The Pathology of Shin Splints JANET KUES, PT' The purpose of this review is to critically evaluate experimental evidence describing the pathology associated with shin splints. Shin splints are defined as medial or posteromedial leg pain which is brought about by walking, running, or related activities and which decreases with rest. The evidence indicates that shin splints may be due to pathology of the posteromedial tibia1 cortex, the periosteum of the posteromedial tibia, or the crural fascia of the deep posterior compartment of the leg. Research is needed to determine if increased pressure in the deep posterior compartment of the leg or pathology of the muscles, tendons, or interosseous membrane of the leg are associated with shin splints. "Shin splints" is a term commonly used to describe exercise-induced leg pain. Several areas of the leg have been cited as the focus of this pain. Among these are the posteromedial aspect of the tibia (2, 3,7,8,12,19), the anterolateral aspect of the tibia (3, 19), and the medial border of the tibia (15). Although different areas of the leg have been cited as the focus of pain, there is agreement about the nature of the symptoms associated with shin splints. The leg pain develops gradually during walking, running, or jumping (2, 4, 7-9,11-13,15,19). The pain initially occurs toward the end of physical activity and decreases with rest. If the activity is continued, the intensity and duration of the pain increases and pain may even be present at rest. Most individuals will have tenderness to palpation and some may have visi- ble swelling at the painful site (2, 4, 11, 13,15, 19). Symptoms associated with shin splints and the types of activity which cause the pain are consistently described in the literature. There is, however, considerable disagreement concerning the pathological basis of the pain. Authors have suggested that shin splints are due to stress fractures of the tibia (4, 8,16), myositis (3, 19- 21), periostitis (2, 7,12,17), increased pressure in a muscular compartment of the leg (1,IS), ' Staff physical therapist. Department of Physical Therapy. Mediil College of Virginia Hospital. 401 N. 12th St.. Richmond. VA 23298. Ms Kues is currently a graduate student. Department of Physical Therapy. School of Allied Health Professions. Medical College of Virginia. V~rgln~a Commonwealth University. P.O. Box 224. MCV Station. R~chrnond. VA 23298-0224. 01 90-601 1/90/1203-0115$02.00/0 THE JOURNAL OF ORTHOPAED~C AND SPORTS PHYSICAL THERAPY Copyright (O 1990 by The Orthopaedii and Sports Physical Therapy Sections of the American Physical Therapy Association JOSPT 12:3 September 1990 PATHOLOGY OF irritation of the interosseous membrane (1 4), or tendonitis (1 8-20). The purpose of this review is to critically evaluate experimental evidence describing the pa- thology associatedwith shin splints. In this review, shin splints are defined as medialor posteromedial leg pain which is brought about by walking, run- ning, or related activities and which decreases with rest. Increased Pressure in the Deep Posterior Compartment of the Leg as a Possible Cause of Shin Splints Puranen (15) examined the deep posterior com- partment of the legs of eight male and three female athletes who reported exercise-induced pain along the medial border of their tibias. The mean age of the athletes was 23 years (SD = 7.2 years). Six of the athletes had right leg pain, four had left leg pain, and one had bilateral leg pain. The athletes had participated in various running activities (i.e., jogging, sprinting, pole vaulting, long jumping, and hurdling) and had experienced pain for several months. Puranen stated that "con- servative treatment" had failed to alleviate their symptoms. He did not define "conservative treat- ment." Most of the athletes in Puranen's study re- ported that they experienced pain only during exercise, although a few reported having pain during walking and while at rest. All of the athletes were tender to palpation along the medial border of their tibias with no signs of vascular or neuro- logical changes. In order to eliminate stress fractures as an etiology, Puranen took radiographs and bone scans of each subject's painful leg. Two subjects SHIN SPLINTS 115 Journal of Orthopaedic & Sports Physical Therapy® Downloaded from www.jospt.org at on April 2, 2023. For personal use only. No other uses without permission. Copyright © 1990 Journal of Orthopaedic & Sports Physical Therapy®. All rights reserved.
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Literature Review: The Pathology of Shin SplintsThe Pathology of Shin Splints JANET KUES, PT'
The purpose of this review is to critically evaluate experimental evidence describing the pathology associated with shin splints. Shin splints are defined as medial or posteromedial leg pain which is brought about by walking, running, or related activities and which decreases with rest. The evidence indicates that shin splints may be due to pathology of the posteromedial tibia1 cortex, the periosteum of the posteromedial tibia, or the crural fascia of the deep posterior compartment of the leg. Research is needed to determine if increased pressure in the deep posterior compartment of the leg or pathology of the muscles, tendons, or interosseous membrane of the leg are associated with shin splints.
