Lower Spine and Lower Extremity Physical Examination

Written by Travis Brege with Dr. Nabil Ebraheim

The steps of any orthopedic examination will follow the pattern of inspection, palpation, range of motion, and tests of strength for the key groups of muscles applying all the appropriate provocative tests and neurovascular examinations. 

First, in the inspection of the spine, look for any visible deformities in the coronal (frontal) and sagittal (longitudinal) planes. In the coronal plane, check for scoliosis and pelvic obliquity1. In the sagittal plane, check for normal cervical lordosis, thoracic kyphosis, and lumbar lordosis2. While assessing the symmetry of the whole body, make sure to assess the skin for lesions, hairy patches, dimples, surgical scars, muscular atrophy, and anything else that may be abnormal.

Next, you want to palpate the iliac crests, posterior superior iliac spines, spinous processes, sacrum, trochanters, and ischial tuberosities. Palpate the soft tissue as well, assessing trigger points such as the gluteus muscles, piriformis, and sciatic nerve. 

Assess the patient’s movement first with their gait as certain gaits may indicate various pathologies (ie. antalgic, Trendelenburg, steppage, and staggering gaits)3. Then, check the movements of the lower spine to identify if any causes pain; for example, extension of the spine creates pain in lumbar stenosis4, while spinal flexion can create pain when a disk pathology is present5.

Now, we can assess the individual nerve roots from L2-S1 using sensory and motor testing, reflex tests, specific provocative tests, and check for Waddell Signs. 

In sensory testing, the areas that can be assessed include pain, light touch, temperature, and proprioception (awareness of the position of one’s body). Sensory testing can indicate a spinal root pathology in the presence of a dermatomal pattern of dysfunction, or it can suggest a neuropathy in the presence of a glove-and-stocking distribution of sensory dysfunction6. The specific pattern of sensory distribution in the lower extremities can be normal, impaired, or completely absent in some cases. 

In motor testing, the action of hip flexion comes largely from the iliopsoas muscle, which is innervated by the L1, L2, and L3 lumbar nerve roots. Hip abduction is completed through the L2, L3, and L4 lumbar nerve roots. Knee extension is innervated by the L2, L3, and L4 lumbar nerve roots. Dorsiflexion is largely performed via the tibialis anterior muscle which is innervated by the L4 lumbar nerve root. Extension of the hallux is mainly innervated by the L5 lumbar nerve root. Ankle plantarflexion is performed using the gastro-soleus complex whose main innervation is from the S1 sacral nerve root7. 

For reflexes, only two exist in the lower extremity that are utilized in physical examination. The Patellar Reflex which is innervated by the L4 lumbar nerve root, and the Achilles Tendon Reflex which is innervated by the S1 sacral nerve root7. 

Provocative and special tests can be used to help differentiate between musculoskeletal pathology and spinal pathology. These include the Straight Leg Raising Test for L5-S1 nerve root irritation8 and the Femoral Stretch Test for L3-L4 nerve root irritation9. Upper motor neuron lesions can be identified or ruled out utilizing the Clonus Test10 and the Babinski Test11. The Bulbocavernosus Reflex can be utilized to detect spinal shock12. The Faber (Flexion, ABduction, External Rotation) Test is a good test for assessing the sacroiliac joint, but it is NOT confirmatory13,14. Sacroiliac joint test is usually confirmed by the injection of an anesthetic with a positive response for reduction of pain15.

Waddell’s Signs are controversial, however, assessing for these signs can be included as a part of a thorough physical examination for a patient that presents with lower back pain. Waddell’s Signs include: (1) superficial tenderness, (2) non-anatomical tenderness (tenderness that exists over a wide area that goes beyond a single anatomical boundary), (3) axial loading pain on the patient’s head that elicits low back pain, (4) acetabular rotation causing low back pain, (5) distracted straight leg discrepancy, (6) regional sensory disturbances, (7) regional muscle weakness that can’t be explained on an anatomical basis, and (8) overreaction to a pain stimulus that isn’t reproduced when the same provocation is applied at a later time16.

