Frozen Shoulder Adhesive Capsulitis - Everything You Need To Know

Frozen Shoulder Adhesive Capsulitis - Everything You Need To Know

https://www.youtube.com/watch?v=VhfaPe8f7g0 

Frozen shoulder (adhesive capsulitis)

The frozen shoulder can be associated with diabetes or thyroid disease.  It may be the initial presenting symptom for these conditions.  The exact details of this relationship remain poorly understood.  Ever patient with a frozen shoulder should have the HbA1c and TSH levels tested.  Also, check for arthritis, rheumatoid factors and antinuclear antibodies.  Most patients with frozen shoulder are female between the ages of 40 and 60 years old.  And frozen shoulder, the patient will lose both the active and the passive range of motion of the shoulder.  The patient develops pain, which means that there is inflammation with early fibrosis of the joint capsule, leading to joint stiffness.  The active and passive global motion, especially external rotation, will be reduced compared to the other side.  The shoulder pain and motion loss is usually not related to trauma.  It is an idiopathic process that results in shoulder pain and loss of motion due to contracture of the capsule.  The essential lesion involves the coracohumeral ligament and the rotator interval.  The synovial inflammation and capsular fibrosis results in pain and joint volume loss.  Check for previous trauma or fractures.  Rule out shoulder joint arthritis and rule out posterior dislocation of the shoulder.  It can also occur post-surgery from a rotator cuff tear.  It may also be associated with dupuytren disease and cervical disc disease.  Check for medical comorbidities such as stroke or cardiac diseases.  The x-ray will exclude trauma, malignancy, arthritis, calcific tendinitis, impingement, and AC joint arthritis.  And frozen shoulder, the humeral head will remain in its normal location.

 

MRI

There is a space reduction in the axillary recess.  Rotator cuff strength is normal by exam and on the MRI.  The pain and stiffness lasts beyond 6 months, then you can do manipulation of the shoulder under anesthesia.  There is a 50% failure rate in diabetics.  The diabetes is associated with a much worse prognosis and poor outcome for surgical and nonsurgical treatment.

 

Treatment

·         Nonoperative

o   This should be done for at least 3 to 6 months.

o   Supervised or home-based capsular stretching program +/-intra-articular steroid joint injection.

o   Nonsteroidal anti-inflammatory medication

·         Surgery

o   Capsular release (arthroscopic or open) and release the intra-articular and subacromial adhesions.

o   The axillary nerve may be injured during release of the capsule.

o   Utilize surgery in patients that have failure of initial conservative treatment for 3 months, and the patient remains functionally limited.

Neck and Upper Extremities Examination

 Written by Ryan Jones with Dr. Nabil Ebraheim

Neck and upper extremities spine examination or cervical spine physical examination involves assessment of vertebrae C3-T2, cranial nerve roots C4-T1, and all the muscles innervated by these nerve roots along with the muscles associated with basic neck movement. This examination follows the typical pattern of orthopedic examination of inspection, palpation, range of motion, neurological evaluation, and special tests¹.

Inspection

Check for any visual deformities or abnormal anatomical alignments in the coronal and sagittal plane including typical cervical lordosis and thoracic kyphosis¹. Also, look for any surgical scars, skin defects like café au lait spots, or muscular atrophy². Muscular atrophy can present as shoulder imbalance, scapular winging, or a general unilateral reduction in size of muscles of the upper extremities.

Palpation

Palpate for local tenderness along the spinal axis while also looking for any asymmetry². This includes palpations of the spinous processes and facet joints of the vertebrae along with palpation of the scapula to look for any asymmetry. Palpate the paraspinal muscles while looking for any tenderness or asymmetry. The muscles of importance include the trapezius, rhomboids, and levator scapulae muscles^1,3.

Range of Motion

Range of motion for the cervical spine involves checking cervical flexion (normal = 50), extension (normal = 60), rotation (normal = 80), and lateral bending (normal = 45)². A thorough range of motion examination should also be done for the shoulder due to the extensive nerve root innervation. Shoulder range of motion involves testing abduction (normal = 180), adduction (normal = 45), flexion (normal = 90), extension (normal = 45), internal rotation (normal = 55), and external rotation (normal = 45)⁴. Any abnormalities in range of motion can be indicative of muscular or neurological pathologies.

Neurological Examination

Test the motor ability and strength of the muscles associated with each cranial root for strength by grading it 0-V based on the muscle manual testing grading system^2,3. Any weakness is a sign of muscular or neurological pathology. Next, test for sensory function for pain (with a paper clip) and light touch (finger) sensation at the dermatome for each cranial nerve¹. Any abnormalities may be a result of neurological pathologies. Test the biceps reflex for C5, brachioradialis reflex for C6, and triceps reflex for C7 cranial nerve root abnormalities¹.

Special Tests

Use the following provocative test to differentiate neck pathologies from other upper extremity:

·         Spurling’s test is indictive of acute radioculopathy².

·         Hoffman’s test is indictive of cervical myelopathy².

·         Lhermitte’s test is indicative of compression and myelopathy of the cervical spine².

·         Stretch test is indicative of brachial plexus pathology.

·         Compression test is indicative of narrowing of the neural foramen, facet joint pressure, or muscle spasms from the paraspinal muscles³.

·         Observation of steppage, lateral, or wide-base gait are all indicative of myelopathy or neurological pathology².

Remember that an MRI may be required to confidently differentiate between shoulder and neck pathologies¹.

References

1.       Ebraheim N. Spine Exam & Upper Extremity – Everything You Need to Know – Dr. Nabil Ebraheim [Internet]. Toledo (OH): University of Toledo Medical Center, Department of Orthopedics; 2021 Aug 4 [cited 2021 Oct 23]. Available from: https://www.youtube.com/watch?v=hIiV-xi2TiE.