"Shin splints" is a term commonly used to describe exercise-induced leg pain. Several areas of the leg have been cited as the focus of this pain. Among these are the posteromedial aspect of the tibia (2, 3, 7, 8, 12, 19), the anterolateral aspect of the tibia (3, 19), and the medial border of the tibia (15). Although different areas of the leg have been cited as the focus of pain, there is agreement about the nature of the symptoms associated with shin splints. The leg pain develops gradually during walking, running, or jumping (2, 4, 7-9, 11-13, 15, 19). The pain initially occurs toward the end of physical activity and decreases with rest. If the activity is continued, the intensity and duration of the pain increases and pain may even be present at rest. Most individuals will have tenderness to palpation and some may have visi- ble swelling at the painful site (2, 4, 11, 13, 15, 19).
Symptoms associated with shin splints and the types of activity which cause the pain are consistently described in the literature. There is, however, considerable disagreement concerning the pathological basis of the pain. Authors have suggested that shin splints are due to stress fractures of the tibia (4, 8, 16), myositis (3, 19- 21), periostitis (2, 7, 12, 17), increased pressure in a muscular compartment of the leg (1, IS),
' Staff physical therapist. Department of Physical Therapy. Mediil College of Virginia Hospital. 401 N. 12th St.. Richmond. VA 23298. Ms Kues is currently a graduate student. Department of Physical Therapy. School of Allied Health Professions. Medical College of Virginia. V~rgln~a Commonwealth University. P.O. Box 224. MCV Station. R~chrnond. VA 23298-0224.
01 90-601 1/90/1203-0115$02.00/0 THE JOURNAL OF ORTHOPAED~C AND SPORTS PHYSICAL THERAPY Copyright (O 1990 by The Orthopaedii and Sports Physical Therapy Sections of the American Physical Therapy Association
JOSPT 12:3 September 1990 PATHOLOGY OF
irritation of the interosseous membrane (1 4), or tendonitis (1 8-20).
The purpose of this review is to critically evaluate experimental evidence describing the pa- thology associated with shin splints. In this review, shin splints are defined as medial or posteromedial leg pain which is brought about by walking, run- ning, or related activities and which decreases with rest.
Increased Pressure in the Deep Posterior Compartment of the Leg as a Possible Cause of Shin Splints
Puranen (15) examined the deep posterior com- partment of the legs of eight male and three female athletes who reported exercise-induced pain along the medial border of their tibias. The mean age of the athletes was 23 years (SD = 7.2 years). Six of the athletes had right leg pain, four had left leg pain, and one had bilateral leg pain. The athletes had participated in various running activities (i.e., jogging, sprinting, pole vaulting, long jumping, and hurdling) and had experienced pain for several months. Puranen stated that "con- servative treatment" had failed to alleviate their symptoms. He did not define "conservative treat- ment."
Most of the athletes in Puranen's study re- ported that they experienced pain only during exercise, although a few reported having pain during walking and while at rest. All of the athletes were tender to palpation along the medial border of their tibias with no signs of vascular or neuro- logical changes.
In order to eliminate stress fractures as an etiology, Puranen took radiographs and bone scans of each subject's painful leg. Two subjects
SHIN SPLINTS 115
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had periosteal thickenings along the medial border of their tibias. One subject had a significant in- crease in radiotracer uptake along the medial border of his tibia. Because fractures could not be seen on the radiographs of these three sub- jects, Puranen concluded that the subjects did not have stress fractures of their tibias. He also concluded that the subjects' pain was not of a bony origin. These conclusions may have been inappropriate. Periosteal thickening on radio- graphs and increased radiotracer uptake on bone scans are often the initial signs of a stress fracture (16, 21). The leg pain of the three subjects may have been due to the tibia's response to stress.
Puranen incised the crural fascia of the deep posterior compartment of the involved leg in all 11 subjects. The incision was made near the insertion of the crural fascia on the medial border of the tibia. Puranen stated that in all of the subjects the fascia was "tense" and "thickened." He did not state what criteria he used to determine that the fascia was "tense" or "thickened."
Puranen also visually inspected the muscles of the deep posterior compartment of each leg. According to Puranen, there appeared to be small areas of necrotic tissue in the flexor digitorum longus muscle of one subject. Although Puranen stated that a histological examination confirmed that the muscle tissue was necrotic, he did not report any of the details of this histological analy- sis.
The crural fascia of the deep posterior com- partment of the leg in all subjects was also ex- amined histologically. Puranen removed a small portion of the crural fascia near its site of insertion on the medial border of the tibia. In nine of the subjects he found signs of "chronic inflammatory infiltration." Puranen did not describe what these signs were.
