Tuesday, December 24, 2013

Pulled elbow & dislocation of radial head at elbow

Traumatic disruption of radio-humeral architecture may take many forms & a cause of lateral elbow pain with elbow stiffness. Subluxation & dislocation occur at this joint without fracture. We are herewith presenting a small review of pulled elbow in children & radial dislocation in adults. The purpose of doing so is to present the clinician to better identify these seemingly equal entities.

Pulled elbow:
It is also known as nursemaid's elbow. It is a common injury in young children. It is considered a minor condition in medicine but cause mush distress to parents of a child.
It results from a sudden longitudinal traumatic pull on pronated and extended forearm, usually by an adult or taller person. This sudden pull pulls the radius through the annular ligament, resulting in subluxation (partial dislocation) of the radial head.
The child experiences sudden acute pain and loss of function in the affected arm.

It appears to be infrequently recognized or diagnosed. Differential diagnosis of traumatic radial head subluxation from traumatic radial head dislocation, congenital radial head dislocation, brachial plexus palsy and "invisible" elbow fractures should be considered. Congenital radial head dislocation is the most common congenital elbow abnormality. Patients generally remain asymptomatic until adolescence and, at that time, may benefit from radial head resection. Open reduction and ligament reconstruction may offer advantages over late radial head resection if performed before the age of 2 years.

Variants of pulled elbow:
It is postulated here that there are two types of traumatic rotary radial head subluxation in pronation, the simple type and the lateral type. Careful analysis of AP view of elbow reveals the change of the shape and position of the radial tuberosity indicating the simple type, or concommitant with lateral displacement of the radial head on the ulna indicating the lateral type.

Treatment procedure:
Pulled elbow is usually treated by manual reduction of the subluxed radial head. Various manoeuvres can be applied. Flexion & supination is believed to be common method employed however few authorities recommend hyperpronation. Most textbooks recommend supination of the forearm, as opposed to pronation and other approaches. It is unclear which manoeuvre is most successful.
According to a Cochrane reviw (2009) pronation method might be more effective and less painful than the supination method for manipulating pulled elbow in young children.
However premanipulative roentgenograms are compared with postmanipulative roentgenograms in such cases to check repositioning.

Dislocation cases:
In closed reduction followed by plaster cast immobilisation for 4 weeks give a good result. In neglected cases where reduction is delayed neocapsule is believed to form hence even arthrography is therefore of little help to differentiate a long standing traumatic dislocation from a congenital dislocation. Various authors prefer & avoid open reduction, which carries a risk of joint stiffness, it is unnecessary to mention old unreduced dislocations cannot be reduced by manipulation. 

Adult cases of dislocation of radial head: 

In adults, isolated radial head dislocation is an extremely rare injury. Isolated traumatic dislocation can be either anterior or posterior. The mechanism leading to an isolated radial dislocation has been variously described. Most authors describe an indirect mechanism. The proximal radioulnar joint is most stable in supination: in this position, the contact between radius and ulna is maximal and the interosseous membrane, the annular ligament, and the anterior fibres of the quadrate ligament are all taut, thus drawing the radial head snugly against its notch in the ulna. Cadaveric studies have shown that posterior dislocation of the radial head cannot occur without the rupture of the annular ligament; in addition, partial tear of the quadrate ligament and the proximal interosseous membrane takes place.
The speculated the mechanism to be a hyperextension of the elbow with forearm in prone position leads to a posterior dislocation of the radial head.

Posterior dislocation of radial head: only few more than 20 cases are described in medical literature but there are no guidelines for treatment. An inability to pronate/supinate while able to flex the elbow should suggest posterior radial head dislocation. There is swelling obvious on the lateral and posterior aspect of the elbow. The elbow is held in flexion and partial supination. Tenderness is present laterally at the elbow, and the radial head is palpable posteriorly. There is no swelling or tenderness over the ulna.

Treatment approach in posterior dislocation: Under general anesthesia, gentle traction, pronation, and direct pressure over the radial head is used to reduce the dislocation. Postreduction, the elbow is generally stable. Immobilization is done in a long-arm cast for 4 weeks in either flexion (110 degres) & supination or uncommonly flexion & pronation. Patient generally recovers complete range of motion.
The diagnosis may be easily missed on radiographs and, therefore, require a high index of suspicion. Authors have reported isolated anterior dislocation of the radial head in young woman without functional disorders. Early reduction is important in order to avoid the necessity for excision of the head of radius and its attendant complications.

If missed or neglected, an open reduction must to be done with either an annular ligament reconstruction or a radial head excision; in these conditions, the results were poor with a restriction of forearm supination and pronation and significant risk of degenerative arthritis of the elbow and the distal radioulnar joints. Closed reduction of an elbow dislocation is unlikely to be successful if attempted later than 21 days after the injury. The results are acceptable if open reduction is undertaken within 3 months of the injury, but after 6 months the results are disappointing and arthroplasty is an alternative.

1. Krul M et al Cochrane Database Syst Rev. 2012 Jan 18;1:CD007759. doi: 10.1002/14651858.CD007759.pub3. (Manipulative interventions for reducing pulled elbow in young children.)
2. Woo CC; J Manipulative Physiol Ther. 1987 Aug;10(4):191-200. (Traumatic radial head subluxation in young children: a case report and literature review.)
.3. Obert L et al; Chir Main. 2003 Aug;22(4):216-9. (Isolated traumatic luxation of the radial head in adults: report of a case and review of the literature.)
4. Damak B et al; Acta Orthop Belg. 1998 Dec;64(4):413-7. (Isolated traumatic anterior dislocation of the radial head).
5. Bruce C et al; J Trauma. 1993 Dec;35(6):962-5. (Unreduced dislocation of the elbow: case report and review of the literature.)
6. Sachar K et al; Hand Clin. 1998 Feb;14(1):39-47. (Congenital radial head dislocations.)
7. Koulali-Idrissi K et al; Chir Main. 2005 Apr;24(2):103-5. [Isolated dislocation of the radial head in an adult (case report and literature review)].
8. J Emerg Trauma Shock. 2010 Oct;3(4):422-4. doi: 10.4103/0974-2700.70767. Isolated, traumatic posterior dislocation of the radial head in an adult: A new case treated conservatively.