2.       Moore DW. Neck & Upper Extremity Spine Exam [Internet]. Santa Barbara (CA): Santa Barbara Orthopedic Associates; 2021 June 27 [cited 2021 Oct 23]. Available from: https://www.orthobullets.com/spine/2001/neck-and-upper-extremity-spine-exam

3.       Iyer KM. Examination of the Cervical Spine. In: Clinical Examination in Orthopedics. London: Springer; 2012. pp 97-107.

4.       Iyer KM. Examination of the Shoulder. In: Clinical Examination in Orthopedics. London: Springer; 2012. pp 9-18.

 

 

               

What is Bursitis? - Everything You Need to Know

 What is Bursitis?

Written by Braden Womack with Dr. Nabil Ebraheim

Bursas are synovium-lined, sac-like structures located throughout the body between skin and tendon or tendon and bone (1,2). The main function of bursa is to reduce the friction between areas of movement and some common locations are the shoulder, knee, hip, and elbow (1). When these areas become swollen or inflamed it is known as bursitis. During this abnormality the bursa will enlarge with fluid causing any movement against or direct pressure upon the area to produce pain for the patient (2).

There are many causes of bursitis that one should be aware of, five of which are prolonged pressure, trauma, sepsis, autoimmune conditions, and idiopathic origins. Prolonged pressure is when the bursa is stressed between a hard surface and bony prominence. Examples of this prolonged pressure include over-use of the area with repetitive motions, frequently resting one’s elbow on their desk, and working on one’s knees without adequate padding. Traumatic bursitis is caused when direct pressure is applied to the bursa, often unknowingly as it may have seemed benign at the time (2). Traumatic bursitis does put the patient at risk of developing septic bursitis, often difficult to distinguish against aseptic bursitis, which is most induced by invasive procedures (2,3). Staphylococcus aureus causes roughly 80% of septic bursitis through what is believed to be a direct inoculation, instead of a hematogenous route due to the poor blood flow seen to bursas (4). Bursitis can also be caused by autoimmune conditions such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, scleroderma, spondyloarthropathy, and gout. The last common cause of bursitis is idiopathic in origin (2).

Bursitis can be broken up further to acute bursitis and chronic bursitis. Acute bursitis is typically caused by trauma, infection, or crystalline joint disease resulting in pain on palpation of the bursa as well as a decrease in range of motion that is secondary to pain. Whereas chronic bursitis is typically caused by inflammatory arthropathies, repetitive motions, or microtraumas most often causing painless swelling and thickening of the bursa. Examination of the skin is an important distinguishing factor for acute and chronic bursitis as trauma, erythema, and warmth should all be evaluated to make a proper diagnosis (2).

Diagnosis of many types of bursitis can be made clinically without further studies, however in the case of trauma, concern for foreign bodies, or fractures imaging can play an important role in diagnosis. Basic plain film imaging can be used when evaluating a superficial bursa however, for a deeper bursa MRI and ultrasound can be used (1). Ultrasound will also provide the added benefit of showing real-time images to observe changes in active and passive movements (2). When evaluating an inflamed bursa, aspiration is a critical tool to distinguish between septic and aseptic bursitis as the aspirated fluid should be sent for a basic cell count and cell cultures (3).

Treatment for bursitis depends on the type and causative agent as most bursitis will heal on their own without intervention. To combat the patient’s pain, bursitis can be treated with a conservative treatment plan involving rest, ice, compression, and elevation as well as NSAIDS and/or acetaminophen for pain (2). With deeper bursitis corticosteroid injections can provide symptomatic relief however, this course of treatment is not recommended for superficial bursa and can delay the diagnosis of another condition such as a tear. Physical therapy is another important treatment method to strengthen the muscles that support the area around the bursa (2). For septic bursitis the typical course of treatment is oral antibiotics as an outpatient but systemic IV antibiotics may be needed if signs of widespread sepsis are present (4). The last line of treatment is surgery which is most often used only as a last resort when all other conservative treatment methods fail (2).

References

1. Chatra PS. Bursae around the knee joints. Indian J Radiol Imaging. 2012 Jan;22(1):27-30. doi: 10.4103/0971-3026.95400. PMID: 22623812; PMCID: PMC3354353.

2. Williams CH, Jamal Z, Sternard BT. Bursitis. [Updated 2021 Aug 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513340/ 

3. Aaron, Daniel L. MD; Patel, Amar MD; Kayiaros, Stephen MD; Calfee, Ryan MD Four Common Types of Bursitis: Diagnosis and Management, American Academy of Orthopaedic Surgeon: June 2011 - Volume 19 - Issue 6 - p 359-367

4. Cea-Pereiro JC, Garcia-Meijide J, Mera-Varela A, Gomez-Reino JJ. A comparison between septic bursitis caused by Staphylococcus aureus and those caused by other organisms. Clin Rheumatol. 2001;20(1):10-4. doi: 10.1007/s100670170096. PMID: 11254233.

 

Hypermobile Ehlers-Danlos Syndrome (hEDS)

Hypermobile Ehlers-Danlos Syndrome

Written by Sarit Dhar with Dr. Nabil Ebraheim

While some people know what Ehlers-Danlos Syndrome (EDS) is, not many know that it is actually a group of 13 different disorders or types. One of the most prevalent types is Hypermobile Ehlers-Danlos Syndrome (hEDS), accounting for 80-90% of EDS cases [1]. The Ehlers-Danlos Syndromes are defined as inherited connective tissue disorders, affecting structural proteins (namely collagen) that leads to joint hypermobility, skin hyperextensibility, and tissue fragility [2]. hEDS is the only EDS subtype that does not have a currently known genetic basis, though it is a hereditary disorder with autosomal dominant inheritance pattern [2]. Therefore, hEDS is in part a diagnosis of exclusion, as genetic testing can be done for the other subtypes. 

