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Medial tibial stress syndrome – A case report
International Emergency Nursing (2009) 17, 233– 236
available at www.sciencedirect.com
journal homepage: www.elsevierhealth.com/journals/aaen
CASE STUDY
Medial tibial stress syndrome – A case report Matthew Crabtree BSc (Hons) DipHe RN (Charge Nurse/Emergency Nurse Practitioner) * Emergency Department/Minor Injury Unit, North Bristol NHS Trust, Bristol BS16 1LE, United Kingdom Received 25 November 2008; received in revised form 11 March 2009; accepted 17 March 2009
Introduction The role of the Emergency Nurse Practitioner (ENP) is an ongoing educational one for the nurse. The practitioner will at some point encounter situations and cases that they have had little or no experience of before in their career. This case report is an example of just such a presentation for the author who examined a patient with Medial Tibial Stress Syndrome (MTSS) who came to an ENP led minor injury unit (MIU) in Bristol. MTSS is a term which is used to describe the three main causes of MTSS. These are: stress fractures, periostitis and deep posterior compartment syndrome (DPCS) ( Detmer, 1986). It is noted that while still popular, the term ‘shin splints’ will not be discussed due to many authors considering it to be an ill defined lay term used to describe overuse injuries in the lower leg (Beck and Osternig, 1994; Ugalde and Batt, 2001; Story and Cymet, 2006; Bouche and Johnson, 2007)) and should therefore be disregarded as a final diagnosis.
Case presentation A 32 year old male presented to the MIU complaining of pain to his right lower leg which had started 4 weeks ago and had gradually been getting worse especially after finishing a run. There was no history of trauma and the patient was otherwise fit and well with no known allergies. On examination the patient was found to have point tenderness approxi* Tel.: +44 117 9701212x3830; fax: +44 117 9572335. E-mail address: [email protected]
mately 7 cm above his medial malleolus with slight localised swelling. The area was not hot or inflamed and had no wounds. He had full range of movement to knee and ankle while the only movement to cause increase tenderness to the area was eversion of the ankle. There was no neurological or vascular deficit to his leg. A provisional diagnosis of MTSS was made and the patient was advised to rest from running for three weeks, take a course of anti-inflammatory medicine and return at the end of the three weeks to assess any improvement. A physiotherapy review was offered if there was no improvement. Although this can be considered a reasonable and safe treatment plan, a lack of underlying knowledge of this condition was highlighted and reflected on. The following discussion examines the condition of MTSS, its causes, diagnosis and treatments.
Discussion Medial tibial stress syndrome (MTSS) is a commonly used term to define pain along the posteriomedial aspect of the distal two thirds of the tibia (Kortebein et al., 2000; Bouche and Johnson, 2007). Sakryd (1998) notes that MTSS encompasses a group of terms and conditions used to describe pain along the medial tibial border. These include shinsplints, stress fractures, stress reactions, periostitis, fasciitis and deep posterior compartment syndrome. Edwards et al. (2005) add that nerve entrapment, popliteal artery entrapment syndrome and bone tumours should all be part of an examiners differential diagnosis. The available literature describes many causes of MTSS and often a clinician will find more than one intrinsic or
1755-599X/$ - see front matter ª 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.ienj.2009.03.007
234 extrinsic factor in their patient’s history and examination. Couture and Karlson (2002) describe intrinsic factors as being unique to the patient. These include previous injuries, anatomical malalignment and poor exercise technique. Extrinsic factors include training methods, surface type and footwear (Pell et al., 2004). Beck (1998) emphasises that running is most commonly associated with tibial stress injuries. Edwards et al. (2005) acknowledge that the highest incidence of MTSS occurs in runners but advises caution not to overlook other sports such as tennis and basketball as potential causes of MTSS. Couture and Karlson (2002) recommend careful attention to the patients anatomical characteristics that may have caused their pain such as hind foot and forefoot varus. These cause subtalar pronation which in turn increases the stress generated by the soleus. Beck and Osternig (1994) report the soleus is a contributor to stress on the medial tibial border. Their study of fifty cadaverous legs found the soleus, flexor digitorum longus (FDL) and deep crural fascia most frequently attached at the site of pain described in MTSS. Other earlier work by Saxena et al. (1990) also implicated the tibialis posterior