Dr. Jeremy Rawlinson and Dr. Norm G. Ducharme
Dr. Jeremy Rawlinson
Dr. Norm G. Ducharme
The upper airway of horses is subjected to large stresses (pressure and airflow turbulence), which may cause the larynx (voice box) and the nasopharynx (area in front of voice box) to collapse during exercise. These two main upper airway areas are the subject to collapse in horses during exercise because they are not supported by bone and require muscle stabilization. Some form of nasopharyngeal collapse is estimated to affect 10 to 20% of racehorses (Standardbred and Thoroughbred) and laryngeal collapse (roaring or paralyzed flapper) reportedly affects 3-to-8% of Thoroughbreds. Laryngeal collapse is not limited to racehorses but is also similarly prevalent in Warm Bloods and is seen in up to 42% of draft horses. Recently we have been able to demonstrate that collapse in the voice box changes the wall pressure in the nasopharynx linking these two conditions- treatment of one should take into considerations treatment of the other. The purpose of this study is to develop more integrated and effective treatments for these two conditions targeting a restoration of normal airway size and function with fewer complications. Indeed, complications after surgery can be quite significant and include feed aspiration into the windpipe and coughing. Use of a combined approach will avoid later duplication in terms of animal use and funding.
For years, we have been able to measure the speed of airflow at the nose and airway pressures in one area of the windpipe of horses at exercise and then test the effect various treatments have on those parameters in horses exercising on a high-speed treadmill. This has led to incremental increases in treatment success for horses with “throat problems.” Success is defined here as a percentage of horses returning to race competition and a level of earnings (purse money) equivalent to pre-disease levels - a very different measure from restoring normal airway patency. Furthermore, some treatments are initially successful but fail after a few months, presumably because of cyclic loading on the repair or the wall in the adjacent part of the airway. This indicates that knowing windpipe pressure or airflow speed at the nose without identifying airflow patterns (i.e. “eddy” currents) and the wall pressure along every aspect of the upper airways is insufficient. In addition, the minimum degree of voice box opening required to restore “normal” airway function has not been determined.
Recently, collaboration with a Biological and Environmental Engineering program headed by Professor Datta has generated a validated computer model that has provided important insight into how air flows through the horse’s upper airway. This has highlighted regions in the airway of high wall pressure and turbulence in horses at exercise and the effects when an area like the voice box is restricted. This has opened up exciting possibilities for new treatments. For example, we knew that laryngeal hemiplegia restricts the diameter of the voice box, but we now know that it also affects the increase wall pressure in the nasopharynx at specific locations. This information will allow areas susceptible to collapse because of this altered wall pressure to be reinforced. Beyond new treatment approaches, it became evident that equine investigators and surgeons must now redefine successful treatment to include minimizing wall pressures that lead to airway collapse while restoring the normal airway pressures and airflow speed. The contribution of all collapsible sections of the upper airway to the stability or instability must now be considered. The biomechanical consequences and respective dysfunction of palate displacement and roaring are interrelated and must be considered in conjunction with functional and biomechanical data to expose potential new treatments. In this proposal, we plan parallel, interlinked studies to increase our understanding of factors contributing to upper airway stability (both palate and voice box).
We now know the magnitude of forces present on the collapsible walls of the upper airway (voice box and nasopharynx) but we do not know the normal structural capacity of those walls (i.e. compliance), what forces act on the structures that stabilize the walls, and how the voice box and nasopharynx interrelationship provides strength or weakness to the walls. To develop more effective treatments, we need to understand the stiffness these walls require to resist collapse and understand more the mechanisms that stabilize the overall upper airways (palate and voice box) at exercise. The study proposed will acquire some information through live animal studies and some through biomedical testing on cadavers followed by computer modeling. The larynx will be the first focus to investigate the structural properties needed to resist collapsing forces. In this area, we know the dorsal cricoarytenoid (DCA) muscle resists collapse where it attaches to the muscular process on the flappers (i.e. arytenoid cartilages). This is akin to opening a door in a wind tunnel. We know how much force is on the wall due to the wind, but we do not know how much force is needed on the door handle to open it, the amount of force needed to open the door at different degrees, nor the actual strength of the door (e.g. wood versus fiberglass versus metal). Regarding the voice box, we do not know the force acting on the muscular process (i.e. door handle) at various degrees of opening; and we do not know the biomechanical properties of the arytenoid cartilage (flapper). MRI images of the voice box with the flapper opened to different degrees of abduction will enable us to construct a three-dimensional model of the flapper’s relationship with that joint and other laryngeal cartilages. Biomechanical analysis to determine the material properties of the cartilage will then be performed using fresh specimens from horses euthanized for reasons unrelated to airway disease. Computer modeling will be performed next to determine the forces applied to the laryngeal cartilage, the amount of deformation or bending, and the specific forces acting on the muscular process (i.e. door handle). Potentially, this would help in the design of stabilizing implants that would be biocompatible and not cut through the cartilage, a problem that has plagued the common tie-back surgery treatment for roaring.
Parallel studies aim to increase knowledge about the factors and mechanisms that stabilize the nasopharynx by inducing collapse (palate displacement) at exercise utilizing a new physiological finding that focuses on the hypoglossal nerve and increasing stiffness of the palate. In a recent breakthrough, soft palate displacement in horses at exercise was reproduced by a specifically located block of the hypoglossal nerve. The anatomical and physiological function of the hypoglossal nerve in humans with snoring and sleep apnea bears much resemblance to palate displacement in horses. The muscle(s) responsible for nasopharyngeal collapse will be identified by electromyelography (EMG) of horses at exercise prior to and after hypoglossal block. This will provide the lines of action of the muscle forces for computer modeling. The effects of increasing stiffness of the palate upon collapsibility and downstream effects to other areas of the airway will be evaluated. In addition, the resulting change in position of the voice box and hyoid apparatus (bones that suspend the voice box) after the block is made will be characterized by radiography and CT scan. This biomechanical and fluid dynamical modeling information will then be entered into our computer model to understand how these mechanisms provide stability.
In summary the proposed studies will answer the following questions. What are the material properties of the arytenoid cartilage, including the muscular process (door handle), and what are the forces acting on the muscular process? What would be the best biomechanical implant on the muscular process to neutralize these forces? How does a horse’s voice box position influence palatal instability? Does the voice box position cause a change in soft palate stiffness and is the palate stiffness irrelevant to airway stability?