The Ehlers-Danlos Syndromes as whole are related to the Joint Hypermobility Spectrum, a spectrum of disorders intended to classify different severities of Hypermobility Spectrum Disorders (HSD). At the most extreme end of the hypermobile spectrum lies hEDS [3]. hEDS differs from the other EDS subtypes in its presentation as well. hEDS includes general joint hypermobility (GJH) but has less severe skin involvement compared to classical or vascular EDS types [1]. Easy bruising and impaired wound healing are also common. The definition of hEDS has evolved to include chronic pain and chronic fatigue as common presentations in those affected by the disease. The current diagnostic criteria include confirmation of GJH using the Beighton scoring system, positive musculoskeletal and pain symptoms or family history, and exclusion of other EDS subtypes or HSDs [4]. 

(Visit this link for the full diagnostic criteria of hEDS)

Apart from acute complications such as dislocation and subluxation, hEDs treatment revolves around chronic pain management and prevention of complications [1]. Acute exacerbations should be treated accordingly using joint reduction techniques and acute pain management. Physical therapy can be used to increase joint stability using low resistance exercises and stretching to increase muscle tone, thereby reducing the chance of acute joint injury. Patients should generally avoid hyperextension and high impact exercise. Oral acetaminophen, NSAIDs, and COX-2 inhibitors can be used as analgesics for chronic pain, as well as after acute injury. Cannabinoids can be considered for chronic pain, but opiates should rarely be used. If an hEDS patient must undergo surgery, careful technique should be used to minimize the wound site and promote healing. In summary, it is important to understand hEDS and how it differs from EDS and other HSDs to properly diagnose and treat patients.

References

1. Tinkle B, Castori M, Berglund B, Cohen H, Grahame R, Kazkaz H, et al. Hypermobile Ehlers-Danlos syndrome (a.k.a. Ehlers-Danlos syndrome Type III and Ehlers-Danlos syndrome hypermobility type): Clinical description and natural history. American Journal of Medical Genetics Part C: Seminars in Medical Genetics. 2017 Feb 1;175(1):48–69.

2. The Types of EDS [Internet]. The Ehlers Danlos Society. 2017. Available from: https://www.ehlers-danlos.com/eds-types/

3. What are the hypermobility spectrum disorders? [Internet]. The Ehlers Danlos Society. 2017. Available from: https://www.ehlers-danlos.com/what-is-hsd/

4. Forghani I. Updates in Clinical and Genetics Aspects of Hypermobile Ehlers Danlos Syndrome. Balkan Medical Journal. 2019 Jan 10;36(1):12–6.

Fractures of the Calcaneus: Everything You Need to Know

Fractures of the Calcaneus: Everything You Need to Know

Written by Dominic Ruwe and Dr. Nabil Ebraheim

Fractures of the calcaneus can be open or closed.¹ Open fractures are more serious than closed fractures.¹ The primary fracture line is caused by an axial load injury.¹ The primary fracture line goes from anterolateral to posteromedial.¹ The primary fracture line divides the calcaneus into two main fragments: the superomedial fragment which is also called the constant or sustentacular (SAS) fragment and the superolateral or tuberosity fragment.¹ The superomedial fragment includes the sustentaculum tali and is stabilized to the talus by ligaments. So, the talus is attached to the constant fragment.¹ The sustentacular fragment is a useful reference point for fracture reduction.² The flexor hallucis longus tendon lies underneath the sustentaculum. If screw placement to the sustentacular fragment is too long, the flexor hallucis longus tendon could be affected, causing fixed flexion of the big toe.³

                The Essex-Lopresti classification system is a useful way to differentiate between different joint fractures. There are two types of Essex-Lopresti fractures: a tongue-type fracture and a joint depression type fracture.¹ In the tongue-type, the posterior facet is attached to the tuberosity. In the joint depression type, the posterior facet is not attached to the tuberosity.⁴ In the tongue-type, the primary fracture line exits anterolaterally and posteromedially.⁵ The secondary fracture line appears beneath the posterior facet and exits posteriorly through the tuberosity.⁵ The superolateral fragment and posterior facet are attached to the tuberosity. The tongue-type fracture can be treated with open reduction and internal fixation.⁶

                In the joint depression type, the primary fracture line splits the calcaneus obliquely through the posterior facet and exits anterolaterally and posteromedially.¹ The secondary fracture line exits superiorly just behind the posterior facet.¹ The posterior facet is a free fragment. The lateral portion of the posterior facet is usually involved and depressed.⁴

The Sander’s classification of calcaneal fractures is used to guide the treatment and predict the outcome of the treatment. This classification system is based on the number of posterior facet fracture fragments seen on a coronal CT scan.⁷ Type I is a nondisplaced fracture which requires nonoperative treatment.⁷ Type II is a two-part fracture of the posterior facet.⁷ Type III is a three-part fracture of the posterior facet.⁷ Type II and III calcaneal fractures benefit from surgery of reduction and fixation.¹ Type III fractures normally result in more arthritis because it has more fracture fragments and may end by fusion.⁸ Type IV fractures are highly comminuted.⁹ They may require primary subtalar arthrodesis.¹