as causing pain in MTSS. A study by Beck and Osternig (1994) refutes this and offers mistakes in the dissection of the cadavers and small sample size (10 legs) as potential weaknesses in the study. However, Bouche and Johnson (2007) in their study of three cadaverous legs attached to a load frame and strain gauge found that the tibialis posterior, soleus and the FDL all had a similar exertional force on the tibial fascia which is the only structure to insert into the medial tibial crest. These findings support Couture and Karlson (2002) who found patients which pronate their ankle excessively have increased leg flexor contractions stressing the tibial fascia and symptoms are localised to the medial tibial crest. This is also supported by Yates and White (2004) who studied risk factors for developing MTSS among navel recruits. They found using a foot posture index which has been shown previously to have a good intratester and intertester reliability showed statistically significant (p = .002) results, finding persons with a pronated foot type as having a higher risk of developing MTSS. Wilder and Sethi (2004) and Pell et al. (2004) acknowledge other risk factors such as hard surfaces and changes in inclination as effecting and causing MTSS. Bouche and Johnson (2007) also emphasise that hard surfaces can add to the contractions of leg muscles and thereby increase the strain on the tibial fascia. Story and Cymet (2006) support this by describing changes in activity, surface type and route inclination as contributing factors to MTSS. Worn out shoes are also discussed and noted that after approximately 300 miles shoes can lose their shock absorbing ability and should therefore be changed. The forces created by the fascial pull in any of the above scenarios are transmitted to underlying bone via the Sharpey’s fibres (Couture and Karlson, 2002). Ugalde and Batt (2001) describe a stress/bone time continuum where over time increases in stress/repetition cause normal bone remodelling to accelerate. If the stress/repetition is not reduced then bone fatigue is likely and may result in a possible stress fracture. Wilder and Sethi (2004) describe this period of time as the most likely to develop micro damage in the
M. Crabtree bone if excessive strain is not reduced. If this damage accumulates then a stress fracture may result. However, if the Sharpey’s fibres tear instead of applying a continued pressure, a condition called periostitis occurs ( Sakryd, 1998). Detmer (1986) explains that this inflammation of the periostium can result in an avulsion of the periostium away from the bone (likely to be caused by the soleus muscle) and in chronic cases adipose tissue may be found between the periostium and bone. Stretching the fibres located in the avulsed periostium is likely to produce medial tibial pain. Detmer (1986) suggests that in this situation periostalgia may be a more accurate term to describe the condition than periostitis. Exertional compartment syndrome (ECS) is another cause of medial tibial pain and is described by Wilder and Sethi (2004) as recurrent exercise induced leg discomfort that occurs at a well defined period in exercise and relief of symptoms only occurs with the stopping of activity. They refer to increased pressures in the two posterior compartments of the lower leg as being responsible for possible causes of medial tibial pain. This is previously supported by Ugalde and Batt (2001), Beck and Osternig (1994) and Detmer (1986) in their anatomical placement of structures which apply stress to the medial tibial border. Ugalde and Batt (2001) summarise that the deep and superficial crural fascia from the soleus and deep posterior compartments are a realistic cause of pain along the medial tibia in exertional compartment syndrome.
Classification As discussed, the literature has yielded three main conditions (stress fracture, periostitis/periostalgia and raised posterior compartment pressures) as the major causes of medial tibial pain. Detmer (1986) has attempted to classify the causes into three categories. MTSS type I is the stress micro fracture and bone stress reactions. Type II is the avulsion of the periostium with possible depositing of adipose tissue. Type III is the chronic compartment syndrome. Coexistence between types was noted. This study and classification by Detmer (1986) has been widely used and cited in other articles throughout this paper and subject matter and is therefore considered valid despite its age. However, it is not without its criticisms and Kortebein et al. (2000) make two evaluations. They first note that the classification is only a clinical stratagem since each disorder may be differentiated by clinical evaluation and laboratory studies. Secondly the findings of adipose tissue between the avulsed periostium and bone had not been replicated in subsequent studies to date Kortebein et al. (2000).