Friday, October 25, 2013

Manage LBA & SIJ pain by Hip intervention

Crucial role of hip in Hip-spine syndrome

Cervical & dorsal spine can produce lumbar spine pain along with lower extremity pain that may mimic sciatica. Similarly muscle imbalances & hip capsular problems may produce SI joint & lumbar spine pain with radiating symptoms in the lower extremity.

In the following article we are trying to focus on hip producing spine & SI joint problems producing radiating & non-radiating symptoms.

Concomitant presence of hip & spine problem named hip-spine syndrome is reported in medical literature but amount of research in this area is scanty. As relates to physiotherapy it becomes difficult to chuck out action plan as every bit of physical intervention must be directed to exact tissue at fault. What causes what, hip gives rise to spine fault or vice versa is yet to be concretely ascertained. Burns SA et al (2) found joint mobilization/manipulation and strengthening exercises directed at the hip alleviates both hip & lumbar spine pain. They have concluded patients with lumbopelvic-hip pain respond favorably to manual therapy and exercise targeting regions adjacent to the lumbar spine and further individuals with a primary complaint of LBP with hip impairments may benefit from interventions to reduce hip impairments.

Many crucial hip joint functions are maintained by pelvifemoral muscles during static & dynamic functions. Hip also has a strong capsule that may suffer from tightness & contracture which may further affect muscle function of hip leading to altered biomechanics of pelvic & lumbar spine producing pain in the mentioned areas. As mentioned above hip mobilization may not only alleviate lumbar spine pain it may also improve muscle function & capsular flexibility. According to Howard M et al (3) use of grade IV non-thrust mobilization improves hip abductor strength immediately post-intervention in healthy individuals assumed to be because of stimulation of mechanoreceptors. In a study by Yerys et al (4) it is revealed that a significant increase in gluteus maximus strength in response to Grade IV P-A mobilizations performed on the anterior hip capsule. Clinicians can utilize these findings in everyday practice to improve muscle strength by integrating manual therapy with therapeutic exercises.

A review of biomechanical prospective of spino-pelvic organization & lumbo-coxa chain in sagital plane:
i. Standing & static posture & lumbar spine curvature to pelvis:  Standing in an erect position is a human property (5). According to Mehta VA et al (8) relation of the pelvis to the spine is overlooked as a contributor to sagittal balance. However, it is now recognized that spinopelvic alignment is important to maintain an energy-efficient posture in normal and disease states. Sagital pelvic alignment is very much dependant on the hip joints. Similarly pelvis anatomy and position, defined by the pelvis incidence, interact with the spinal organization in shape and position to regulate the sagittal balance between both the spine and pelvis. Sagittal balance of the human body may be defined by a setting of different parameters such as (a) pelvic parameters: pelvic incidence (PI), pelvic tilt (PT) and sacral slope (SS); (b) C7 positioning: spino-pelvic angle (SSA) and C7 plumb line; (c) shape of the spine: lumbar lordosis. The genuine shape of the spine is probably one of the main mechanical factors of degenerative evolution. This shape is oriented by a shape pelvis parameter, the pelvis incidence. In case of pathology, this constant parameter is the only signature to determine the original spine shape we have to restore the balance of the patient.

ii. Bending & lifting: Bending and lifting activities are associated with injury to the lumbar discs and ligaments, and cadaveric experiments suggest that this damage is most attributable to a high bending moment (bending stress) acting on the osteoligamentous spine. Dolan P et al (6) examined the hypothesis that people with poor sagittal mobility in the lumbar spine and hips apply higher bending stresses to their spines during everyday lifting activities. They found all subjects flattened or reversed their lumbar lordosis when lifting, and most came close to or exceeded their static in vivo limit of lumbar flexion in many of the activities. The bending moment acting on the lumbosacral junction rose to about 30 Nm, which is about 50% of that required to cause injury in a single lift. Bending moments were significantly lower in subjects who had good sagittal mobility in the lumbar spine. Good hip mobility was similarly associated with a reduction in bending moment, but this reached significance only in subjects who reported a history of low back pain.

iii. Hip Lateral Rotation (HLR) test: Pattern of hip lateral rotation vary in different back pain suffers i.e. they move their hip differently (9). Linda R et al (7) examined whether lumbopelvic motion associated with a clinical test of active hip lateral rotation (HLR) systematically varied between people classified into 1 of 2 low back pain (LBP) subgroups: lumbar rotation (Rot) or lumbar rotation with extension (RotExt). And they further examined whether the timing of hip and lumbopelvic rotation with HLR would be more symmetric, right versus left, in people in the Rot subgroup compared with the RotExt subgroup.

They found People in the Rot and RotExt subgroups displayed systematic differences in how they moved the hip and lumbopelvic region with the clinical test of active HLR. These findings are potentially important because such differences in movement patterns between subgroups of people with LBP suggest different contributing factors and may require different treatments to affect the movement patterns. Here normalizing faulty movement i.e. hip lateral rotation may lead to alleviation of LBA. 

Patterns of hip contracture & it’s genesis: 
 Analysis of patterns in poliomyelitis reveals that fibrosis of gluteus maximus muscle may lead to limited flexion of the hips and various degrees of contracture of the abductor and external rotator muscles (1). In such cases affected hip could not be flexed in the usual sagittal plane, but had to be flexed in abduction. If gluteus maximus tightness & contracture is addressed excellent correction of the other hip contractures are achieved.