Calcaneal avulsion fractures are typically serious. These types of fractures require urgent reduction and internal fixation to prevent skin complications.¹⁰ In joint depression fractures of the calcaneus, the swelling must go down before surgery. Avulsion fractures of the calcaneus are emergencies, so emergency surgery is performed before the swelling goes down. Open reduction and internal fixation of the calcaneus is generally delayed for 1-2 weeks to allow for improvement of the soft tissue swelling, except with avulsion fractures.¹ Avulsion fractures can cause skin tenting and urgent reduction is recommended.¹⁰

There are many associated conditions with calcaneal fractures. Ten percent are associated with spinal fractures.¹¹ Ten percent are associated with compartment syndrome of the foot.¹² If this is neglected, it will lead to claw toes due to contracture of the intrinsic flexor muscles.¹² Approximately ten percent are associated with bilateral fractures.¹³ Sixty percent are associated with calcaneocuboid joint fractures.¹⁴ Calcaneal fractures may also be associated with peroneal tendon subluxation. Peroneal tendon subluxation may be detected on axial CT scans or it may be seen as an avulsion fracture of the fibula on x-rays.¹⁵

                Complication rates for calcaneal fractures are high. Factors associated with poor outcomes are age greater than 50, smoking, early surgery, history of a fall, heavy manual labor, males, bilateral injury, workman’s compensation, and peripheral vascular disease.^1,16,17 Men do worse with calcaneal fractures than women. Calcaneal fractures in men are normally associated with workman’s compensation, heavy labor, and a 0˚ Bohler angle.¹ These fractures typically need subtalar fusion.¹⁸ Calcaneal fractures in females have a simple fracture pattern. Since calcaneal fractures in males are usually more severe, it follows that better outcomes are seen in females with calcaneal fractures.¹⁹

                The Bohler angle is measured on lateral x-rays.¹ This angle is normally between 20˚-40˚.¹ The Bohler angle is formed by a line drawn from the highest point of the anterior process of the calcaneus to the highest point of the posterior facet and a line drawn tangential to the superior edge of the tuberosity.¹ A decrease in this angle indicates a collapse of the posterior facet.¹ When viewing calcaneal fractures with the Harris view, the calcaneus appears to be shortened and widened with varus.¹ When viewing calcaneal fractures through CT scans, the axial cut shows the calcaneocuboid joint and peroneal tendon subluxation.^1,20 The sagittal view shows the subtalar joint and its depression.²¹ The coronal view shows the displacement of the posterior facet.²² Coronal CT scans can also show the number of the joint fracture fragments.¹ The surgical outcome of calcaneal fractures correlate with the number of the joint fracture fragments and the quality of reduction.¹ MR imaging shows stress fractures of the calcaneus and the integrity of the peroneal tendons.^23,24

Stress fractures of the calcaneus may be misdiagnosed as plantar fasciitis.²⁵ Stress fractures usually occur in female runners.²⁶ It is characterized by swelling and tenderness with medial and lateral compression of the hindfoot during the squeeze test.²⁷ If the X-ray is negative, an MRI should be obtained. The fracture will be seen in T1 MR imaging as a linear streak or a band of low signal intensity in the posterior calcaneal tuberosity.²⁸ In T2 imaging, the signal will be increased.²⁸

                There are several complications with calcaneal fractures. Wound-related complications are the most common complication.²⁹ Wound-related complications occur more in smokers, diabetics, and patients with open fractures.¹ Open fractures of the calcaneus is another common complication. Open fractures of the calcaneus can lead to amputation.³⁰ There is also a high risk of infection with open fractures.³⁰ Grade I and Grade II open fractures have wounds that open medially. Open reduction and internal fixation (ORIF) can be done to treat this complication.³⁰ Open reduction and internal fixation should not be done in Grade III medial wounds and in most lateral wounds.³⁰ Another complication is malunion of the calcaneus.³¹ This is characterized by widening of the heel, varus deformity, and loss of height.³¹ The talus is dorsiflexed, limiting dorsiflexion of the ankle.³¹ Peroneal tendon irritation and impingement from the lateral wall is another complication.³²

                Surgery on the calcaneus decreases the risk of post-traumatic arthritis.³³ Tongue-type and joint depression type fractures may benefit from open reduction and internal fixation.⁶ Subtalar distraction arthrodesis is a good operation to treat calcaneal fractures associated with loss of height and limited dorsiflexion of the ankle.³¹ This operation improves talar inclination and decreases anterior ankle impingement.³¹ Additionally, it takes care of arthritis in the subtalar joint.³¹ Another surgical approach is extensile lateral approach. The lateral calcaneal artery provides blood supply to the lateral flap associated with the calcaneal extensile approach.³⁴ It is important to be aware that the Sural nerve is in the vicinity of the surgical area.³⁵ Delayed wound healing is a common complication in the extensile lateral approach.³⁵

 

References:

1. Trompeter A, Razik A, Harris M. Calcaneal fractures: Where are we now? Strategies in Trauma and Limb Reconstruction. 2017;13(1):1–11.

2. Berberian W, Sood A, Karanfilian B, Najarian R, Lin S, Liporace F. Displacement of the SUSTENTACULAR fragment in INTRA-ARTICULAR CALCANEAL FRACTURES. Journal of Bone and Joint Surgery. 2013;95(11):995–1000.

3. Carr JB. Complications of CALCANEUS fractures entrapment of the Flexor hallucis longus. Journal of Orthopaedic Trauma. 1990;4(2):166–8.

4. Rothberg DL, Yoo BJ. Posterior facet cartilage injury in OPERATIVELY Treated Intra-articular CALCANEUS FRACTURES. Foot & Ankle International. 2014;35(10):970–4.