Diagnostic procedures To differentiate between the causes of medial tibial pain Couture and Karlson (2002) advocate using these three diagnostic tools. They are plain film X-rays, triple phase bone scan (TPBS) and magnetic resonance imaging (MRI). Ugalde and Batt (2001) agree that using these three tests offer the best diagnostic potential for identifying the cause of the pain.
Medial tibial stress syndrome – A case report Pell et al. (2004) and Ugalde and Batt (2001) also acknowledge that these tests are not without their limitations and especially note that X-rays are invariably normal. This is reflected by Wilder and Sethi (2004) who state that in approximately two thirds of symptomatic patients X-rays are initially negative with only half ever going on to develop positive findings. Despite their low diagnostic value Edwards et al. (2005) value X-ray’s and advocate obtaining them to exclude other abnormalities including tumours. Wilder and Sethi (2004) acknowledge the most common positive finding on an X-ray is a focal region of periosteal thickening suggesting a stress fracture. Kortebein et al. (2000) note that the TPBS is very useful in differentiating between a stress fracture (Detmers type I) and a tibial stress reaction (Detmers type II). Couture and Karlson (2002) agree and describe a classic longitudinal orientated diffuse tracer uptake visible only on the delayed phase for tibial stress reactions. This is in comparison to a stress fracture which appears as a focal fusiform tracer uptake. The negative side to TPBS is the exposure of the patient to radiation and its inability to image tendon pathology (Ugalde and Batt, 2001). Brukner (2000) adds difficulty in identifying specific fracture sites, tumours, osteomyelitis and other bony abnormalities as weaknesses to its effectiveness. Using an MRI is the alternative choice to TPBS. Although slightly less available and more expensive the MRI has advantages in that the patient is not exposed to radiation, has excellent anatomical visualisation and can therefore differentiate between conditions such as tumours and stress fractures while pinpointing any fracture origins (Brukner 2000). Kortebein et al. (2000), Ugalde and Batt (2001), Couture and Karlson (2002) and Wilder and Sethi (2004) agree that TPBS and MRI have very similar sensitivity in identifying stress fractures. However, Story and Cymet (2006) add that MRI has the added advantage of showing acute changes such as periosteal fluid and bone marrow oedema. To effect a diagnosis of compartment syndrome Ugalde and Batt (2001) describe using either a wick or slit catheter to measure the compartment pressure during exercise or a needle manometer for resting pressures post exercise. These tests are not without their disadvantages and can yield different results depending on limb placement, catheter placement in the muscle and patient compliance. Wilder and Sethi (2004) agree with the disadvantages and recommend using a battery powered, hand held digital fluid pressure monitor. They found their device to be more accurate, versatile, convenient and less time consuming while also providing reproducible measurements among different operators. Both Ugalde and Batt (2001) and Wilder and Sethi (2004) agree that with examination and history consistent with compartment syndrome, finding one or more pressure P15 mm hg pre-exercise; P30 mm hg 1 min post exercise or P20 mm hg 5 min post exercise constitutes a diagnosis. Additionally, Wilder and Sethi (2004) note that TPBS and MRI also have roles to play in diagnosis. The TPBS may show a decreased radionuclide concentration near the area of increased pressure with an increase of concentration in the soft tissues both superior and inferior to the abnormality. An MRI can show swelling within a compartment, which, if has not returned to baseline by 25 min post exercise is considered diagnostic.