Sitting posture: In relaxed sitting posture hip rolls in to abduction & external rotation being flexed. This may lead to contracture of hip external rotators & abductors. That may also lead to tightness of posterior hip capsule.

If hip remains or maintains an abduction, external rotation position then there is compensatory pelvic posture for example iliac out-flare. Hence all of this may lead to altered dynamic sagital balance of the whole lumbopelvocoxa region which may further lead to a degenerative pathogenesis in any of the above.

1.    Patients with lower back or buttock pain that radiates into the posterior or lateral leg are often referred to physical therapy with a diagnosis of sciatica. Often the physical exam does not reveal neurologic findings indicative of radiculopathy. Instead, there is hip abductor muscle pain and weakness. This syndrome involves muscle imbalances that result in overuse strain of the gluteus medius and gluteus minimus muscles, Myofascial trigger points, and trochanteric bursitis. This paper describes hip abductor pain syndrome and provides a rationale for the diagnosis and treatment. Treatment salient points are discussed above (9).
2.    According to a case study by Boyle KL interventions to restore and maintain the optimal position of pelvis and hip (femoral head in the acetabulum) may be beneficial for treating patients with chronic LBP/SIJP. The patient’s pain may be alleviated in just a few days performing exercises to reposition the pelvis and restore posterior hip capsule extensibility and internal rotation (11) anterior interior chain pattern of postural asymmetry.         


1.    YS Hang; J Bone Joint Surg Am, 1979 Jan 01;61(1):52-55. Contracture of the hip secondary to fibrosis of the gluteus maximus muscle.
2.    Burns SA et al Physiother Theory Pract. 2011 Jul;27(5):384-97. doi: 10.3109/09593985.2010.509382. Epub 2010 Aug 26. Clinical decision making in a patient with secondary hip-spine syndrome.
3.    Howard Makofsky et al, J Man Manip Ther. 2007; 15(2): 103–110. Immediate Effect of Grade IV Inferior Hip Joint Mobilization on Hip Abductor Torque: A Pilot Study.
4.    Yerys et al; Journal of Manual & Manipulative Therapy, Volume 10, Number 4, 2002 , pp. 218-224(7). Effect of Mobilization of the Anterior Hip Capsule on Gluteus Maximus Strength.
5.    Roussouly P et al; Eur Spine J. 2011 Sep;20 Suppl 5:609-18. doi: 10.1007/s00586-011-1928-x. Epub 2011 Aug 2. Biomechanical analysis of the spino-pelvic organization and adaptation in pathology.
6.    Dolan P et al; Clinical Biomechanics, Volume 8, Issue 4, July 1993, Pages 185–192. Influence of lumbar and hip mobility on the bending stresses acting on the lumbar spine.
7.    Linda R. Van Dillen et al; Archives of Physical Medicine and Rehabilitation, Volume 88, Issue 3, March 2007, Pages 351–360. Symmetry of Timing of Hip and Lumbopelvic Rotation Motion in 2 Different Subgroups of People With Low Back Pain.
8.    Mehta VA et al; Neurosurgery. 2012 Mar;70(3):707-21. Implications of spinopelvic alignment for the spine surgeon.
9.    Dennis C et al; The Iowa Orthopaedic Journal, Volume 23 57. RATIONALE FOR TREATMENT OF HIP ABDUCTOR PAIN SYNDROME.
10.    Barbee E et al; phys ther.1990,70:537-541. Patters of hip rotation range of motion: A comparison between healthy subjects & patients with low back pain.
11.    Boyle KL. Physiother Can. 2010;preprint. doi:10.3138/ptc.2009-37. Managing a female patient with left low back pain and sacroiliac joint pain with therapeutic exercise: a case report.

Monday, September 30, 2013

Chronic fatigue syndrome

Severe fatigue is a common complaint among patients. Often, the fatigue is transient or can be attributed to a definable organic illness. Some patients present with persistent and disabling fatigue, but show no abnormalities on physical examination or screening laboratory tests. In these cases, the diagnosis of chronic fatigue syndrome (CFS) should be considered.

According to Centers for Disease Control and Prevention (CDC, USA) Chronic fatigue syndrome (CFS) currently is defined as:
(1) fatigue of at least 6 months' duration, seriously interfering with the patient's life; and (2) without evidence of various organic or psychiatric illnesses that can produce chronic fatigue.

The World Health Organization classifies myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs) as a nervous system disease. Together with other diseases under the G93 heading, ME/cfs shares a triad of abnormalities involving elevated oxidative and nitrosative stress (O&NS), activation of immuno-inflammatory pathways, and mitochondrial dysfunctions with depleted levels of adenosine triphosphate (ATP) synthesis.

Clinical features:
Elaborately CFS is characterized by debilitating fatigue with associated myalgias, tender lymph nodes, arthralgias, chills, feverish feelings, and postexertional malaise. According to Komaroff there may be abrupt onset with an 'infectious-like' illness, intermittent unexplained fevers, arthralgias and 'gelling' (stiffness), sore throats, cough, photophobia, night sweats, and post-exertional malaise with systemic symptoms.
According to Clauw 4 of the following criteria need to be present: sore throat, impaired memory or cognition, unrefreshing sleep, postexertional fatigue, tender glands, aching stiff muscles, joint pain, and headaches.

While chronic, debilitating fatigue is common in medical outpatients, CFS is relatively uncommon. Prevalence depends substantially on the case definition used.
It is known that CFS is a heterogeneous disorder possibly involving an interaction of biologic systems. Medical research continues to examine the many possible etiologic agents for CFS (infectious, immunologic, neurologic, and psychiatric), but the answer remains elusive.