 

References

1. Janicki JA, Alman B. Scoliosis: Review of diagnosis and treatment. Paediatr Child Health. 2007 Nov;12(9):771-6. doi: 10.1093/pch/12.9.771. PMID: 19030463; PMCID: PMC2532872. 

2. Scheer JK, Tang JA, Smith JS, Acosta FL Jr, Protopsaltis TS, Blondel B, Bess S, Shaffrey CI, Deviren V, Lafage V, Schwab F, Ames CP; International Spine Study Group. Cervical spine alignment, sagittal deformity, and clinical implications: a review. J Neurosurg Spine. 2013 Aug;19(2):141-59. doi: 10.3171/2013.4.SPINE12838. Epub 2013 Jun 14. PMID: 23768023. 

3. Lim MR, Huang RC, Wu A, Girardi FP, Cammisa FP Jr. Evaluation of the elderly patient with an abnormal gait. J Am Acad Orthop Surg. 2007 Feb;15(2):107-17. doi: 10.5435/00124635-200702000-00005. PMID: 17277257.

4. Katz JN, Harris MB. Clinical practice. Lumbar spinal stenosis. N Engl J Med. 2008 Feb 21;358(8):818-25. doi: 10.1056/NEJMcp0708097. PMID: 18287604.

5. Kuai S, Liu W, Ji R, Zhou W. The Effect of Lumbar Disc Herniation on Spine Loading Characteristics during Trunk Flexion and Two Types of Picking Up Activities. J Healthc Eng. 2017;2017:6294503. doi: 10.1155/2017/6294503. Epub 2017 Jun 11. PMID: 29065628; PMCID: PMC5485332.

6. Scott K, Kothari MJ. Evaluating the patient with peripheral nervous system complaints. J Am Osteopath Assoc. 2005 Feb;105(2):71-83. doi: 10.7556/jaoa.2005.105.2.71. PMID: 15784929.

7. Basit H. Anatomy, Back, Spinal Nerve-Muscle Innervation [Internet]. StatPearls [Internet]. U.S. National Library of Medicine; 2021 [cited 2021Oct25]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538322/?report=classic

8. Capra F, Vanti C, Donati R, Tombetti S, O'Reilly C, Pillastrini P. Validity of the straight-leg raise test for patients with sciatic pain with or without lumbar pain using magnetic resonance imaging results as a reference standard. J Manipulative Physiol Ther. 2011 May;34(4):231-8. doi: 10.1016/j.jmpt.2011.04.010. Epub 2011 May 5. PMID: 21621724.

9. Suri P, Rainville J, Katz JN, Jouve C, Hartigan C, Limke J, Pena E, Li L, Swaim B, Hunter DJ. The accuracy of the physical examination for the diagnosis of midlumbar and low lumbar nerve root impingement. Spine (Phila Pa 1976). 2011 Jan 1;36(1):63-73. doi: 10.1097/BRS.0b013e3181c953cc. PMID: 20543768; PMCID: PMC2978791.

10. Zimmerman B, Hubbard JB. Clonus. 2021 Aug 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 30521283.

11. van Gijn J. The Babinski reflex. Postgrad Med J. 1995 Nov;71(841):645-8. doi: 10.1136/pgmj.71.841.645. PMID: 7494766; PMCID: PMC2398330.

12. Ko HY. Revisit Spinal Shock: Pattern of Reflex Evolution during Spinal Shock. Korean J Neurotrauma. 2018 Oct;14(2):47-54. doi: 10.13004/kjnt.2018.14.2.47. Epub 2018 Oct 31. PMID: 30402418; PMCID: PMC6218357.

13. Cattley P, Winyard J, Trevaskis J, Eaton S. Validity and reliability of clinical tests for the sacroiliac joint. A review of literature. Australas Chiropr Osteopathy. 2002 Nov;10(2):73-80. PMID: 17987177; PMCID: PMC2051080.