235 Because of the overlap of pathophysiology between the three main causes of medial tibial pain, treatment should be similar for each cause (Ugalde and Batt, 2001). Story and Cymet (2006) recommend an appropriate period of rest and using appropriate footwear designed to correct running abnormalities such as hyperpronation if appropriate. Also using appropriate surfaces for the chosen type of sport or activity, for example using a padded dirt surface for running instead of concrete or grass (too hard/soft, respectively). If conservative methods fail then a surgical alternative may be required. Detmer (1986) found encouraging results on patients with types II, III and combined II/III. He found that that by performing a periosteal cauterisation and faciotomy on type II and type II/III patients while performing only faciotomy on type III patients the following improvements were recorded (non-surgical treatment for type I, surgical procedures were under local anaesthetic on an outpatients basis – follow up on average at 6 months). Improved performance documented as follows: type II 93%, type III 100%, type II/III 86%. Complete cures as follows: type II 78%, type III 75%, type II/III 57% (Detmer 1986). Yates et al. (2003) enrolled patients with a positive TPBS for MTSS (diffuse linear uptake consistent with periostitis) and a 12 month history of failed conservative treatment. Their study was different to Detmer (1986) in that patients were operated on under general anaesthetic and had a slightly different surgical technique. However, Yates et al. (2003) found a significant decrease in symptoms following surgical intervention (p < 0.001) with a mean reduction in pain of 71.6%. Although these two studies have their weaknesses (Detmer (1986) had a relatively small study while no purpose for the cauterisation was noted. Yates et al. (2003) had only a 59% response rate to follow up) results show that if conservative methods fail then surgery can be offered as a treatment with an evidence based foundation of improving symptoms.
Conclusions It can be acknowledged that although MTSS is not a frequent presentation for Emergency Nurse Practitioners it is still valuable to be able to diagnose, treat and refer potential cases. The literature suggests the diagnosis may be reliant on a thorough examination, detailed history, plain film Xrays, TPBS and MRI. It is recognised that TPBS and MRI tests will not be available for use by ENP’s, therefore the ENP role in diagnosis of MTSS may be in recognising the differential diagnosis of MTSS, excluding more worrying causes and appropriately referring the patient on to others for definitive diagnosis and treatment. ENP’s can also safely commence an initial conservative treatment plan of rest and analgesia while also evaluating the patients individual intrinsic and extrinsic factors. As an ENP it is important to be able to advise a patient on all aspects of possible treatment and outcomes. The patient may present at any stage of symptoms. Pell et al. (2004) acknowledge a timely diagnosis and treatment plan can help ensure the quickest possible return to activity. Therefore, an informed ENP will be able to work with the patient to implement a plan of action to resolve their
236 condition, which may involve other multidisciplinary health care professionals.
References Beck, B.R., 1998. Tibial stress injuries: an aetiological review for the purposes of guiding management. Sports Medicine 26 (4), 265–279. Beck, B.R., Osternig, R., 1994. Medial tibial stress syndrome. The location of muscles in the leg in relation to symptoms. Journal of Bone and Joint Surgery 76-A (7), 1057–1061. Bouche, R.T., Johnson, C.H., 2007. Medial tibial stress syndrome (Tibial Fasciitis). A proposed pathomechanical model involving fascial traction. Journal of the American Podiatric Medical Association 97 (1), 31–36. Brukner, P., 2000. Exercise related lower leg pain: bone. Medicine and Science in Sports and Exercise 32 (2), s15–s26. Couture, C.J., Karlson, K.A., 2002. Tibial stress injuries. The Physician and Sports Medicine 30 (6), 29–36. Detmer, D.E., 1986. Chronic shin splints: classification and management of medial tibial stress syndrome. Sports Medicine 3, 436–446. Edwards, P.H., Wright, M.L., Hartman, J.F., 2005. A practical approach for the differential diagnosis of chronic leg pain in the athlete. The American Journal of Sports Medicine 33 (8), 1241– 1249.