Following his exploration of the deep poste- rior compartment of each subject's leg, Puranen left the incision in the crural fascia open and sutured the skin. After 4 weeks of rest, all of the athletes were able to return to training with com- plete relief of their symptoms. Based on these results and on the findings (i.e., tense and thick- ened fascia with inflammatory infiltration), Pura- nen concluded that the pain was due to the build up of excessive pressure in the deep posterior compartments during exercise. Although this ex- planation may be plausible, an alternate hypoth- esis is that the 4 weeks of rest led to relief of symptoms because the source of pain was due to bone or muscle injury. Without measuring pres- sure, it seems highly speculative to conclude that the athletes' pain was due to increased pressure in the deep posterior compartments.
Puranen's findings suggest that pathology of the crural fascia of the deep posterior compart- ment may be associated with shin splints. Pura-
nen did not provide evidence to support his hy- pothesis that an increase in pressure in the deep posterior compartment causes the pain of shin splints.
Mubarak et a/. (1 3) measured the pressure in the deep posterior compartment of the legs of 7 male and 5 female subjects who had a mean age of 24.6 years (SD = 8.7 years). The subjects complained of exercise-induced pain along the posteromedial aspects of their tibias. Two of the subjects had bilateral leg pain and 10 had unilat- eral leg pain. Ten of the subjects were joggers, and one was a sprinter, and one a football player. Mubarak et a/. stated that the subjects' leg pain increased with weightbearing activities and de- creased with rest. Weightbearing activities were not defined.
Mubarak et a/. reported that each subject had tenderness over the distal one-third of their posteromedial tibias. There were no signs of mo- tor, sensory, or circulatory changes. Radiographs and bone scans were taken of the subjects' pain- ful legs. In 2 subjects, mild cortical hypertrophy over the medial tibias was seen. Two subjects also had mild diffuse areas of increased radiotra- cer uptake along the medial portion of their tibias.
Mubarak et a/. used a wick catheter con- nected to a pressure transducer to measure the pressure in the deep posterior compartment of the legs of the subjects. Pressure measurements were taken before, during, and after exercise. Each subject exercised on an isokinetic device. The foot on the involved side was attached to the device and the subject performed dorsiflexion and plantarflexion until he fatigued or until he felt medial tibia1 pain. Apparently, the isokinetic exer- cise did not cause leg pain in all of the subjects. Because Mubarak et a/. appeared to be testing the hypothesis that shin splints are due to in- creased pressure in a muscular compartment of the leg during exercise, it would seem necessary to have the subjects perform an exercise that would cause them leg pain.
The pressure measurements obtained from the deep posterior compartment of the legs of all 12 subjects, during each condition (i.e., before, during, and after exercise), were averaged and compared to average intracompartmental pres- sure values obtained from a group of control subjects. Details were not provided about the control subjects or about how the pressure values were obtained from these subjects.
Mubarak et a/. stated that the average pres- sure values obtained before, during, and after exercise for the subjects with leg pain were similar to the average pressure values obtained from the control subjects. They concluded that their sub- jects' leg pain was not due to increased pressure in the deep posterior compartments. However, if the subjects' individual pressure measurements
116 KUES JOSPT 12:3 September 1990
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are compared to the average control values, the conclusion may be different. Measurements ob- tained during exercise in three of the subjects were considerably greater than the average con- trol value. The subjects' pressures were 125,130, and 150 mm Hg versus 60 mm Hg for the control group.
According to D'Ambrosia et a/. (2), if pressure in a muscular compartment of the leg is greater than approximately 60 mm Hg, the fine intramus- cular arteries will be occluded. The pressure measurements in the legs of three subjects in Mubarak et a1.k study appear to have been at pathological levels during exercise. The leg pain these subjects experienced may have been due to ischemia.
The majority of the subjects in Mubarak et a1.k study appeared to have pressure measure- ments within normal limits. The authors, however, failed to report the reliability of their measure- ments. The exercise performed in this study was also not sufficient to provoke a painful episode in every subject. The results of this study, therefore, must be interpreted with caution.
Mubarak et al.'s (13) findings are similar to those of D'Ambrosia et a/. (2). D'Ambrosia et a/. found no increase in the pressure of the anterior or deep posterior compartments of the legs in 14 track and field athletes who reported exercise- induced posteromedial leg pain. Five males and 9 females with a mean age of 19.6 years (SD = 1.4 years) were the subjects. All the subjects com- plained of unilateral exercise-induced pain along the posteromedial aspect of their tibias. The pain increased with exercise and decreased with rest. Bone scans were taken of each subject's leg and the authors reported that there were no signs of stress fractures of the tibia.