14. Nejati P, Sartaj E, Imani F, Moeineddin R, Nejati L, Safavi M. Accuracy of the Diagnostic Tests of Sacroiliac Joint Dysfunction. J Chiropr Med. 2020 Mar;19(1):28-37. doi: 10.1016/j.jcm.2019.12.002. Epub 2020 Sep 12. PMID: 33192189; PMCID: PMC7646135.

15. Jung MW, Schellhas K, Johnson B. Use of Diagnostic Injections to Evaluate Sacroiliac Joint Pain. Int J Spine Surg. 2020 Feb 10;14(Suppl 1):30-34. doi: 10.14444/6081. PMID: 32123655; PMCID: PMC7041665.

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.

 

 

               

Neck Pain Causes and Treatment -Everything You Need to Know

Written by Katherine Esser and Dr. Nabil Ebraheim

Neck pain is a common ailment of the American population, affecting 30 to 50% of adults annually¹. While there are numerous etiologies of neck pain, this is a brief review of the more common causes and modes of treatment².

Firstly, radiculopathy from disc herniation. In addition to neck pain, the patient will complain of arm pain that typically follows a myotomal pattern, and sensory symptoms (like burning and tingling) that follow a specific dermatome in the hand³. There may also be motor weakness of the upper extremity³. This is due to compression of a nerve root either by a disc herniation or by arthritis that narrows the foramen². A neurological exam assessing motor, sensory and reflex testing should be done to determine cervical spine disc herniation. Treatment should first be non-surgical with anti-inflammatory medication, isometric exercises, physical therapy, and muscle relaxants². An MRI should be ordered if symptoms do not improve after 6-12 weeks of conservative treatment. If there is an indication for surgery, it often involves decompression and fusion of the involved disc space. 26% of patients with cervical radiculopathy require surgery³.

Secondly, neck pain may be due to cervical myelopathy. This is the most common cause of non-traumatic spinal cord dysfunction⁴. It is due to direct compression of the spinal cord or surrounding blood vessels, and presents in a variety of ways clinically⁴. Indications of cervical myelopathy are an unstable and wide-based gait, clumsiness of the hands, occipital headaches, and discomfort of the neck². The pain may not be severe, but insidious, gradual, and poorly characterized. An MRI may be ordered which will show compression of the spine^2. Due to the slow, stepwise deterioration in cervical myelopathy, each stage may be treated differently⁴. There is conflicting evidence regarding the conservative versus surgical approach to treatment of cervical myelopathy. The goal for surgery is cord decompression with expansion of the spinal canal, restoration of cervical lordosis, and stabilisation if the risk of cervical kyphosis is high⁴. The evidence suggests mild cervical myelopathy should be treated conservatively with careful observation, whereas surgical intervention should be employed for moderate to severe cases⁴.

Thirdly, neck pain may be due to a whiplash injury. This is the most common traumatic cause of neck pain⁵. Specifically, neck hyperreflexia and neck pain after a car collision from behind. Pain may refer to the head, shoulder, or arm. There are usually no neurological deficits. The patient will have a soft tissue injury and an x-ray will show cervical lordosis due to muscle spasm. Treatment for a whiplash injury is aggressive physical therapy and mobilization.

Cervical spondylosis may also cause neck pain. This is arthritis of the spine. It is a natural degenerative process of cervical spine which will be shown on X-Ray. Degenerative changes start in the intervertebral discs with osteophyte formation and involvement of soft tissue structures. It is important to note many people over 30 years of age display similar abnormalities on imaging of the cervical spine and it may be difficult to delineate normal aging and disease. Cervical spondylosis can be diagnosed clinically based on characteristic exacerbation by neck movement. Although pain is focused in the cervical area, it is also referred to a wide area⁶. Cervical spondylosis should be managed medically and surgery should only be done if there is instability or neurological deficit³. In fact, there is evidence that suggests various exercise regiments may be more effective than usual medicinal care (analgesics, muscle relaxants) or stress management⁶.