Diagnosis of CFS is primarily by exclusion with no definitive laboratory test or physical findings.
Differential diagnosis should be considered carefully as similarities with fibromyalgia & teperomadibular joint disorder exist and concomitant illnesses include irritable bowel syndrome, depression, and headaches.
Course of CFS:
According to Komaroff the illness can last for years and is associated with marked impairment of functional health status.

Therefore, treatment of CFS may be variable and should be tailored to each patient. Therapy should include graded exercise (SF-36 is useful in assessing functional status), diet, good sleep hygiene, antidepressants, and other medications, depending on the patient's presentation.
It is note worthy that for graded exercises to be implemented one need to assess the exercise capacity of the individual.

References:1.    Komaroff AL et al, Am J Med. 1996 Jan;100(1):56-64. An examination of the working case definition of chronic fatigue syndrome.
2.    Craig T et al Am Fam Physician. 2002 Mar 15;65(6):1083-90. Chronic fatigue syndrome: evaluation and treatment.
3.    Komaroff AL, Ciba Found Symp. 1993;173:43-54; discussion 54-61.Clinical presentation of chronic fatigue syndrome.
4.    Buchwald D Am J Med. 1996 Oct;101(4):364-70. Functional status in patients with chronic fatigue syndrome, other fatiguing illnesses, and healthy individuals.
5.    Bates DW et al Arch Intern Med. 1993 Dec 27;153(24):2759-65. Prevalence of fatigue and chronic fatigue syndrome in a primary care practice.
6.    Clauw DJ, PM R. 2010 May;2(5):414-30. doi: 10.1016/j.pmrj.2010.04.010. Perspectives on fatigue from the study of chronic fatigue syndrome and related conditions.
7.    Aaron LA et al Best Pract Res Clin Rheumatol. 2003 Aug;17(4):563-74. Chronic diffuse musculoskeletal pain, fibromyalgia and co-morbid unexplained clinical conditions.
8.    Morris G et al; Mol Neurobiol. (2013).The Emerging Role of Autoimmunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/cfs).

Monday, July 15, 2013

Why i was not writing any blog since january 2013?

I was engrossed in building my new multi specialty hospital.

Losing my father who was more than god to me.

Following the view of entrance of  my hospital

website: www.medcarehospitalodisha.com
Tel: 0674-2436217

Soon i will be writing again as intensely as before.


Saturday, January 5, 2013

Diagnosis of Posterior heel pain & role of eccentric exercise in mid-portion Achilles tendinopathy


Degenerative disorders of tendons present an enormous clinical challenge. They are extremely common, prone to recur and existing medical and surgical treatments are generally unsatisfactory. Posterior heel pain is a common complaint in both athlete and non-athlete. Posterior heel pain is multifactorial and includes paratenonitis, tendinosis, tendinosis with partial rupture, insertional tendinitis, retrocalcaneal bursitis, and subcutaneous tendo-Achilles bursitis. Each of these entities is distinct, but they often occur in combination.

To avoid stereotyped treatment programs and there by failure of treatment, we need to know & classify homogenous appearing clinical entities into it’s own due place. With respect to posterior heel pain we encounter similar appearing entities in the Achilles tendon itself. Hence Van dijk et al in 2011 has sought clear terminology to delineate each of pain syndromes arising out of posterior heel. Following is an outline of new terminology they proposed; the definitions hereof encompass the anatomic location, symptoms, clinical findings and histopathology.

1. Mid-portion Achilles tendinopathy: a clinical syndrome characterized by a combination of pain, swelling and impaired performance. It includes, but is not limited to, the histopathological diagnosis of tendinosis.

Anatomic location: 2–7 cm from the insertion onto the calcaneus.
Symptoms: A combination of pain, swelling and impaired performance.
Signs: Diffuse or localized swelling
Histopathology: Includes, but is not limited to, the histopathological diagnosis of tendinosis: implies histopathological diagnosis of tendon degeneration without clinical or histological signs of intratendinous inflammation, not necessarily symptomatic

2. Achilles paratendinopathy: Achilles tendon is a weight-bearing tendon that lack a true tendon sheath but ia surrounded by paratenon. There is an acute or chronic inflammation and/or degeneration of the thin membrane around the Achilles tendon in this entity. There are clear distinctions between acute paratendinopathy and chronic paratendinopathy, both in symptoms as in histopathology.

Acute Achilles paratendinopathy:
Anatomic location: Around the mid-portion Achilles tendon
Symptoms: Edema and hyperaemia
Signs: Palpable crepitations, swelling
Histopathology: Edema and hyperaemia of paratenon, with infiltration of inflammatory cells, possibly with production of a fibrinous exudate that fills the space between tendon sheath and tendon

Chronic Achilles paratendinopathy:
Anatomic location: Around the mid-portion Achilles tendon
Symptoms: Exercise induced pain
Signs: Crepitations & swelling less pronounced than it’s acute counterpart
Histopathology: Paratenon thickened as a result of fibrinous exudate, prominent and widespread proliferation of (myo)fibroblasts, formation of new connective tissue and adhesions between tendon, paratenon, and crural fascia

3. Insertional Achilles tendinopathy: located at the insertion of the Achilles tendon onto the calcaneus, bone spurs and calcifications in the tendon proper at the insertion site may exist.

Anatomic location: Insertion of Achilles tendon onto calcaneus, most often with formation of bone spurs and calcifications in tendon proper at insertion site
Symptoms: Pain, stiffness, sometimes a (solid) swelling
Signs: Painful tendon insertion at the mid-portion of the posterior aspect of the calcaneus, swelling may be visible and a bony spur may be palpable
Histopathology: Ossification of enthesial fibrocartilage, and sometimes small tendon tears occurring at tendon-bone junction

4. Retrocalcaneal bursitis: an inflammation of the bursa in the recess between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess).