M. Crabtree Kortebein, P.M., Kaufman, K.R., Basford, J.R., Stuart, M.J., 2000. Medial tibial stress syndrome. Medicine and Science in Sports and Exercise 32(2) Supplement March, s27–s33. Pell, R.F., Khanuja, H.S., Cooley, R.G., 2004. Leg pain in the running athlete. Journal of the American Academy of Orthopaedic Surgeons 12, 396–404. Sakryd, G., 1998. Medial tibial stress syndrome. Athletic Therapy Today (January), 41–44. Saxena, A., O’Brien, T., Bunce, D., 1990. Anatomic dissection of the tibialis posterior muscle and its correlation to medial tibial stress syndrome. Journal of Foot Surgery 29, 105–108. Story, J., Cymet, T.C., 2006. Shin splints, painful to have and to treat. Comprehensive Therapy 32 (3), 192–195. Ugalde, V., Batt, M.E., 2001. Shin splints: current theories and treatment. Critical Reviews in Physical and Rehabilitation Medicine 13 (3), 217–253. Wilder, R.P., Sethi, S., 2004. Overuse injuries: tendinopathies, stress fractures, compartment syndrome and shin splints. Clinics in Sports Medicine 23, 55–81. Yates, B., Allen, M.J., Barnes, M.R., 2003. Outcome of surgical treatment of medial tibial stress syndrome. Journal of Bone and Joint Surgery 85-A (10), 1974–1980. Yates, B., White, S., 2004. The incidence and risk factors in the development of medial tibial stress syndrome among navel recruits. The American Journal of Sports Medicine 32 (3), 772– 780.
available at www.sciencedirect.com
journal homepage: www.elsevierhealth.com/journals/aaen
CASE STUDY
Medial tibial stress syndrome – A case report Matthew Crabtree BSc (Hons) DipHe RN (Charge Nurse/Emergency Nurse Practitioner) * Emergency Department/Minor Injury Unit, North Bristol NHS Trust, Bristol BS16 1LE, United Kingdom Received 25 November 2008; received in revised form 11 March 2009; accepted 17 March 2009
Introduction The role of the Emergency Nurse Practitioner (ENP) is an ongoing educational one for the nurse. The practitioner will at some point encounter situations and cases that they have had little or no experience of before in their career. This case report is an example of just such a presentation for the author who examined a patient with Medial Tibial Stress Syndrome (MTSS) who came to an ENP led minor injury unit (MIU) in Bristol. MTSS is a term which is used to describe the three main causes of MTSS. These are: stress fractures, periostitis and deep posterior compartment syndrome (DPCS) ( Detmer, 1986). It is noted that while still popular, the term ‘shin splints’ will not be discussed due to many authors considering it to be an ill defined lay term used to describe overuse injuries in the lower leg (Beck and Osternig, 1994; Ugalde and Batt, 2001; Story and Cymet, 2006; Bouche and Johnson, 2007)) and should therefore be disregarded as a final diagnosis.
Case presentation A 32 year old male presented to the MIU complaining of pain to his right lower leg which had started 4 weeks ago and had gradually been getting worse especially after finishing a run. There was no history of trauma and the patient was otherwise fit and well with no known allergies. On examination the patient was found to have point tenderness approxi* Tel.: +44 117 9701212x3830; fax: +44 117 9572335. E-mail address: [email protected]
mately 7 cm above his medial malleolus with slight localised swelling. The area was not hot or inflamed and had no wounds. He had full range of movement to knee and ankle while the only movement to cause increase tenderness to the area was eversion of the ankle. There was no neurological or vascular deficit to his leg. A provisional diagnosis of MTSS was made and the patient was advised to rest from running for three weeks, take a course of anti-inflammatory medicine and return at the end of the three weeks to assess any improvement. A physiotherapy review was offered if there was no improvement. Although this can be considered a reasonable and safe treatment plan, a lack of underlying knowledge of this condition was highlighted and reflected on. The following discussion examines the condition of MTSS, its causes, diagnosis and treatments.