D'Ambrosia et a/. measured the pressures in the anterior and deep posterior compartments with a needle connected to a pressure transducer. The pressure in the anterior compartment of the leg was measured in all subjects. The pressure in the deep posterior compartment of three subjects' legs was measured. D'Ambrosia et a/. did not indicate why they only measured the pressure in the deep posterior compartments of three sub- jects. Because their subjects were complaining of posteromedial leg pain, it would have been more appropriate to measure the deep posterior com- partment pressure in all subjects. The pressure measurements were also obtained with the sub- jects at rest. The subjects, however, experienced their pain during exercise. Methodological issues and the failure of D'Ambrosia et a/. to report the reliability of their pressure measurements bring into question their results.
Summary of Pressure Studies
Exercise-induced increases in pressure in the deep posterior compartment have been hypothe-
sized as a cause of shin splints. An increase in pressure in the deep posterior compartment may cause pain due to ischemia. Studies, however, have failed to support this hypothesis.
Stress Fractures of the Tibia as a Possible Cause of Shin Splints
Devas (4) attributed exercise-induced pain along the posteromedial aspect of the tibia to stress fractures. Devas stated that out of a 'consider- able number" of patients he had seen for exer- cise-induced leg pain, 13 males and 3 females had radiological confirmation of stress fractures. The mean age of these patients was 18.1 years (SD = 5.4 years). Fifteen of these patients had unilateral leg pain. One patient had bilateral leg pain. The patients had participated in various run- ning sports and stated that they began to expe- rience pain on the medial side of their legs as they were completing running. The intensity and dura- tion of the pain was mild at first and, with contin- ued running, increased. The pain ultimately be- came so severe that running could not be contin- ued. Although the pain decreased or disappeared with rest, any running caused the pain to increase or return. The duration of the subjects' symptoms ranged from 3 weeks to 5 months.
Devas reported that all 16 patients had ten- derness along the medial border of their tibias and some had visible swelling in this area. In 6 pa- tients, a localized area of subperiosteal new bone formation along the posteromedial cortex of the tibia was visible on radiographs. In the other 10 patients, an incomplete fracture extending through the posteromedial cortex of the tibia was seen on radiographs.
Devas only noted radiological changes in 16 of the "considerable number" of patients he had seen for exercise-induced leg pain. He stated that all of his patients, with histories similar to those 16, had stress fractures of their tibias. He con- cluded that radiological changes were a late man- ifestation of stress fractures and that fractures would not be seen in all patients.
Devas hypothesized that a stress fracture results from a series of events. He believed that with the repeated stress of running the postero- medial cortex of the tibia "disrupts" causing pain but little or no changes on radiographs. Devas believed that if the athlete rested, tibia1 changes would not progress to the point where the changes were demonstrable on a radiograph. De- vas believed that if the athlete continued to run, the continued stress would lead to subperiosteal new bone formation which would be visible on radiographs. If the stress continued, a fracture of the cortex would be evident on radiographs.
Stress fractures may not be immediately vis- ible on radiographs (1 0); however, it seems spec-
JOSPT 12:3 September 1990 PATHOLOGY OF SHIN SPLINTS 117
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ulative to assume that all of the patients Devas saw (with exercise-induced leg pain and no radi- ological changes) had stress fractures of their tibias. The source of the leg pain may have been from nonosseous tissues.
The process of stress fracture formation de- scribed by Devas was purely hypothetical and appears to have been based solely on his clinical experience. Roub et a/. (1 6) offer some evidence to support Devas' hypothesis. Roub et a/. found that some individuals with exercise-induced leg pain have localized changes in the tibia1 cortex which never progress to the point of being visible on radiographs.
Roub et a/. examined 35 college athletes who had 1- to 12-week histories of exercise-induced medial leg pain. The athletes were members of track, gymnastics, or field hockey teams. Thirteen of the athletes had bilateral leg pain. According to Roub et a/., the severity of the symptoms were similar in all of the athletes. Details of the athletes' symptoms were not provided.
Roub et a/. obtained radiographs and radio- nuclide images (bone scans) from the involved leg($ of each athlete. Athletes who exhibited no radiological changes but who had increased radi- otracer uptake on the bone scan had a second radiograph taken 1 month later. A control group of 13 asymptomatic athletes from the same teams also underwent radionuclide imaging and had ra- diographs taken of both their legs.
All subjects in the control group and six of the athletes with leg pain had no signs of stress fractures on the initial radiographs or bone scans. Details describing these subjects were not pro- vided.
On the initial bone scans, seven male and seven female athletes (15 legs) with leg pain ex- hibited focal, longitudinal, fusiform areas of in- creased radiotracer uptake along the medial cor- tex of their tibias. These athletes had no signs of stress fractures on the initial radiographs. How- ever, on the radiographs taken 1 month later, there were signs of stress fractures. Roub et a/. did not state what these signs were.