Anatomic location: Bursa in the recess between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of the calcaneus (Retrocalcaneal recess)
Symptoms: Painful swelling superior to calcaneus
Signs: Painful soft tissue swelling, medial and lateral to the Achilles tendon at the level of the posterosuperior calcaneus
Histopathology: Fibro-cartilaginous bursal walls show degeneration and/or calcification, with hypertrophy of the synovial infoldings and accumulation of fluid in the bursa. Alternatively, the bursa may be primarily involved by inflammatory or infectious bursitis due to an inflammatory arthropathy

5. Superficial calcaneal bursitis: inflammation of the bursa located between a calcaneal prominence or the Achilles tendon and the skin.

Anatomic location: Bursa located between calcaneal prominence or the Achilles tendon and the skin
Symptoms: Visible, painful, solid swelling postero-lateral calcaneus (often associated with shoes with rigid posterior portion)
Signs: Visible, painful, solid swelling and discoloration of skin. Most often located at posterolateral calcaneus; sometimes posterior or posteromedial

Histopathology: An acquired adventitious bursa, developing in response to friction. When inflamed, lined by hypertrophic synovial tissue and fluid.

Finally, they suggested that previous terms as Haglund's disease; Haglund's syndrome; Haglund's deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucumber heel), are no longer used.

Pathology of Achilles tendon disorders:

Tendinopathy is essentially an 'overuse', degenerative condition. Histopathology studies indicate intratendinous failed healing response and neoangiogenesis in achilles tendinopathy. Neovascularisation evident on Doppler ultrasound correlates well with pain and poor function. Power Doppler study shows microvessels arise on the ventral side of the TA tendon. However according to Richards PJ (2005) there is non-linear relationship between tendonopathy, TA size and the amount of microvascularity.
Mid portion achilles tendionopathy: Tendinopathy of the main body of tendo Achillis affects athletic and sedentary patients. Mechanical loading is thought to be a major causative factor. However, the exact mechanical loading conditions which cause tendinopathy are poorly defined. Repetitive mechanical loading induces a non-inflammatory pathology, and repetitive microtrauma ultimately exceeds the healing response.

Diagnostic clues:

A Haglund's deformity or precisely RCB (Retrocalcaneal bursitis) is present in asymptomatic patients & more to that it does not indicate presence of insertional Achilles tendinitis. A vast majority of the insertional Achilles tendinitis patients have calcification at the tendon insertion (Kang , 2012).

On the basis of X-ray Singh R(2008) for diagnosis of etiology of posterior heel pain described certain angles, lines and soft tissue parameters that focus to describe the calcaneal prominence and its relationship to Achilles tendon and its bursae. Following are the points of diagnosis:
Parallel pitch lines, Chauveaux-Liet angle, ill-defined retrocalcaneal recess, superficial tendo-Achilles bursa and anteroposterior diameter of Achilles tendon more than 9 mm about 2 cm above insertion are reliable objective diagnostic indicators of bony deformity of calcaneus and soft tissue affection in patients with posterior heel pain.

Skeletal US imaging:
A study by Richards PJ (2005) reveal that power doppler is more sensitive to reveal tendon microvascularity than colour doppler in TA tendonopathy. Morphologically abnormal adult TAs were larger than 5.9 mm but power doppler flow is only seen in TAs above 6.5 mm.

Treatment of posterior heel pain:

Although most cases of this disorder are successfully treated nonoperatively, a small subgroup of recalcitrant cases may benefit from surgical intervention. (Impact of conservative treatment is discussed below.)

If paratenonitis is present, the paratenon is partially excised, and adhesions are released. Areas of symptomatic tendinosis are excised with repair of the residual defect in the Achilles tendon. An alternative for patients with tendinosis who are at increased risk for wound problems or who do not want a large open incision is percutaneous or endoscopic tenotomy. A symptomatic Haglund's deformity or inflamed retrocalcaneal bursa is excised. Augmentation of the Achilles tendon may be considered if debridement threatens the structural integrity of the tendon, in older patients, and in revision surgery (6).

Complete ruptures in active, athletic persons should be treated operatively in most cases and result in predictably good outcomes. There may be some cases that escape early recognition and require a reconstructive procedure to salvage a potentially severe functional deficit.

Extracorporeal shock wave therapy, Peritendinous injections and eccentric training decrease neovascularity, relieve pain and improve outcome. Although surgery is the last resort in those patients failing conservative management, it is still unclear how the removal of adhesions and excision of affected tendinopathic areas affects healing and vascularity, or resolves pain.

Other options commonly taken:
US therapy with or without phonophoresis, shoe modification (heel raise) & biomechanical correction through shoe, contrast heat, night splintage in TA stretched position.

Impact of conservative treatment:

According to Richard PJ (2005) in patient with conservatively managed tendinopathy of the mid-Achilles tendon over 1 year there was a reduction of MRI enhancement and number of vessels on power Doppler, followed by morphological improvements and a reduction in size. Vessels per se related to the abnormal morphology and size of the tendon rather than symptoms. Symptoms improve before the Achilles size reduces and the restoration of normal imaging over time.

Role of Eccentric exercise in management of posterior heel pain arising out of achilles tendinopathy:
Recently eccentric, but not concentric, exercises have been shown to be highly effective in managing tendinopathy of the Achilles (and other) tendons. The mechanism for the efficacy of these exercises is unknown although it has been speculated that forces generated during eccentric loading are of a greater magnitude.

