Investigation of Corticosteroid Versus Placebo Injection in Patients With Syndesmotic Ligament Injury or High Ankle Sprain
Status: | Terminated |
---|---|
Conditions: | Hospital, Orthopedic |
Therapuetic Areas: | Orthopedics / Podiatry, Other |
Healthy: | No |
Age Range: | 16 - Any |
Updated: | 9/27/2018 |
Start Date: | April 2016 |
End Date: | September 21, 2018 |
Single-site, Double Blinded, Randomized Investigation of Corticosteroid Versus Placebo Injection Under Ultrasound Guidance in Patients With Syndesmotic Ligament Injury or High Ankle Sprain
This study evaluates the use of corticosteroids acutely as an adjuvant treatment of the high
ankle sprain. Subjects will receive either a corticosteroid or a local anesthetic injection.
ankle sprain. Subjects will receive either a corticosteroid or a local anesthetic injection.
The term "high ankle sprain" refers to injury to the syndesmotic ligaments of the ankle. It
has become a much more common injury comprising up to 24.6% of all ankle sprains , with an
incidence of 2.4 per 1000 athlete exposures. These can present a significant therapeutic
challenge for the sports physician and typically result in a prolonged morbidity and delayed
return to activity. The literature shows a lack of information for definitive care of these
athletes. Typical recovery for the high ankle sprain is almost twice as long as the more
common lateral ankle inversion sprain with a mean time to return to play of 45 days. There is
also a higher incidence of residual chronic pain comparing high ankle sprains to an isolated
lateral ankle sprain. The current standard for treatment of this injury has been to depend on
symptomatic treatment with an initial phase of rest and protected splinting. This is followed
by the use of NSAID's with a graduated rehabilitation program to reduce swelling, improve
range of motion, and regain strength and proprioception of the ankle. This is followed by
protective taping or bracing and return to activities as tolerated. Inflammation is one of
the body's first reactions to injury. Release of damaged cells and tissue debris occurs upon
injury. These expelled particles act as antigens to stimulate a nonspecific immune response
and to cause the proliferation of leukocytes. Local blood flow increases to transport the
polymorphonuclear leukocytes, macrophages, and plasma proteins to the injured area. A
redistribution of arteriolar flow produces stasis and hypoxia at the injury site. The
resulting infiltration of tissues by the leukocytes, plasma proteins, and fluid causes the
redness, swelling, and pain that are characteristic of inflammation. Initially, the
inflammatory reaction serves several important purposes. The influx of leukocytes facilitates
the process of phagocytosis and the removal of damaged cells and other particulate matter.
Pain and tenderness remind the patient to protect the injured area; however, the inflammatory
reaction eventually becomes counterproductive. The mechanism of corticosteroid action
includes a reduction of the inflammatory reaction by limiting the capillary dilatation and
permeability of the vascular structures. These compounds restrict the accumulation of
polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins.
They also inhibit the release of destructive enzymes that attack the injury debris and
destroy normal tissue indiscriminately. Additionally, new research suggests that
corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby
reducing the formation of prostaglandins, which contribute to the inflammatory process. There
are no previous prospective, randomized studies that look at utilization of corticosteroids
in treatment of the high ankle sprain. Only anecdotal information is available in simple case
reports for treatment. There was one study looking at treatment with platelet rich plasma
injection which demonstrated shorter return to play times and less long term residual pain.
has become a much more common injury comprising up to 24.6% of all ankle sprains , with an
incidence of 2.4 per 1000 athlete exposures. These can present a significant therapeutic
challenge for the sports physician and typically result in a prolonged morbidity and delayed
return to activity. The literature shows a lack of information for definitive care of these
athletes. Typical recovery for the high ankle sprain is almost twice as long as the more
common lateral ankle inversion sprain with a mean time to return to play of 45 days. There is
also a higher incidence of residual chronic pain comparing high ankle sprains to an isolated
lateral ankle sprain. The current standard for treatment of this injury has been to depend on
symptomatic treatment with an initial phase of rest and protected splinting. This is followed
by the use of NSAID's with a graduated rehabilitation program to reduce swelling, improve
range of motion, and regain strength and proprioception of the ankle. This is followed by
protective taping or bracing and return to activities as tolerated. Inflammation is one of
the body's first reactions to injury. Release of damaged cells and tissue debris occurs upon
injury. These expelled particles act as antigens to stimulate a nonspecific immune response
and to cause the proliferation of leukocytes. Local blood flow increases to transport the
polymorphonuclear leukocytes, macrophages, and plasma proteins to the injured area. A
redistribution of arteriolar flow produces stasis and hypoxia at the injury site. The
resulting infiltration of tissues by the leukocytes, plasma proteins, and fluid causes the
redness, swelling, and pain that are characteristic of inflammation. Initially, the
inflammatory reaction serves several important purposes. The influx of leukocytes facilitates
the process of phagocytosis and the removal of damaged cells and other particulate matter.
Pain and tenderness remind the patient to protect the injured area; however, the inflammatory
reaction eventually becomes counterproductive. The mechanism of corticosteroid action
includes a reduction of the inflammatory reaction by limiting the capillary dilatation and
permeability of the vascular structures. These compounds restrict the accumulation of
polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins.
They also inhibit the release of destructive enzymes that attack the injury debris and
destroy normal tissue indiscriminately. Additionally, new research suggests that
corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby
reducing the formation of prostaglandins, which contribute to the inflammatory process. There
are no previous prospective, randomized studies that look at utilization of corticosteroids
in treatment of the high ankle sprain. Only anecdotal information is available in simple case
reports for treatment. There was one study looking at treatment with platelet rich plasma
injection which demonstrated shorter return to play times and less long term residual pain.
Inclusion Criteria:
- Age 16 years or older
- Musculoskeletal ultrasound performed which demonstrates injury pattern consistent with
high ankle sprain.
- Must sign the informed consent form and agree to meet the needs of the study
- Clinically and ultra sound confirmed and isolated syndesmotic ligament injury or high
ankle sprain without associated fracture
- Injury occurred within the previous 7 days
Exclusion Criteria:
- Surgical intervention required to stabilize the ankle
- Unable to read and understand the consent form
- Unable to meet the needs of the follow-up examinations
- Allergic to the betamethasone
- Current fungal infection
- Pregnancy or currently breast feeding
We found this trial at
1
site
2301 25th Street South
Fargo, North Dakota 58103
Fargo, North Dakota 58103
Phone: 701-417-6292
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