Discussion Medial tibial stress syndrome (MTSS) is a commonly used term to define pain along the posteriomedial aspect of the distal two thirds of the tibia (Kortebein et al., 2000; Bouche and Johnson, 2007). Sakryd (1998) notes that MTSS encompasses a group of terms and conditions used to describe pain along the medial tibial border. These include shinsplints, stress fractures, stress reactions, periostitis, fasciitis and deep posterior compartment syndrome. Edwards et al. (2005) add that nerve entrapment, popliteal artery entrapment syndrome and bone tumours should all be part of an examiners differential diagnosis. The available literature describes many causes of MTSS and often a clinician will find more than one intrinsic or
1755-599X/$ - see front matter ª 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.ienj.2009.03.007
234 extrinsic factor in their patient’s history and examination. Couture and Karlson (2002) describe intrinsic factors as being unique to the patient. These include previous injuries, anatomical malalignment and poor exercise technique. Extrinsic factors include training methods, surface type and footwear (Pell et al., 2004). Beck (1998) emphasises that running is most commonly associated with tibial stress injuries. Edwards et al. (2005) acknowledge that the highest incidence of MTSS occurs in runners but advises caution not to overlook other sports such as tennis and basketball as potential causes of MTSS. Couture and Karlson (2002) recommend careful attention to the patients anatomical characteristics that may have caused their pain such as hind foot and forefoot varus. These cause subtalar pronation which in turn increases the stress generated by the soleus. Beck and Osternig (1994) report the soleus is a contributor to stress on the medial tibial border. Their study of fifty cadaverous legs found the soleus, flexor digitorum longus (FDL) and deep crural fascia most frequently attached at the site of pain described in MTSS. Other earlier work by Saxena et al. (1990) also implicated the tibialis posterior as causing pain in MTSS. A study by Beck and Osternig (1994) refutes this and offers mistakes in the dissection of the cadavers and small sample size (10 legs) as potential weaknesses in the study. However, Bouche and Johnson (2007) in their study of three cadaverous legs attached to a load frame and strain gauge found that the tibialis posterior, soleus and the FDL all had a similar exertional force on the tibial fascia which is the only structure to insert into the medial tibial crest. These findings support Couture and Karlson (2002) who found patients which pronate their ankle excessively have increased leg flexor contractions stressing the tibial fascia and symptoms are localised to the medial tibial crest. This is also supported by Yates and White (2004) who studied risk factors for developing MTSS among navel recruits. They found using a foot posture index which has been shown previously to have a good intratester and intertester reliability showed statistically significant (p = .002) results, finding persons with a pronated foot type as having a higher risk of developing MTSS. Wilder and Sethi (2004) and Pell et al. (2004) acknowledge other risk factors such as hard surfaces and changes in inclination as effecting and causing MTSS. Bouche and Johnson (2007) also emphasise that hard surfaces can add to the contractions of leg muscles and thereby increase the strain on the tibial fascia. Story and Cymet (2006) support this by describing changes in activity, surface type and route inclination as contributing factors to MTSS. Worn out shoes are also discussed and noted that after approximately 300 miles shoes can lose their shock absorbing ability and should therefore be changed. The forces created by the fascial pull in any of the above scenarios are transmitted to underlying bone via the Sharpey’s fibres (Couture and Karlson, 2002). Ugalde and Batt (2001) describe a stress/bone time continuum where over time increases in stress/repetition cause normal bone remodelling to accelerate. If the stress/repetition is not reduced then bone fatigue is likely and may result in a possible stress fracture. Wilder and Sethi (2004) describe this period of time as the most likely to develop micro damage in the
M. Crabtree bone if excessive strain is not reduced. If this damage accumulates then a stress fracture may result. However, if the Sharpey’s fibres tear instead of applying a continued pressure, a condition called periostitis occurs ( Sakryd, 1998). Detmer (1986) explains that this inflammation of the periostium can result in an avulsion of the periostium away from the bone (likely to be caused by the soleus muscle) and in chronic cases adipose tissue may be found between the periostium and bone. Stretching the fibres located in the avulsed periostium is likely to produce medial tibial pain. Detmer (1986) suggests that in this situation periostalgia may be a more accurate term to describe the condition than periostitis. Exertional compartment syndrome (ECS) is another cause of medial tibial pain and is described by Wilder and Sethi (2004) as recurrent exercise induced leg discomfort that occurs at a well defined period in exercise and relief of symptoms only occurs with the stopping of activity. They refer to increased pressures in the two posterior compartments of the lower leg as being responsible for possible causes of medial tibial pain. This is previously supported by Ugalde and Batt (2001), Beck and Osternig (1994) and Detmer (1986) in their anatomical placement of structures which apply stress to the medial tibial border. Ugalde and Batt (2001) summarise that the deep and superficial crural fascia from the soleus and deep posterior compartments are a realistic cause of pain along the medial tibia in exertional compartment syndrome.