Four male and 12 female athletes (24 legs) with leg pain had increased radiotracer uptake along the medial border of their tibias on the initial bone scans. The pattern of radiotracer uptake in these 16 athletes ranged from focal, longitudinal, fusiform shapes to focal, vague, nondescript shapes. These athletes exhibited no signs of stress fractures on the initial radiographs or the radiographs taken 1 month later.
Roub et a/., like Devas (4), believe that stress fractures form as a result of a series of events. They believe that the fractures begin microscopi- cally and may or may not progress to the point of being radiographically demonstrable.
Roub et a/. stated that a stress fracture r e p
resents a focal acceleration of the remodeling process in cortical bone. In the sequence of re- modeling, resorption of cortical bone is followed by replacement. Osteoclastic activity resorbs bone in areas of stress and the bone is replaced by osteoblastic activity. According to the theory, when there is excessive stress, resorption pro- ceeds rapidly and replacement is slow. During this stage of fracture formation patients complain of pain and bone scans may exhibit a slight, nondes- cript increase in radiotracer concentration in the area of increased stress. Radiological signs of a stress fracture will not be present. If the stress continues, resorption of cortical bone proceeds even more rapidly than replacement. During this stage of stress fracture formation, patients have pain and bone scans will exhibit a focal, intense, fusiform area of increased radiotracer concentra- tion in the area of increased stress. Radiographic signs of a stress fracture (i.e., vague lucent cor- tical areas, periosteal, and endosteal thickening) will be present or will appear within a few weeks. Because at this stage the rate of resorption of cortical bone is much greater than the rate of replacement, the cortex is weakened. Periosteal and endosteal bone formation serve to reinforce the weakened cortex. A fracture that is visible on radiographs occurs only when stress causes the resorption of the cortex to be accelerated beyond the capacity of the periosteal and endosteal re- actions to offer adequate support.
Roub et a/. feel…
The purpose of this review is to critically evaluate experimental evidence describing the pathology associated with shin splints. Shin splints are defined as medial or posteromedial leg pain which is brought about by walking, running, or related activities and which decreases with rest. The evidence indicates that shin splints may be due to pathology of the posteromedial tibia1 cortex, the periosteum of the posteromedial tibia, or the crural fascia of the deep posterior compartment of the leg. Research is needed to determine if increased pressure in the deep posterior compartment of the leg or pathology of the muscles, tendons, or interosseous membrane of the leg are associated with shin splints.
"Shin splints" is a term commonly used to describe exercise-induced leg pain. Several areas of the leg have been cited as the focus of this pain. Among these are the posteromedial aspect of the tibia (2, 3, 7, 8, 12, 19), the anterolateral aspect of the tibia (3, 19), and the medial border of the tibia (15). Although different areas of the leg have been cited as the focus of pain, there is agreement about the nature of the symptoms associated with shin splints. The leg pain develops gradually during walking, running, or jumping (2, 4, 7-9, 11-13, 15, 19). The pain initially occurs toward the end of physical activity and decreases with rest. If the activity is continued, the intensity and duration of the pain increases and pain may even be present at rest. Most individuals will have tenderness to palpation and some may have visi- ble swelling at the painful site (2, 4, 11, 13, 15, 19).
Symptoms associated with shin splints and the types of activity which cause the pain are consistently described in the literature. There is, however, considerable disagreement concerning the pathological basis of the pain. Authors have suggested that shin splints are due to stress fractures of the tibia (4, 8, 16), myositis (3, 19- 21), periostitis (2, 7, 12, 17), increased pressure in a muscular compartment of the leg (1, IS),
' Staff physical therapist. Department of Physical Therapy. Mediil College of Virginia Hospital. 401 N. 12th St.. Richmond. VA 23298. Ms Kues is currently a graduate student. Department of Physical Therapy. School of Allied Health Professions. Medical College of Virginia. V~rgln~a Commonwealth University. P.O. Box 224. MCV Station. R~chrnond. VA 23298-0224.
01 90-601 1/90/1203-0115$02.00/0 THE JOURNAL OF ORTHOPAED~C AND SPORTS PHYSICAL THERAPY Copyright (O 1990 by The Orthopaedii and Sports Physical Therapy Sections of the American Physical Therapy Association
JOSPT 12:3 September 1990 PATHOLOGY OF
irritation of the interosseous membrane (1 4), or tendonitis (1 8-20).
The purpose of this review is to critically evaluate experimental evidence describing the pa- thology associated with shin splints. In this review, shin splints are defined as medial or posteromedial leg pain which is brought about by walking, run- ning, or related activities and which decreases with rest.