5. White EA, Skalski MR, Matcuk GR, Heckmann N, Tomasian A, Gross JS, et al. Intra-articular tongue-type fractures of the calcaneus: Anatomy, injury patterns, and an approach to management. Emergency Radiology. 2018;26(1):67–74.

6. Chhabra N, Sherman SC, Szatkowski JP. Tongue-type calcaneus fractures: a threat to skin. The American Journal of Emergency Medicine. 2013;31(7).

7. Jiménez-Almonte JH, King JD, Luo TD, Aneja A, Moghadamian E. Classifications in Brief: Sanders classification OF INTRAARTICULAR fractures of the calcaneus. Clinical Orthopaedics & Related Research. 2018;477(2):467–71.

8. Rammelt S, Marx C. Managing severely malunited calcaneal fractures and fracture-dislocations. Foot and Ankle Clinics. 2020;25(2):239–56.

9. Piovesana LG, Lopes HC, Pacca DM, Ninomiya AF, Dinato MC, Pagnano RG. Assessment of reproducibility of sanders classification for calcaneal fractures. Acta Ortopédica Brasileira. 2016;24(2):90–3.

10. Berringer R. Avulsion fracture of the calcaneus. Canadian Medical Association Journal. 2018;190(45).

11. Rowe CR. Fractures of the os calcis. JAMA. 1963;184(12):920.

12. Myerson Mark, Manoli Arthur. Compartment syndromes of the foot after calcaneal fractures. Clinical Orthopaedics and Related Research. 1993;&NA;(290).

13. Popelka V. Súčasné trendy v liečbe intraartikulárnych zlomenín pätovej kosti [Current Concepts in the Treatment of Intra-Articular Calcaneal Fractures]. Acta Chir Orthop Traumatol Cech. 2019;86(1):58-64. Slovak. PMID: 30843515.14.

14. Kinner B, Schieder S, Müller F, Pannek A, Roll C. Calcaneocuboid joint involvement IN CALCANEAL FRACTURES. Journal of Trauma: Injury, Infection & Critical Care. 2010;68(5):1192–9.

15. Park C-H, Gwak H-C, Kim J-H, Lee C-R, Kim D-H, Park C-S. Peroneal tendon Subluxation and dislocation In CALCANEUS FRACTURES. The Journal of Foot and Ankle Surgery. 2021;60(2):233–6.

16. Su J, Cao X. Can operations achieve good outcomes in elderly patients with SANDERS II–III calcaneal fractures? Medicine. 2017;96(29).

17. Clare MP, Crawford WS. Managing complications of CALCANEUS FRACTURES. Foot and Ankle Clinics. 2017;22(1):105–16.

18. Csizy M, Buckley R, Tough S, Leighton R, Smith J, McCormack R, et al. Displaced Intra-articular CALCANEAL FRACTURES. Journal of Orthopaedic Trauma. 2003;17(2):106–12.

19. Barla J, Buckley R, McCormack R, Pate G, Leighton R, Petrie D, et al. Displaced intraarticular calcaneal fractures: Long-term outcome in women. Foot & Ankle International. 2004;25(12):853–6.

20. Toussaint RJ, Lin D, Ehrlichman LK, Ellington JK, Strasser N, Kwon JY. Peroneal tendon DISPLACEMENT Accompanying INTRA-ARTICULAR CALCANEAL FRACTURES. Journal of Bone and Joint Surgery. 2014;96(4):310–5.

21. Badillo K, Pacheco JA, Padua SO, Gomez AA, Colon E, Vidal JA. Multidetector CT evaluation Of CALCANEAL FRACTURES. RadioGraphics. 2011;31(1):81–92.

22. Buckley R. Displaced fracture of the calcaneus body [Internet]. AO Foundation Surgery Reference. [cited 2021Sep29]. Available from: https://surgeryreference.aofoundation.org/orthopedic-trauma/adult-trauma/calcaneous/displaced-body-fractures/definition

23. Kato M, Warashina H, Kataoka A, Ando T, Mitamura S. Calcaneal insufficiency fractures following ipsilateral total knee arthroplasty. Injury. 2021;52(7):1978–84.

24. Park HJ, Cha SD, Kim HS, Chung ST, Park NH, Yoo JH, et al. Reliability of MRI findings OF PERONEAL Tendinopathy in patients with LATERAL CHRONIC Ankle Instability. Clinics in Orthopedic Surgery. 2010Nov5;2(4):237.

25. Weber JM, Vidt LG, Gehl RS, Montgomery T. Calcaneal stress fractures. Clinics in Podiatric Medicine and Surgery. 2005;22(1):45–54.

26. Labronici P, Pires RE, Amorim L. Calcaneal stress fractures in civilian patients. Journal of the Foot & Ankle. 2021;15(1):54–9.

27. Kiel J, Kaiser K. Stress Reaction and Fractures. 2021 Aug 4. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 29939612.

28. Lawrence DA, Rolen MF, Morshed KA, Moukaddam H. MRI of heel pain. American Journal of Roentgenology. 2013Apr18;200(4):845–55.

29. Ding L, He Z, Xiao H, Chai L, Xue F. Risk factors for postoperative wound complications of calcaneal fractures following plate fixation. Foot & Ankle International. 2013;34(9):1238–44.

30. Heier KA, Infante AF, Walling AK, Sanders RW. Open fractures of THE Calcaneus: Soft-tissue Injury DETERMINES OUTCOME. The Journal of Bone and Joint Surgery-American Volume. 2004;86(11):2569.

31. Guang-Rong Y, Xiao Y. Surgical management Of Calcaneal Malunion. Journal of Orthopaedics, Trauma and Rehabilitation. 2013;17(1):2–8.