Classification As discussed, the literature has yielded three main conditions (stress fracture, periostitis/periostalgia and raised posterior compartment pressures) as the major causes of medial tibial pain. Detmer (1986) has attempted to classify the causes into three categories. MTSS type I is the stress micro fracture and bone stress reactions. Type II is the avulsion of the periostium with possible depositing of adipose tissue. Type III is the chronic compartment syndrome. Coexistence between types was noted. This study and classification by Detmer (1986) has been widely used and cited in other articles throughout this paper and subject matter and is therefore considered valid despite its age. However, it is not without its criticisms and Kortebein et al. (2000) make two evaluations. They first note that the classification is only a clinical stratagem since each disorder may be differentiated by clinical evaluation and laboratory studies. Secondly the findings of adipose tissue between the avulsed periostium and bone had not been replicated in subsequent studies to date Kortebein et al. (2000).
Diagnostic procedures To differentiate between the causes of medial tibial pain Couture and Karlson (2002) advocate using these three diagnostic tools. They are plain film X-rays, triple phase bone scan (TPBS) and magnetic resonance imaging (MRI). Ugalde and Batt (2001) agree that using these three tests offer the best diagnostic potential for identifying the cause of the pain.
Medial tibial stress syndrome – A case report Pell et al. (2004) and Ugalde and Batt (2001) also acknowledge that these tests are not without their limitations and especially note that X-rays are invariably normal. This is reflected by Wilder and Sethi (2004) who state that in approximately two thirds of symptomatic patients X-rays are initially negative with only half ever going on to develop positive findings. Despite their low diagnostic value Edwards et al. (2005) value X-ray’s and advocate obtaining them to exclude other abnormalities including tumours. Wilder and Sethi (2004) acknowledge the most common positive finding on an X-ray is a focal region of periosteal thickening suggesting a stress fracture. Kortebein et al. (2000) note that the TPBS is very useful in differentiating between a stress fracture (Detmers type I) and a tibial stress reaction (Detmers type II). Couture and Karlson (2002) agree and describe a classic longitudinal orientated diffuse tracer uptake visible only on the delayed phase for tibial stress reactions. This is in comparison to a stress fracture which appears as a focal fusiform tracer uptake. The negative side to TPBS is the exposure of the patient to radiation and its inability to image tendon pathology (Ugalde and Batt, 2001). Brukner (2000) adds difficulty in identifying specific fracture sites, tumours, osteomyelitis and other bony abnormalities as weaknesses to its effectiveness. Using an MRI is the alternative choice to TPBS. Although slightly less available and more expensive the MRI has advantages in that the patient is not exposed to radiation, has excellent anatomical visualisation and can therefore differentiate between conditions such as tumours and stress fractures while pinpointing any fracture origins (Brukner 2000). Kortebein et al. (2000), Ugalde and Batt (2001), Couture and Karlson (2002) and Wilder and Sethi (2004) agree that TPBS and MRI have very similar sensitivity in identifying stress fractures. However, Story and Cymet (2006) add that MRI has the added advantage of showing acute changes such as periosteal fluid and bone marrow oedema. To effect a diagnosis of compartment syndrome Ugalde and Batt (2001) describe using either a wick or slit catheter to measure the compartment pressure during exercise or a needle manometer for resting pressures post exercise. These tests are not without their disadvantages and can yield different results depending on limb placement, catheter placement in the muscle and patient compliance. Wilder and Sethi (2004) agree with the disadvantages and recommend using a battery powered, hand held digital fluid pressure monitor. They found their device to be more accurate, versatile, convenient and less time consuming while also providing reproducible measurements among different operators. Both Ugalde and Batt (2001) and Wilder and Sethi (2004) agree that with examination and history consistent with compartment syndrome, finding one or more pressure P15 mm hg pre-exercise; P30 mm hg 1 min post exercise or P20 mm hg 5 min post exercise constitutes a diagnosis. Additionally, Wilder and Sethi (2004) note that TPBS and MRI also have roles to play in diagnosis. The TPBS may show a decreased radionuclide concentration near the area of increased pressure with an increase of concentration in the soft tissues both superior and inferior to the abnormality. An MRI can show swelling within a compartment, which, if has not returned to baseline by 25 min post exercise is considered diagnostic.