Increased Pressure in the Deep Posterior Compartment of the Leg as a Possible Cause of Shin Splints
Puranen (15) examined the deep posterior com- partment of the legs of eight male and three female athletes who reported exercise-induced pain along the medial border of their tibias. The mean age of the athletes was 23 years (SD = 7.2 years). Six of the athletes had right leg pain, four had left leg pain, and one had bilateral leg pain. The athletes had participated in various running activities (i.e., jogging, sprinting, pole vaulting, long jumping, and hurdling) and had experienced pain for several months. Puranen stated that "con- servative treatment" had failed to alleviate their symptoms. He did not define "conservative treat- ment."
Most of the athletes in Puranen's study re- ported that they experienced pain only during exercise, although a few reported having pain during walking and while at rest. All of the athletes were tender to palpation along the medial border of their tibias with no signs of vascular or neuro- logical changes.
In order to eliminate stress fractures as an etiology, Puranen took radiographs and bone scans of each subject's painful leg. Two subjects
SHIN SPLINTS 115
. A ll
ri gh
ts r
es er
ve d.
had periosteal thickenings along the medial border of their tibias. One subject had a significant in- crease in radiotracer uptake along the medial border of his tibia. Because fractures could not be seen on the radiographs of these three sub- jects, Puranen concluded that the subjects did not have stress fractures of their tibias. He also concluded that the subjects' pain was not of a bony origin. These conclusions may have been inappropriate. Periosteal thickening on radio- graphs and increased radiotracer uptake on bone scans are often the initial signs of a stress fracture (16, 21). The leg pain of the three subjects may have been due to the tibia's response to stress.
Puranen incised the crural fascia of the deep posterior compartment of the involved leg in all 11 subjects. The incision was made near the insertion of the crural fascia on the medial border of the tibia. Puranen stated that in all of the subjects the fascia was "tense" and "thickened." He did not state what criteria he used to determine that the fascia was "tense" or "thickened."
Puranen also visually inspected the muscles of the deep posterior compartment of each leg. According to Puranen, there appeared to be small areas of necrotic tissue in the flexor digitorum longus muscle of one subject. Although Puranen stated that a histological examination confirmed that the muscle tissue was necrotic, he did not report any of the details of this histological analy- sis.
The crural fascia of the deep posterior com- partment of the leg in all subjects was also ex- amined histologically. Puranen removed a small portion of the crural fascia near its site of insertion on the medial border of the tibia. In nine of the subjects he found signs of "chronic inflammatory infiltration." Puranen did not describe what these signs were.
Following his exploration of the deep poste- rior compartment of each subject's leg, Puranen left the incision in the crural fascia open and sutured the skin. After 4 weeks of rest, all of the athletes were able to return to training with com- plete relief of their symptoms. Based on these results and on the findings (i.e., tense and thick- ened fascia with inflammatory infiltration), Pura- nen concluded that the pain was due to the build up of excessive pressure in the deep posterior compartments during exercise. Although this ex- planation may be plausible, an alternate hypoth- esis is that the 4 weeks of rest led to relief of symptoms because the source of pain was due to bone or muscle injury. Without measuring pres- sure, it seems highly speculative to conclude that the athletes' pain was due to increased pressure in the deep posterior compartments.
Puranen's findings suggest that pathology of the crural fascia of the deep posterior compart- ment may be associated with shin splints. Pura-
nen did not provide evidence to support his hy- pothesis that an increase in pressure in the deep posterior compartment causes the pain of shin splints.
Mubarak et a/. (1 3) measured the pressure in the deep posterior compartment of the legs of 7 male and 5 female subjects who had a mean age of 24.6 years (SD = 8.7 years). The subjects complained of exercise-induced pain along the posteromedial aspects of their tibias. Two of the subjects had bilateral leg pain and 10 had unilat- eral leg pain. Ten of the subjects were joggers, and one was a sprinter, and one a football player. Mubarak et a/. stated that the subjects' leg pain increased with weightbearing activities and de- creased with rest. Weightbearing activities were not defined.
Mubarak et a/. reported that each subject had tenderness over the distal one-third of their posteromedial tibias. There were no signs of mo- tor, sensory, or circulatory changes. Radiographs and bone scans were taken of the subjects' pain- ful legs. In 2 subjects, mild cortical hypertrophy over the medial tibias was seen. Two subjects also had mild diffuse areas of increased radiotra- cer uptake along the medial portion of their tibias.