While there are various pathologies to include in the differential of neck pain, typically, patients with neck pain will have no injury. Pain will be in the posterior neck, tender to palpation with no radiation to the arm, no neurological deficits, and an X-Ray will show mild arthritis. Often, patients will be prescribed anti-inflammatory medication and referred to physical therapy.

 

References

1.       Goode AP, Freburger J, Carey T. Prevalence, practice patterns, and evidence for chronic neck pain. Arthritis Care Res (Hoboken). 2010 Nov;62(11):1594-601. doi: 10.1002/acr.20270. Epub 2010 Jun 2. PMID: 20521306; PMCID: PMC2974793.

          Ebraheim N. Neck pain causes and treatment - everything you need to know - Dr. Nabil Ebraheim [Internet]. YouTube. YouTube; 2021 [cited 2021Nov24]. Available from: https://www.youtube.com/watch?v=bwM5uskViJ4&ab_channel=nabilebraheim

3.       Wong JJ, Côté P, Quesnele JJ, Stern PJ, Mior SA. The course and prognostic factors of symptomatic cervical disc herniation with radiculopathy: a systematic review of the literature. Spine J. 2014; 14(8):1781-9.

4.       Bakhsheshian J, Mehta VA, Liu JC. Current Diagnosis and Management of Cervical Spondylotic Myelopathy. Global Spine J. 2017 Sep;7(6):572-586. doi: 10.1177/2192568217699208. Epub 2017 May 31. PMID: 28894688; PMCID: PMC5582708.

5.       MacDermid JC, Walton DM, Bobos P, Lomotan M, Carlesso L. A Qualitative Description of Chronic Neck Pain has Implications for Outcome Assessment and Classification. Open Orthop J. 2016 Dec 30;10:746-756. doi: 10.2174/1874325001610010746. PMID: 28217199; PMCID: PMC5301418.

6.       Binder AI. Cervical spondylosis and neck pain. BMJ. 2007 Mar 10;334(7592):527-31. doi: 10.1136/bmj.39127.608299.80. PMID: 17347239; PMCID: PMC1819511.

 

ACL Ganglion Cyst, Meniscal Cyst, Baker Cyst - Everything You Need to Know

ACL Ganglion Cyst, Meniscal Cyst, Baker Cyst - Everything You Need to Know

Written by Ali Mahmoud with Dr. Nabil Ebraheim

 There are many cysts that can occur in and around the knee joint. These types of cysts include an anterior cruciate ligament (ACL) ganglion cyst, meniscal cyst, and baker’s cyst.

Ganglion cysts contain yellow viscous fluid surrounded by a thin capsule, and are considered rare when associated with the ACL (1). Theorized pathogenesis of an ACL ganglion cyst includes synovial tissue herniation, post-traumatic mucoid degeneration mediated by local release of hyaluronic acid, ectopic synovial tissue theory, and displacement of synovial fluid during embryogenesis. These cysts are often discovered during knee MRI or knee arthroscopy while evaluating symptoms of knee pain or limited knee motion. There are no defining symptoms of ACL ganglion cysts, but they should be suspected in patients with knee pain or limited range of motion in their knees. MRI’s are the gold standard for diagnosing ACL ganglion cysts, with the diagnostic criteria being a fluid signal in the substance of the ligament with two of the following three criteria: 1) mass effect on ACL fibers, 2) lobulated margins, and 3) ACL fluid disproportionate to the joint. The treatment of choice for an ACL ganglion cyst is an arthroscopic decompression with debridement of the cyst for instant relief of pain, range of motion improvement, and return to physical activities. In cases where arthroscopic decompression is not available, aspiration under CT or ultrasound have shown excellent results in treating these cysts. These cysts do not recur after resection (2).

Meniscal cysts are believed to occur when the meniscal fibrocartilage tears, allowing synovial fluid to extrude through the meniscal tear and become encysted. Meniscal cysts can be classified into 3 subtypes: parameniscal, intrameniscal, and synovial. Parameniscal cysts appear on MRI as a loculated fluid-intensity lesion with a clear connection to the adjacent meniscus (4). Intrameniscal cysts appear as an abnormally increasing signal within an enlarged meniscus. Synovial meniscal cysts are cystic outpouchings of the joint capsule that are not associated with trauma. They are frequently asymptomatic, and are found incidentally on MRIs performed to assess for other knee pathologies. Symptomatic meniscal cysts can be treated with arthroscopic resection and repair of the causative meniscal tear (3).

