New Findings About Trigger Finger and How to Treat ItLittle by little, researchers are coming to understand what's behind the problem of trigger finger. Trigger finger (and trigger thumb) are conditions affecting the movement of the tendons as they bend the fingers or thumb toward the palm of the hand. This movement is called flexion. The tendons that move the fingers are held in place on the bones by a series of ligaments called pulleys. These ligaments form an arch on the surface of the bone that creates a sort of tunnel for the tendon to follow along the bone. To keep the tendons moving smoothly under the ligaments, the tendons are wrapped in a slippery coating called tenosynovium. The tenosynovium reduces the friction and allows the flexor tendons to glide through the tunnel formed by the pulleys as the hand is used to grasp objects. When the flexor tendon gets pinched or stuck under the A1 pulley, a trigger digit develops.
A series of studies have been done examining this pulley mechanism called the A1 pulley under high-powered microscope called light microscopy. So far, the scientists have found that normal pulleys have three layers: an outer, middle, and inner layer. Each layer is made up of different types of cells and a different mixture of those cells. For example, the outer layer is formed by loose connective tissue with a good blood supply. The middle layer contains dense connective tissue. And the inner layer is the gliding layer made up of fibrous chondrocytes (cartilage cells).
In this study, hand specialists take a closer look at the histology of these three layers with four things in mind. Histology refers to the cellular make up of the tissues. The four areas of study focused on 1) histology of normal A1 pulleys, 2) histology of the abnormal A1 pulleys seen in trigger fingers, 3) creating a way to classify trigger finger based on histology, and 4) looking at how the histology compares with patient's symptoms and clinical presentation.
In order to examine normal pulleys from human fingers, the authors relied upon human cadavers (hands preserved after death for study). They were able to obtain 55 normal A1 pulleys from adult fingers this way. The abnormal pulleys came from 80 live patients who had surgery to release a total of 104 trigger fingers. The pathologic pulleys were removed at the time of surgery and sent to the lab for close inspection and analysis.
Any time a comparative study like this is done, the researchers must also take a look at the patients to see if there are any major differences in the two groups or factors that might be linked with the problem. In this case, background data on the cadavers was not available. But the patient profile showed an even mix between men and women ranging in ages from as young as 18 up to nearly 80 years old. Two-thirds of the group had been involved in light-to-heavy manual labor. At least half of the group had some other problem affecting the hand such as diabetes, carpal tunnel syndrome, or Dupuytren's disease.
Dupuytren's first shows up as a thick nodule (knob) or a short cord in the palm of the hand, just below the ring finger. More nodules form, and the tissues thicken and shorten until the finger cannot be fully straightened. Dupuytren's contracture usually affects only the ring and little finger. The contracture spreads to the joints of the finger, which can become permanently immobilized (unable to move).
For each patient with a trigger finger, before surgery, the severity of symptoms was labeled as Stage I, II, or III. Stage I patients had tenderness and pain at the surface of the A1 pulley along the palm side of the hand. No nodules or triggering were present. Patients considered in Stage II had tenderness, swelling, and/or tendon nodules that got caught under the pulley when the finger was actively flexed. And Stage III was a more severe form of stage II with more catching and possibly a flexion contracture (finger stuck in a bent position).
The authors described their findings for each of the three normal layers of A1 pulleys examined. Most notable is the fact that the first two layers form a fibrocartilaginous portion of the lining or sheath around the tendon right where the pulleys are located. This helps them move, slide, and glide more smoothly. Very few (if any) blood vessels were present in those two layers. The outermost layer on the palm side of the pulley had very tiny capillaries to bring blood supply to the area. This layer is right next to the tendon sheath and helps bring blood to the area.
Light microscopy made it possible to look at the tissues with increasing magnification. The borders between each layer were visible, thickness of the layers could be measured, and the surfaces were easy to see, too. Pulleys from the trigger fingers showed various amounts of damage and destruction of the fibrocartilaginous layers of the pulley. Sometimes it was so thin, it disappeared. Tiny cracks called fissures were common along with scar tissue and increased blood supply to the damaged area. Despite all of those changes, there was no sign of inflammation anywhere in the area.
Using the histologic findings, a three-grade classification model was proposed. Grade 1 included mild abnormalities. The fibrocartilaginous gliding surface was still fairly normal. There was no swelling, no cysts, no fissures, and no evidence of blood vessels forming in the area. Grade 2 had more moderate changes. The gliding surface was fissured and thinning. The middle layer did not appear to be getting thicker yet (from scar tissue) but the inner layer was replaced with fibrous (scar) tissue. And in Grade 3 (severe) lesions, the gliding surface was very thin with skips in the fibrocartilaginous layer and places where it was missing (destroyed) altogether.
In summary, this study takes a closer look at the A1 pulley mechanism associated with trigger finger. Other studies have focused on the flexor tendon instead. Histologic abnormalities of the pulley are described. Because of these findings, a greater appreciation for the role of A1 pulleys in trigger finger is reported. It appears that increased mechanical stress from repetitive use of the fingers results in abnormalities that can be graded 1 to 3 (mild to severe). As the condition gets worse, more and more of the gliding surface is destroyed and replaced by fibrosis (scar tissue) that has its own blood supply. As the pulley gets thicker and thicker, the tendon is less able to slide and glide underneath it.
The authors report that they have changed how they treat trigger finger as a result of their findings. Now they try steroid injection(s) before surgery. They plan to report on results of patients who have injection therapy for trigger fingers compared with those who do not. Placement of the injection may make a difference in outcomes if the pulleys are treated instead of the flexor tendons. Time will tell!
K. Drossos, MD, et al. Correlations Between Clinical Presentations of Adult Trigger Digits and Histologic Aspects of the A1 Pulley. In The Journal of Hand Surgery. October 2009. Vol. 34-A. No. 8. Pp. 1429-1435.
|*Disclaimer:* The information contained herein is compiled from a variety of sources. It may not be complete or timely. It does not cover all diseases, physical conditions, ailments or treatments. The information should NOT be used in place of visit with your healthcare provider, nor should you disregard the advice of your health care provider because of any information you read in this topic.|
|All content provided by eORTHOPOD® is a registered trademark of Medical Multimedia Group, L.L.C.. Content is the sole property of Medical Multimedia Group, LLC and used herein by permission.|