235 Because of the overlap of pathophysiology between the three main causes of medial tibial pain, treatment should be similar for each cause (Ugalde and Batt, 2001). Story and Cymet (2006) recommend an appropriate period of rest and using appropriate footwear designed to correct running abnormalities such as hyperpronation if appropriate. Also using appropriate surfaces for the chosen type of sport or activity, for example using a padded dirt surface for running instead of concrete or grass (too hard/soft, respectively). If conservative methods fail then a surgical alternative may be required. Detmer (1986) found encouraging results on patients with types II, III and combined II/III. He found that that by performing a periosteal cauterisation and faciotomy on type II and type II/III patients while performing only faciotomy on type III patients the following improvements were recorded (non-surgical treatment for type I, surgical procedures were under local anaesthetic on an outpatients basis – follow up on average at 6 months). Improved performance documented as follows: type II 93%, type III 100%, type II/III 86%. Complete cures as follows: type II 78%, type III 75%, type II/III 57% (Detmer 1986). Yates et al. (2003) enrolled patients with a positive TPBS for MTSS (diffuse linear uptake consistent with periostitis) and a 12 month history of failed conservative treatment. Their study was different to Detmer (1986) in that patients were operated on under general anaesthetic and had a slightly different surgical technique. However, Yates et al. (2003) found a significant decrease in symptoms following surgical intervention (p < 0.001) with a mean reduction in pain of 71.6%. Although these two studies have their weaknesses (Detmer (1986) had a relatively small study while no purpose for the cauterisation was noted. Yates et al. (2003) had only a 59% response rate to follow up) results show that if conservative methods fail then surgery can be offered as a treatment with an evidence based foundation of improving symptoms.
Conclusions It can be acknowledged that although MTSS is not a frequent presentation for Emergency Nurse Practitioners it is still valuable to be able to diagnose, treat and refer potential cases. The literature suggests the diagnosis may be reliant on a thorough examination, detailed history, plain film Xrays, TPBS and MRI. It is recognised that TPBS and MRI tests will not be available for use by ENP’s, therefore the ENP role in diagnosis of MTSS may be in recognising the differential diagnosis of MTSS, excluding more worrying causes and appropriately referring the patient on to others for definitive diagnosis and treatment. ENP’s can also safely commence an initial conservative treatment plan of rest and analgesia while also evaluating the patients individual intrinsic and extrinsic factors. As an ENP it is important to be able to advise a patient on all aspects of possible treatment and outcomes. The patient may present at any stage of symptoms. Pell et al. (2004) acknowledge a timely diagnosis and treatment plan can help ensure the quickest possible return to activity. Therefore, an informed ENP will be able to work with the patient to implement a plan of action to resolve their
236 condition, which may involve other multidisciplinary health care professionals.
References Beck, B.R., 1998. Tibial stress injuries: an aetiological review for the purposes of guiding management. Sports Medicine 26 (4), 265–279. Beck, B.R., Osternig, R., 1994. Medial tibial stress syndrome. The location of muscles in the leg in relation to symptoms. Journal of Bone and Joint Surgery 76-A (7), 1057–1061. Bouche, R.T., Johnson, C.H., 2007. Medial tibial stress syndrome (Tibial Fasciitis). A proposed pathomechanical model involving fascial traction. Journal of the American Podiatric Medical Association 97 (1), 31–36. Brukner, P., 2000. Exercise related lower leg pain: bone. Medicine and Science in Sports and Exercise 32 (2), s15–s26. Couture, C.J., Karlson, K.A., 2002. Tibial stress injuries. The Physician and Sports Medicine 30 (6), 29–36. Detmer, D.E., 1986. Chronic shin splints: classification and management of medial tibial stress syndrome. Sports Medicine 3, 436–446. Edwards, P.H., Wright, M.L., Hartman, J.F., 2005. A practical approach for the differential diagnosis of chronic leg pain in the athlete. The American Journal of Sports Medicine 33 (8), 1241– 1249.
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