32. Davis D, Seaman TJ, Newton EJ. Calcaneus Fractures. 2021 Aug 9. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 28613611.

33. Vilá-Rico J, Ojeda-Thies C, Mellado-Romero MÁ, Sánchez-Morata EJ, Ramos-Pascua LR. Arthroscopic posterior subtalar arthrodesis for salvage of posttraumatic arthritis following calcaneal fractures. Injury. 2018;49.

34. Mehta CR, An VV, Phan K, Sivakumar B, Kanawati AJ, Suthersan M. Extensile lateral versus sinus Tarsi approach For displaced, intra-articular Calcaneal Fractures: A meta-analysis. Journal of Orthopaedic Surgery and Research. 2018;13(1).

35. Buckley R. Extended lateral approach to the calcaneus [Internet]. AO Foundation Surgery Reference. [cited 2021Sep29]. Available from: https://surgeryreference.aofoundation.org/orthopedic-trauma/adult-trauma/calcaneous/approach/extended-lateral-approach-to-the-calcaneus

Olecranon Fractures

Fractures of the olecranon may occur due to a direct blow to the elbow or from a fall onto an outstretched hand. Nondisplaced fractures have less than 2mm of separation and are considered stable. Fracture separation will not increase with elbow flexion. Extensor mechanism is intact and the patient will be able to extend the elbow against gravity. Displaced fractures could be an avulsion, oblique, transverse, comminuted, or dislocated.

Olecranon fracture dislocations can be anterior (transolecranon) or posterior (similar to monteggia fracture dislocation). An examination will show that the patient is unable to extend the elbow with these displaced fracture types. A true lateral view x-ray will clearly show the olecranon fracture. Usually, these fractures are followed by stiffness of the elbow in about 50% of the patients. However, this does not affect the function.

The goal of treatment for olecranon fractures should be restoration of the articular surface, preservation of the continuity of extensor mechanisms, maintain elbow stability, and avoid stiffness of the elbow. Nonoperative treatment is used for nondisplaced fractures and it may be used for some displaced fractures in elderly patients (treat elbow in some flexion with a splint). I would personally use minimally invasive techniques in these patients unless the skin is very bad, or the fracture is very comminuted.

There are three techniques used for surgical treatment: the tension band technique, detach olecranon and reattach triceps, and plate and screw fixation. The tension band technique is only used for transverse fractures with no comminution. K-wires and screws are used, and the surgeon may use either a 6.5mm screw or Kwires for the tension band. When doing the tension band technique, you want to engage the anterior cortex of the ulna. The surgeon should avoid over penetration to avoid affecting the forearm rotation or injuring the anterior interosseous nerve. The surgeon needs to be sure that the pins are not fixing the radius and that after the operation, the patient can perform pronation and supination of the forearm (pull the pins out slightly if needed). The distractive force of the triceps is converted to compression force at the articular surgace, especially when bending the elbow. The drill hole for the K-wire should be positioned about 4-5cm from the fracture which gives enough safe distance so that the fracture will not propagate. Place the tension band wire through the drilled holes before application of the K wires. The surgeon should be sure that the hook to the K-wire is posterior. Make sure that the tension band wire is close to the bone so there is no laxity in the fixation and instability. An intramedullary screw could be used. This screw fixation may need a washer to capture the tension band wire. Intramedullary 6.5mm screw fixation is a reasonable option for fixation but it may need to be supplemented with tension band wires. Never use cancellous screw alone. The tension band technique are for transverse fractures of the olecranon. If fractures comminution is present, change the plan of fixation.

When detaching the olecranon and reattaching the triceps, an excision of the fracture fragment and triceps advancement is used:

• If the fracture is less than 50%
• To treat elderly patients (especially if fracture is comminuted)
• For some nonunions when the fracture is small and cannot be fixed

The surgeon must be sure that the procedure is done with the elbow is stable. If the elbow has ligamentous instability and excision of the fracture fragment is done, this will make the elbow very unstable. The triceps should be attached closer to the articular surface.

Special olecranon plates are available when using a plate and screw fixation technique. The bridge plate and screw fixation technique is used in comminuted, Monteggia, oblique fractures extending to the coranoid, and fracture dislocation. The plate is placed on the tension side of the olecranon (dorsal side). Sometimes, an opening is made through the triceps and the plate is placed against the bone, then suturing the triceps tendon over the plate to avoid hardware prominence.

In summary, if the patient is elderly with a small, comminuted fracture fragment less than 50% of the joint space, excise the fragment, and reattach the triceps tendon to the olecranon. If the olecranon fracture is transverse and proximal to the base of the coranoid process, then use the tension band technique. Use plate fixation for all olecranon fracture scenerios, such comminuted fractures, oblique fractures, unstable fractures, dislocation, or fractures distal to the coranoid process. The typical exam question scenario will discuss a comminuted fracture that should be treated with a plate. You probably need to remove above 20% of the plate fixations due to hardware irritation. Hardware irritation is worse with the tension band surgical treatment (may need to remove in more than 50% of cases).

Anterior Interosseous Nerve- The Benedictine and O.K. Sign

A patient with a complete anterior interosseous nerve injury or a high medial nerve injury should be asked to make a fist. The first and second digits will have difficulty in flexing, while the other digits will flex. The third digit will be weak, while the fourth and fifth digits are normal. This position of the hand is similar to the position taken during a hand blessing. The Benedictine sign is different from an “ulnar claw hand”. Ulnar claw hand refers to damage to the ULNAR nerve and is seen when attempting to extend all the digits (leaving the 4^th and 5^th digits flexed). The O.K. sign is used to check for paralysis of the anterior interosseous nerve due to entrapment or compression injury. A patient with paralysis of the anterior interosseous nerve will be unable to make the O.K. sign. This is due to weakness of the flexor pollicis longus and flexor digitorum profundus muscles. A typical pinch attitude is associated with anterior interosseous nerve injury.