All portions of TA suffering achilles tendinopathy do not respond equally to eccentric exercises. Eccentric exercises for the calf muscles have been shown to be effective for chronic non-insertional Achilles tendinopathy (AT). However, the relative effectiveness of various dosages is unknown. Study by Rompe JD et al (2008) found eccentric loading show inferior results to low-energy shock wave therapy in chronic recalcitrant insertional tendinopathy assessed at four months of follow-up. Hence the location of the lesion has a profound effect on efficacy of eccentric exercises.

Dose: Relative effectiveness of various dosages of eccentric exercises for AT is still unclear. However, it appears that highly variable compliance rates result in similar positive outcomes (14).
Possible explanation: According to Rees JD et al; oscillations (while eccentrically loaded) provide a mechanism to explain the therapeutic benefit of eccentric loading in Achilles tendinopathy and parallels recent evidence from bone remodelling, where the frequency of the loading cycles is of more significance than the absolute magnitude of the force.


1. van Dijk CN et al; Knee Surg Sports Traumatol Arthrosc. 2011 May;19(5):835-41. Epub 2011 Jan 11. (Terminology for Achilles tendon related disorders.)
2. Kang S et al; Foot Ankle Int. 2012 Jun;33(6):487-91. (Insertional Achilles tendinitis and Haglund's deformity.)
3. Singh R et al; Foot (Edinb). 2008 Jun;18(2):91-8. Epub 2008 Mar 19. (Diagnostic significance of radiologic measurements in posterior heel pain.)
4. Schepsis AA et al; Am J Sports Med. 2002 Mar-Apr;30(2):287-305. (Achilles tendon disorders in athletes.)
5. Tan SC et al; Disabil Rehabil. 2008;30(20-22):1608-15. doi:10.1080/09638280701792268. (Achilles and patellar tendinopathy: current understanding of pathophysiology and management.)
6. Aronow MS; Clin Podiatr Med Surg. 2005 Jan;22(1):19-43. (Posterior heel pain -retrocalcaneal bursitis, insertional and noninsertional Achilles tendinopathy).
7. Rompe JD et al; Disabil Rehabil. 2008;30(20-22):1666-76. doi: 10.1080/09638280701785825. (Mid-portion Achilles tendinopathy--current options for treatment)
8. McShane JM et al; urr Sports Med Rep. 2007 Oct;6(5):288-92. (Noninsertional Achilles tendinopathy: pathology and management.)
9. Solan M et al; Foot Ankle Clin. 2007 Dec;12(4):597-615, vi. (Management of insertional tendinopathy of the Achilles tendon.)
10. Meyer A et al; Scand J Med Sci Sports. 2009 Oct;19(5):609-15. doi: 10.1111/j.1600-0838.2009.00981.x. Epub 2009 Jul 6. (Eccentric exercise protocols for chronic non-insertional Achilles tendinopathy: how much is enough?)
11. Richards PJ et al; Skeletal Radiol. 2010 Jun;39(6):509-21. doi: 10.1007/s00256-009-0772-0. Epub 2009 Aug 27. (Longitudinal microvascularity in Achilles tendinopathy (power Doppler ultrasound, magnetic resonance imaging time-intensity curves and the Victorian Institute of Sport Assessment-Achilles questionnaire): a pilot study.)
12. Rees JD et al; Br J Sports Med. 2009 Apr;43(4):242-6. doi: 10.1136/bjsm.2008.052910. Epub 2008 Nov 3. (Eccentric exercises; why do they work, what are the problems and how can we improve them?)
13. Rees JD et al; Rheumatology (Oxford). 2008 Oct;47(10):1493-7. doi: 10.1093/rheumatology/ken262. Epub 2008 Jul 22. (The mechanism for efficacy of eccentric loading in Achilles tendon injury; an in vivo study in humans.)
14. Meyer A et al; Scand J Med Sci Sports. 2009 Oct;19(5):609-15. doi: 10.1111/j.1600-0838.2009.00981.x. Epub 2009 Jul 6. (Eccentric exercise protocols for chronic non-insertional Achilles tendinopathy: how much is enough?)

Wednesday, July 18, 2012

Entrapment of medial calcaneal nerve (MCN)

Peripheral nerve entrapment is a rare, but important, cause of foot and ankle pain that often is underdiagnosed and mistreated. A peripheral nerve may become entrapped anywhere along its course, but certain anatomic locations are characteristic (2).

The medial calcaneal nerve (MCN)

The Tibial nerve is called the planter nerve in the sole. The tibial nerve passes to the sole of the foot takes a turn on the medial side of the calcaneum is called MCN. The medial calcaneal nerve arises from tibial nerve of the inner side of the ankle, perforates the laciniate ligament, travels downwards passing below the bony projection on the inner side of the ankle, and supplies the skin over the medial aspect of the heel. Hence it is the most important nerve for heel sensations. MCN have 2 branches. The anterior branch dominate the cutaneous sensation of the anterior part of the medial calcaneal and heel weight loading field, while the posterior branch dominate the sensation of the posterior and median part.

How entrapment occurs?

A nerve can become entrapped on its way through the tissue planes. Usually in case of entrapment, the nerve gets compressed between a static and a mobile surface. As the body moves, the nerve is subjected to repeated sliding or friction, leading to compression and trauma. This trauma may damage the outer sheath of the nerve that helps with signal transmission and cause other structural alterations that eventually lead to pain and loss of function.

Causes of MCN entrapment: The medial calcaneal nerve may become entrapped between the tight fascia at the origin of the abductor hallucis muscle and the heel bone (calcaneus). An excessive pronation of the foot may lead to medial calcaneal nerve entrapment. This can occur as a postoperative complication during the release of the lateral plantar nerve branch (4).

