin oxygenation levels, amount of skin perspiration, and other autonomically related events. We hypothesize that during AD, the blood flow rate below the injury level will drop significantly, translating into meaningful decreases in