The anterior interosseous nerve arises from the median nerve about 4-6cm distal to the elbow, which is about 1/3 of the way down the forearm. It exits from the anterolateral aspect of the median nerve and it runs between the radius and the ulna on the interosseous membrane between and below the muscles of the flexor digitorum profundus and the flexor pollicis longus.

The anterior interosseous nerve supplies the flexor digitorum profundus muscle for the index and long fingers. It also supplies the flexor pollicis longus and the pronator quadratus muscles. The flexor digitorum profundus muscle for the index and long fingers is supplied by the anterior interosseous nerve. The medial part of the FDP is supplied by the ulnar nerve (FDP has dual innervation). The anterior interosseous nerve passes dorsal to the pronator quadratus with the anterior interosseous artery and provides innervation to the volar wrist capsule. The terminal branch of the anterior interosseous nerve innervates the carpal joint capsule.

In patients with Martin-Gruber Connection, the median nerve, or anterior interosseous nerve to the ulnar nerve in the forearm may present with intrinsic muscle weakness. It may be differentiated also from Parsonage-Turner Synrome (acute brachial plexus neuritis) and patient may have pain in the affected extremity. In anterior interosseous nerve entrapment, the median nerve conduction study result will be normal, however the needle EMG of the anterior interosseous innervated muscles will be abnormal.

Tests Orthopaedic Surgeons Should Think About

There are some important tests that every Orthopaedic Surgeon should think about. This doesn’t mean the tests are needed for every patient. It just means that the physician needs to think about these tests to see if it will benefit the patient or not. Some tests commonly ordered are hemoglobin A1C (HbA1c), Vitamin D25, and C-reactive protein (CRP) & sedimentation rate.

Hemoglobin A1C test are ordered for diabetic patients. HbA1c is a good test for monitoring long-term glucose (sugar) control on patients with diabetes. HbA1c is a percentage of the glycanated hemoglobin relative to the total hemoglobin in the blood. The normal range of HbA1c is 4-6%. More than 7% is high. Another test, the 25-Hydroxy Vitamin D blood test is ordered for patients with osteoporosis, nonunions, fragility fractures, and occasionally in patients with infections. If infection is suspected and the physician needs to monitor the progress of treatment, C-reactive protein (CRP) & sedimentation rate tests should be ordered. A Methicillin-resistant staphylococcus aureus (MRSA) screening should be ordered for patients who could be carriers. Nutritional assessments may be necessary for other patients.

Joints should be aspirated prior to injecting of the joint. The physician should additionally be sure that there is no infection when injecting the joint. A fluid analysis from the joint should be completed. Important vascular studies that can be ordered include: A.B.I., CTA, or a Doppler. Some radiological studies are performed with a dye injection. For example, an MRI of the spine will require gadolinium, while an MRI arthrogram may be used for the hip or shoulder. Tests rarely ordered include: alpha-defensin test (infection); Nicotine/Cotinine test (smoking); Protein S, Protein C, or Factor 5 leiden tests. There are some special tests and precautions that must be taken for patients with epilepsy. It is important that the physician does not perform a procedure if the epilepsy is not controlled. It is important to know that anti-epileptic medication can interfere with vitamin D metabolism in the liver.

Patients on anticoagulation medications should be monitored, especially patients with atrial fibrillation, which makes the orthopaedic procedure more complicated. You want to give the patient anticoagulation, but not encroaching on the management of atrial fibrillation. Patients with a short or thick neck, or a history of sleep apnea, may need additional sleep studies before surgery and may need special precautions after surgery. Sleep apnea will affect the post-operative care of the patient. The physician should avoid ordering unnecessary tests and focus on ordering the most important tests. Orthopaedics deal with concepts and every condition will have a reasonable way of diagnosing it and a reasonable way of treating it.  

Adhesive Capsulitis, Frozen Shoulder

Adhesive Capsulitis, or frozen shoulder, is a painful progressive loss of shoulder motion. It affects both active and passive movement of the shoulder joint. The shoulder will be stiff and painful and occurs due to inflammation, fibrosis, scarring, and contraction of the capsule. A normal shoulder joint capsule is elastic and allows great range of motion. Inflammation and thickening of the shoulder capsule and may lead to adhesive capsulitis. Frozen shoulder may occur without any specific cause, however it may be triggered by a mild trauma to the shoulder.

This condition develops slowly and goes through three phases:

1. Pain and freezing
2. Stiffness or frozen
3. Resolution

During the pain and freezing phase, the pain is worse at night and increases with any movement. This phase will last several months. During the second phase, range of motion is limited as pain is diminishing. This may last up to one year. The resolution phase may begin overtime and may last up to three years.

Conditions associated with frozen shoulder include:

• Diabetes
• Thyroid problems
• Auto immune disease
• Stroke
• Rheumatoid arthritis
• Trauma or post-surgery

A patient with frozen shoulder will have loss of both active (movement without assistance) and passive (movement with assistance) motion. External rotation of the shoulder is very limited and the condition is self-limiting and may resolve on its own. X-rays are needed to rule out degenerative arthritis.  An MRI or arthrogram will show small fluid in joint cavity. Rotator cuff may be normal and synovitis and narrowing of the rotator cuff interval is usually seen.