S/S of MCN entrapment:
Stages of nerve entrapment (2):Clinically, any nerve entrapment is divided into three stages. 
Stage I: patients feel rest pain and intermittent paresthesias which are worse at night.
Stage II: continued nerve compression leads to paresthesias, numbness, and, occasionally, muscle weakness that does not disappear during the day.
Stage III: patients describe constant pain, muscle atrophy, and permanent sensory loss.

There is pain and parasthesia (burning or tingling) in the areas supplied by the nerve, that is below the inner bony projection of the ankle and under the heel. The pain usually initiates on the inside of the heel and travels towards the center. Any activity may further aggravate the pain.
When the medial calcaneal nerve is trapped the Tinel’s sign is positive. This test is performed by lightly tapping the skin over the nerve, which leads to tingling in the area supplied by the nerve.
Medial calcaneal nerve entrapment should not be confused with other causes of heel pain, such as plantar fasciitis and tarsal tunnel syndrome. Accurate diagnosis is important to achieve the desired results.

Palpation of MCN:
A thorough understanding of the causes of peripheral nerve entrapment, the anatomic course and variation of the peripheral nerves, the diagnostic modalities, and the treatment options can simplify this complex problem (2).
According to Tang et al anatomical position of MCN is relatively constant with 95% accuracy, MCN can be palpated at the following site:

MCNs arises from the tibial nerve at 3.3 cm up the horizontal plane of the tip of medial malleolus. They sent out anterior branches and posterior branches from 0.3 cm below the horizontal plane of the tip of medial malleolus on average.

Physical Testing:

Although diagnostic confusion abounds because of the multiple etiologies of peripheral nerve entrapments and their complex physical and temporal relation David Butler’s neural tension testing is very important to assess the reduced mobility of the nerve within the tissue plane.

Electrophysiological testing:

Electrodiagnosis is a powerful tool for evaluating lower extremity disorders that stem from the peripheral nervous system. Electrodiagnostic testing can help differentiate neurogenic versus non-neurogenic causes of complaints such as pain, weakness, and paresthesias. It can help practitioners pinpoint the anatomic location and reveal the underlying pathology in peripheral nerve lesions.


The first line of treatment includes rest and supportive therapies. Avoid activities that lead to pain; immobilization may also help. Use cold compresses and anti-inflammatory painkillers to reduce the symptoms. Massage or ultrasound therapy is also useful.
If rest and conservative treatment fail to eradicate the symptoms, surgical decompression of the nerve may be required. Surgical treatment usually produces good results.

Author’s comment:

Try Butler’s nerve gliding exercises & Neurodynamic techniques. I have personally tried alternative digital compression-relaxation at the site where the nerve takes a sharp angulation at heel with varied success rates but it is worth trying.  

1. Tang J et al; Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Apr;35(4):386-9. (Anatomic characteristics and clinic significance of the medial calcaneal nerve).
[Article in Chinese]
2. Hirose CB et al; Foot Ankle Clin. 2004 Jun;9(2):255-69. (Peripheral nerve entrapments).
3. Roy PC; Foot Ankle Clin. 2011 Jun;16(2):225-42. (Electrodiagnostic evaluation of lower extremity neurogenic problems).
4. http://docpods.com/medial-calcaneal-nerve-entrapment

Thursday, July 5, 2012

Planter heel pain: planter fascitis, Fat pad atrophy, combined PF & FPA.

What the following article is on?Discussion on 3 conditions with mostly similar symptom of planter heel pain.

Synonyms of planter heel pain: Subcalcaneal heal pain, calcaneodynia  etc.
Synonyms of Planter fascitis: Planter fasciosis, Planter fasciopathy etc.

Planter foot pain is seemingly the most innocuous yet significant morbid condition affecting the adults hampering their ADLs & QOL. According to a recent research paper (1) Plantar heel pain can be provoked by PF (Planter fascitis), FPA (Fat pad atrophy), combination of PF + FPA and other causes. Patients with PF or FPA typically show different characteristics in clinical features but overall may look quite similar. Plantar heel pain requires differential diagnosis for appropriate treatment.
DD of planter foot pain includes following:

Planter heel pain can be sub-divided in to neural & non-neural pain. The non-neural pain can again be sub-divided into 2 bony & soft tissue pains.
Bony pathology: Calcaneal stress fracture, apophysitis of the calcaneus (Sever's disease), osteomyelitis, or inflammatory arthropathy.

Soft tissue pathology:  Fat pad atrophy (FPA) or contusion, plantar fascia rupture and plantar fasciitis (PF).

Neural pathology: Entrapment or compression of the first branch of the lateral plantar nerve (Baxter's nerve), medial calcaneal branch of posterior tibial nerve, or nerve to abductor digiti quinti muscle.

Other neural causes include S1 radiculopathy, tarsal tunnel syndrome, and peripheral neuropathy.

Many times planter foot pain is due to combination of different pathologies coexisting together. For example it is reported that Planter fascitis & fat pad atrophy coexist to produce planter foot pain. Similarly Labib et al described the heel pain triad (HPT). HPT is a combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome.

We are going to discuss S/S of 2 different pathologies with similar presentation and they often coexists. 

A. Planter fascitis (PF):According to Buchbinder (5) PF is reported to be the most common cause of plantar heel pain. The peak age is between (40-60) years.

Pathology of PF(6):
The pathology is still unknown.
Histopathologic examination of biopsy specimens from patients undergoing excessive extension or microinjuries of the plantar fascia shows secondary degenerative changes in the plantar fascia, with or without fibroblastic proliferation, and without acute inflammation.
However there is aging caused physiological changes are thought leading to PF. There is increased stress on the calcaneus and plantar fascia due to of loss of buffering tissue such as water and collagen of the fat pad.