Mubarak et a/. used a wick catheter con- nected to a pressure transducer to measure the pressure in the deep posterior compartment of the legs of the subjects. Pressure measurements were taken before, during, and after exercise. Each subject exercised on an isokinetic device. The foot on the involved side was attached to the device and the subject performed dorsiflexion and plantarflexion until he fatigued or until he felt medial tibia1 pain. Apparently, the isokinetic exer- cise did not cause leg pain in all of the subjects. Because Mubarak et a/. appeared to be testing the hypothesis that shin splints are due to in- creased pressure in a muscular compartment of the leg during exercise, it would seem necessary to have the subjects perform an exercise that would cause them leg pain.
The pressure measurements obtained from the deep posterior compartment of the legs of all 12 subjects, during each condition (i.e., before, during, and after exercise), were averaged and compared to average intracompartmental pres- sure values obtained from a group of control subjects. Details were not provided about the control subjects or about how the pressure values were obtained from these subjects.
Mubarak et a/. stated that the average pres- sure values obtained before, during, and after exercise for the subjects with leg pain were similar to the average pressure values obtained from the control subjects. They concluded that their sub- jects' leg pain was not due to increased pressure in the deep posterior compartments. However, if the subjects' individual pressure measurements
116 KUES JOSPT 12:3 September 1990
J ou
rn al
o f
O rt
ho pa
ed ic
. A ll
ri gh
ts r
es er
ve d.
are compared to the average control values, the conclusion may be different. Measurements ob- tained during exercise in three of the subjects were considerably greater than the average con- trol value. The subjects' pressures were 125,130, and 150 mm Hg versus 60 mm Hg for the control group.
According to D'Ambrosia et a/. (2), if pressure in a muscular compartment of the leg is greater than approximately 60 mm Hg, the fine intramus- cular arteries will be occluded. The pressure measurements in the legs of three subjects in Mubarak et a1.k study appear to have been at pathological levels during exercise. The leg pain these subjects experienced may have been due to ischemia.
The majority of the subjects in Mubarak et a1.k study appeared to have pressure measure- ments within normal limits. The authors, however, failed to report the reliability of their measure- ments. The exercise performed in this study was also not sufficient to provoke a painful episode in every subject. The results of this study, therefore, must be interpreted with caution.
Mubarak et al.'s (13) findings are similar to those of D'Ambrosia et a/. (2). D'Ambrosia et a/. found no increase in the pressure of the anterior or deep posterior compartments of the legs in 14 track and field athletes who reported exercise- induced posteromedial leg pain. Five males and 9 females with a mean age of 19.6 years (SD = 1.4 years) were the subjects. All the subjects com- plained of unilateral exercise-induced pain along the posteromedial aspect of their tibias. The pain increased with exercise and decreased with rest. Bone scans were taken of each subject's leg and the authors reported that there were no signs of stress fractures of the tibia.
D'Ambrosia et a/. measured the pressures in the anterior and deep posterior compartments with a needle connected to a pressure transducer. The pressure in the anterior compartment of the leg was measured in all subjects. The pressure in the deep posterior compartment of three subjects' legs was measured. D'Ambrosia et a/. did not indicate why they only measured the pressure in the deep posterior compartments of three sub- jects. Because their subjects were complaining of posteromedial leg pain, it would have been more appropriate to measure the deep posterior com- partment pressure in all subjects. The pressure measurements were also obtained with the sub- jects at rest. The subjects, however, experienced their pain during exercise. Methodological issues and the failure of D'Ambrosia et a/. to report the reliability of their pressure measurements bring into question their results.
Summary of Pressure Studies
Exercise-induced increases in pressure in the deep posterior compartment have been hypothe-
sized as a cause of shin splints. An increase in pressure in the deep posterior compartment may cause pain due to ischemia. Studies, however, have failed to support this hypothesis.
Stress Fractures of the Tibia as a Possible Cause of Shin Splints
Devas (4) attributed exercise-induced pain along the posteromedial aspect of the tibia to stress fractures. Devas stated that out of a 'consider- able number" of patients he had seen for exer- cise-induced leg pain, 13 males and 3 females had radiological confirmation of stress fractures. The mean age of these patients was 18.1 years (SD = 5.4 years). Fifteen of these patients had unilateral leg pain. One patient had bilateral leg pain. The patients had participated in various run- ning sports and stated that they began to expe- rience pain on the medial side of their legs as they were completing running. The intensity and dura- tion of the pain was mild at first and, with contin- ued running, increased. The pain ultimately be- came so severe that running could not be contin- ued. Although the pain decreased or disappeared with rest, any running caused the pain to increase or return. The duration of the subjects' symptoms ranged from 3 weeks to 5 months.