Treatment consists of anti-inflammatory medications, physical therapy, injections, and manipulation under anesthesia. Surgery will be done in the form of a release of the capsule when nonoperative methods fail. The physician should always check the patient for diabetes.  

Anatomy of the Posterior Cutaneous Nerve of the Thigh

The posterior cutaneous nerve of the thigh (small sciatic nerve) arises from the sacral plexus from S1-S3. The posterior cutaneous nerve of the thigh exits from the pelvis through the greater sciatic notch below the piriformis muscle. The nerve descends below the gluteus maximus muscle along with the inferior gluteal artery. It runs into the back of the thigh beneath the fascia lata and over the long head of the biceps femoris muscle to the back of the knee. The nerve then pierces the deep fascia and accompanies the short saphenous vein to the middle of the back of the leg. The posterior cutaneous nerve of the thigh innervates the distal part of the gluteal region, the skin of the perineum and the posterior part of the thigh.

The nerve can become compressed when passing through the tunnel below the piriformis muscle and under the gluteus maximus muscle. This may result in sensitivity disturbances of the innervation area of the nerve. Causes of the syndrome may be hypertrophy or abnormality of the piriformis muscle such as entrapment below the piriformis which compresses the nerve. Compression of the nerve can also occur due to prolonged sitting. During the clinical examination, pain and sensitivity will be evident. Pain and sensitivity disturbances are characteristic of the nerve distribution site in the posterior part of the thigh down the knee. This disturbance can be from hyperesthesia to hypoesthesia or burning sensation similar to meralgia paresthetica of the lateral cutaneous nerve of the thigh.

Differential diagnosis include piriformis syndrome. The patient should avoid sitting for long periods of time, especially on a hard base. Treatment consists of physical therapy, massage, and injection. Surgery is rarely needed.

SLAP Tear- Symptoms, Diagnosis, and Treatment

A SLAP tear is a tear that occurs where the biceps tendon inserts into the superior labrum. A SLAP tear is different from a Bankart lesion. SLAP tears are not common and can be hard to diagnose. Symptoms of a SLAP tear include: pain deep within the shoulder or in the back of the shoulder, as well as catching, popping, or clicking sensations. The patient may also experience pain when throwing a ball with a decrease in velocity and the feeling of having a dead arm after pitching. Patients will also experience pain with overhead activity which mimics impingement syndrome. This typically affects throwing athletes. When the biceps tendon is involved, pain may also be located at the front of the shoulder. A SLAP tear can be an isolated lesion or it can be associated with internal impingement, articular sided cuff tear, or instability.

A SLAP tear is diagnosed with a clinical examination and testing. The O’Brien’s test is the most commonly used test. Multiple tests are usually used including the anterior slide test and the clunk test. An MRI with contrast is the best imaging technique. When performing the O’Brien’s test, the patient is standing or sitting with the arm at 90° of flexion, 10° of adduction, and full internal rotation with the forearm pronated.  The examiner applies pressure to the forearm and instructs the patient to resist the applied downward force. Pain at the shoulder joint suggests a SLAP lesion. Decrease in pain of the shoulder joint on supination of the arm is suggestive of a SLAP tear.

Treatment consists of physical therapy, anti-inflammatory medications, injections, and surgery (when conservative treatment fails). If surgery is necessary, a labral debridement will be performed for minor tearing and fraying. Biceps Tenodesis is becoming popular, as it is a procedure that cuts the biceps tendon where it attaches to the labrum and reinserts it in another area, usually in front of the shoulder. A biceps tenotomy is a procedure that cuts the biceps tendon from the glenoid, releasing the long head of the biceps tendon from its attachment allowing it to fall into the upper arm out of the shoulder joint. A biceps tenotomy is probably best suitable for some elderly patients. A SLAP repair is a procedure which uses sutures to anchor the torn labrum to the glenoid. This repair is usually done for athletes and patients under the age of 40 years.

Massive Rotator Cuff Tear

To view my Youtube video, 'Massive Rotator Cuff Tear- Classic', click here.

Massive rotator cuff tears are a disabling problem. These tears can cause pain, weakness, and sometimes swelling of the shoulder. The rotator cuff consists of four muscles that function to stabilize the shoulder joint: supraspinatus rotator cuff tendon, subscapularis tendon, infraspinatus rotator cuff tendon, and the teres minor rotator cuff tendon. The supraspinatus tendon is the most common of the rotator cuff tendons to become ruptured. Massive tears of the rotator cuff that are greater than 5cm usually involving both the supraspinatus and infraspinatus tendons.

Massive tears of the rotator cuff are defined as tears greater than 5cm, usually involving both the supraspinatus and infraspinatus tendons. Retraction of the rotator cuff tendons along with muscle atrophy and fatty infiltration can occur. This makes surgical reconstruction difficult with the surgical outcome being unpredictable and less than satisfactory.

Treatment varies from physiotherapy to replacement of the humeral head. Arthroscopic or open repair is usually the selected treatment. Reconstruction can be done in selected cases. A rotator cuff arthropathy is performed on massive cuff tears that are associated with superior migration of the humeral head as well as instability and arthritis of the shoulder. The patient will have pseudoparalysis and an x-ray will show shift of the humerus proximally. An MRI will show massive cuff tear with retraction at the level of the glenoid with atrophy of the muscle and fatty infiltration. A reverse shoulder is the treatment of choice for the elderly with rotator cuff arthropathy as it improves the pain and function. Hemiarthroplasty is the treatment for younger patients. A standard head or a big humeral head can be selected.

A patient with a massive tear of the cuff usually develops weakness of the shoulder and becomes unable to actively lift the arm without assistance. Fluid collection within the shoulder may occur with a massive tear of the rotator cuff.