Risk factors for PF:
1.    running excessively (or suddenly increasing running distance)
2.    occupations that involve long periods of standing
3.    pes planus
4.    limited ankle dorsiflexion
5.    obesity

Basis of clinical diagnosis:1. Pain characteristics: first-step morning pain and relief of pain after walking (most significant finding). Medial calcaneal tuberosity pain must be view is association with morning 1st step pain to diagnose PF. Unilateral pain is more common than bilateral.
2. Association with abnormal foot biomechanics: TA tightness & Limited ankle DF is most commonly associated with PF. Both pes planus & Cavus are associated with PF however Pes palnus is more associated with PF than pes cavus.
Explanation of association of pes planus & TA tightness with PF:
Limited ankle dorsiflexion on the involved side significantly increased the risk of PF. According to Inman et al (7) approximately 10 degrees of ankle dorsiflexion with the knee extended is required during a normal gait. If the Achilles tendon is shortened, limiting ankle dorsiflexion, excessive pronation of the foot may occur to compensate for this limitation. Greater the limitation in ankle dorsiflexion, the more load on the plantar fascia. Excessive pronation of the foot increases tensile loads on the plantar aponeurosis.
Hence repetitive pronatory stress that increases tensile force on the plantar fascia causing the plantar arch to lower is the cause of PF. The pronatory effect increases with age, and is related to limited ankle dorsiflexion caused by decreased elasticity of the tendons, and the reduced range of motion that occurs with age.
Digiovanni et al (8) reported relief or absence of plantar heel pain in 52% of patients participating in exercises to stretch the plantar fascia, and 22% after stretching the Achilles tendon. This provides a good target for treatment.
3. Heel spur: Heel spur is a common incidental finding in PF than FPA.
Diagnosis on the basis of US scanning:
Hypoechoic fusiform-shaped swelling more than 4 mm in thickness at the origin of the plantar fascia.

B. Fat pad atrophy (FPA):There is loss of buffering tissue such as water and collagen of the fat pad under the heel mostly due to age. The fat pad atrophies and shock absorbency diminishes in subjects that were older than 40 years. Yi et al (1) used the following criteria to diagnose FPA. FPA is said to the causing planter heel pain if more than 3 of the following criteria are present:
1.    pain at heel center or margin
2.    worsening pain when barefoot 
3.    worsening pain after a long period of standing
4.    palpable calcaneus
In addition to the above following US scan finding: when the patient had a fat pad that was less than 3 mm in thickness.

1. B/L pain is common than U/L.
2. Pain characteristics:
a. aching pain (commonest) but also tingling, cold (5.4%) and burning sensations. (highest to lowest in that order)
b. pain after a long walk, pain at night and resting pain (highest to lowest in that order).
3. Both pes planus & cavus are associated with FPA.
4. Risk factors of FPA: B/L pain which get more severe with prolonged standing is likely to be caused by FPA.

C. PF+FPA (PFFPA):  PF and FPA may share very similar symptoms and are difficult to distinguish from one another further it has been seen. PF can be co-morbid with FPA. PFFPA shares features common to both PF & FPA. In case of mixed characteristics of PF and FPA, PFFPA should be considered first and ultrasonography should be used as an key diagnostic tool.

Treatment options:
It is imperative to diagnose correctly among seemingly similar S/S in planter foot pain. Many FPA & PFFPA cases are misdiagnosed as having PF and treated with conservative therapy including local steroid injection. In cases treated with steroid to PF there are reports of planter fascia rapture in running, hence it is cautioned to diagnose correctly & treat aptly. 
Though many surgical options are available including minimal invasive techniques, there are myriad non-surgical techniques available. Nevertheless, nonsurgical management of plantar fascitis (a predominate cause of planter heel pain) is successful in approximately 90% of patients (2). The options in physical medicinesfor planter heel pain includes: rest, massage, nonsteroidal anti-inflammatory drugs, night splints, heel cups/pads, custom and off-the-shelf orthoses, injections, casts, and physical therapy measures such as shock wave therapy (2). Stretching exercises of the plantar fascia and Achilles tendon can also relieved pain (1). In many studies standing TA stretching is compared with stretching through a prefabricated night splint. Findings suggest that stretching through a prefabricated night splint is a very good option in managing planter foot pain from PF that also is claimed to speeding up the time to recover (4). Heel cushions, heel cups, or low-dye taping can be applied to relieve the pressure on the calcaneus of FPA patients. In those involved in sports correction of training errors and orthotics are essential components in any treatment program (3).
Surgical treatment should be considered in only a small subset of patients with persistent, severe symptoms refractory to nonsurgical intervention for at least 6 to 12 months (2).

1. Yi TI et al; Ann Rehabil Med. 2011 Aug;35(4):507-13. Epub 2011 Aug 31. Clinical characteristics of the causes of plantar heel pain.
2. Neufeld SK et al; J Am Acad Orthop Surg. 2008 Jun;16(6):338-46. Plantar fasciitis: evaluation and treatment.
3. Ryan J; Am Fam Physician. 1995 Sep 1;52(3):891-8, 901-2. Use of posterior night splints in the treatment of plantar fasciitis.
4. Barry LD et al; J Foot Ankle Surg. 2002 Jul-Aug;41(4):221-7. (A retrospective study of standing gastrocnemius-soleus stretching versus night splinting in the treatment of plantar fasciitis.
5. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med. 2004;350:2159–2166.
6. Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc. 2003;93:234–237.
7. Inman VT, Ralston HJ, Todd F. Human walking. 2nd ed. Baltimore: Williams & Wilkins; 1994. pp. 45–72.
8. Digiovanni BF, Nawoczenski DA, Malay DP, Graci PA, Williams TT, Wilding GE, Baumhauer JF. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg. 2006;88:1775–1781. [PubMed]