Devas reported that all 16 patients had ten- derness along the medial border of their tibias and some had visible swelling in this area. In 6 pa- tients, a localized area of subperiosteal new bone formation along the posteromedial cortex of the tibia was visible on radiographs. In the other 10 patients, an incomplete fracture extending through the posteromedial cortex of the tibia was seen on radiographs.
Devas only noted radiological changes in 16 of the "considerable number" of patients he had seen for exercise-induced leg pain. He stated that all of his patients, with histories similar to those 16, had stress fractures of their tibias. He con- cluded that radiological changes were a late man- ifestation of stress fractures and that fractures would not be seen in all patients.
Devas hypothesized that a stress fracture results from a series of events. He believed that with the repeated stress of running the postero- medial cortex of the tibia "disrupts" causing pain but little or no changes on radiographs. Devas believed that if the athlete rested, tibia1 changes would not progress to the point where the changes were demonstrable on a radiograph. De- vas believed that if the athlete continued to run, the continued stress would lead to subperiosteal new bone formation which would be visible on radiographs. If the stress continued, a fracture of the cortex would be evident on radiographs.
Stress fractures may not be immediately vis- ible on radiographs (1 0); however, it seems spec-
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ulative to assume that all of the patients Devas saw (with exercise-induced leg pain and no radi- ological changes) had stress fractures of their tibias. The source of the leg pain may have been from nonosseous tissues.
The process of stress fracture formation de- scribed by Devas was purely hypothetical and appears to have been based solely on his clinical experience. Roub et a/. (1 6) offer some evidence to support Devas' hypothesis. Roub et a/. found that some individuals with exercise-induced leg pain have localized changes in the tibia1 cortex which never progress to the point of being visible on radiographs.
Roub et a/. examined 35 college athletes who had 1- to 12-week histories of exercise-induced medial leg pain. The athletes were members of track, gymnastics, or field hockey teams. Thirteen of the athletes had bilateral leg pain. According to Roub et a/., the severity of the symptoms were similar in all of the athletes. Details of the athletes' symptoms were not provided.
Roub et a/. obtained radiographs and radio- nuclide images (bone scans) from the involved leg($ of each athlete. Athletes who exhibited no radiological changes but who had increased radi- otracer uptake on the bone scan had a second radiograph taken 1 month later. A control group of 13 asymptomatic athletes from the same teams also underwent radionuclide imaging and had ra- diographs taken of both their legs.
All subjects in the control group and six of the athletes with leg pain had no signs of stress fractures on the initial radiographs or bone scans. Details describing these subjects were not pro- vided.
On the initial bone scans, seven male and seven female athletes (15 legs) with leg pain ex- hibited focal, longitudinal, fusiform areas of in- creased radiotracer uptake along the medial cor- tex of their tibias. These athletes had no signs of stress fractures on the initial radiographs. How- ever, on the radiographs taken 1 month later, there were signs of stress fractures. Roub et a/. did not state what these signs were.
Four male and 12 female athletes (24 legs) with leg pain had increased radiotracer uptake along the medial border of their tibias on the initial bone scans. The pattern of radiotracer uptake in these 16 athletes ranged from focal, longitudinal, fusiform shapes to focal, vague, nondescript shapes. These athletes exhibited no signs of stress fractures on the initial radiographs or the radiographs taken 1 month later.
Roub et a/., like Devas (4), believe that stress fractures form as a result of a series of events. They believe that the fractures begin microscopi- cally and may or may not progress to the point of being radiographically demonstrable.
Roub et a/. stated that a stress fracture r e p
resents a focal acceleration of the remodeling process in cortical bone. In the sequence of re- modeling, resorption of cortical bone is followed by replacement. Osteoclastic activity resorbs bone in areas of stress and the bone is replaced by osteoblastic activity. According to the theory, when there is excessive stress, resorption pro- ceeds rapidly and replacement is slow. During this stage of fracture formation patients complain of pain and bone scans may exhibit a slight, nondes- cript increase in radiotracer concentration in the area of increased stress. Radiological signs of a stress fracture will not be present. If the stress continues, resorption of cortical bone proceeds even more rapidly than replacement. During this stage of stress fracture formation, patients have pain and bone scans will exhibit a focal, intense, fusiform area of increased radiotracer concentra- tion in the area of increased stress. Radiographic signs of a stress fracture (i.e., vague lucent cor- tical areas, periosteal, and endosteal thickening) will be present or will appear within a few weeks. Because at this stage the rate of resorption of cortical bone is much greater than the rate of replacement, the cortex is weakened. Periosteal and endosteal bone formation serve to reinforce the weakened cortex. A fracture that is visible on radiographs occurs only when stress causes the resorption of the cortex to be accelerated beyond the capacity of the periosteal and endosteal re- actions to offer adequate support.
Roub et a/. feel…
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