Baker’s cyst (popliteal cyst) is the most common cyst in the knee (3). These are fluid-filled lesions arising in the popliteal fossa as an enlargement of the gastrocnemio-semimembranosus bursa. These cysts can expand into the spaces between muscle and knee capsule. Rarely, they can extend into nearby muscles such as the vastus medialis muscle and the head of the gastrocnemius muscle (6). Complications of a Baker’s cyst include rupture, hemorrhage and infection. Most Baker’s cysts are asymptomatic, but larger ones may cause nerve entrapment, compress nearby veins, or limit knee range of motion (3). Cysts that rupture can cause symptoms similar to phlebitis (5). They can be visualized on MRI along with any associated pathology that is causing the cyst, such as arthritis or meniscal tear. They can be treated conservatively with rest, ice, and anti-inflammatory medications. They can also be treated with aspirations, steroid injections or surgical excisions. If an intra-articular pathology is present that is causing the cyst, then treatment with arthroscopy and debridement of the pathology is recommended to prevent recurrence of the Baker’s cyst.

 

Citations

1.       Plotkin B, Agarwal VK, Varma R. Ganglion Cyst of the Anterior Cruciate Ligament. Radiology Case Reports. 2009;4(3):1-4.

2.       Vaishya R, Esin Issa A, Agarwal AK, Vijay V. Anterior Cruciate Ligament Ganglion Cyst and Mucoid Degeneration: A Review. Cureus. 2017 Sep 13;9(9):e1682. doi: 10.7759/cureus.1682. PMID: 29152439; PMCID: PMC5679775.

3.       Telischak NA, Wu JS, Eisenberg RL. Cysts and cystic-appearing lesions of the knee: A pictorial essay. Indian J Radiol Imaging. 2014 Apr;24(2):182-91. doi: 10.4103/0971-3026.134413. PMID: 25024531; PMCID: PMC4094974.

4.       Crowell MS, Westrick RB, Fogarty BT. Cysts of the lateral meniscus. Int J Sports Phys Ther. 2013 Jun;8(3):340-8. PMID: 23772349; PMCID: PMC3679639.

5.       Handy JR. Popliteal cysts in adults: a review. Semin Arthritis Rheum. 2001 Oct;31(2):108-18. doi: 10.1053/sarh.2001.27659. PMID: 11590580.

6.       Li TY. The Sonographic Spectrum of Baker Cysts. Journal of Diagnostic Medical Sonography. 2017 Sep 9;34(1):38-48. doi: 10.1177/8756479317733750. 

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.

Chronic Exertional Compartment Syndrome

Chronic Exertional Compartment Syndrome

Written by Jonathan Hunyadi with Dr. Nabil Ebraheim

Chronic exertional compartment syndrome (CECS) a pathology in runners usually involving the anterior compartment of the leg. It is believed to result from swelling and hypoperfusion of muscle and nerve during physical activity. Patients typically present with anterior burning leg pain that is exacerbated by exercise and is greatly reduced or completely subsides 15 to 30 minutes after exercise.

The condition can be diagnosed by measuring the pressure of the affected compartment one and five minutes after exercise. A pressure of 30 mmHg one minute and a pressure of 20 mmHg five minutes after exercise is considered diagnostic. Patients with CECS usually have a resting intra-compartment pressure greater than 15 mmHg which greatly increases during running. This typically produces a burning, cramping or aching pain after about 10 minutes of running resulting in cessation of exercise. Additionally, patients sometimes report tingling over the dorsal aspect of the foot while running.

Patients often present following stretching and strengthening therapy without relief. On physical exam, the patient will present with diffuse, nonspecific tenderness over the anterolateral leg without focal tenderness over bone. Pulses and x-ray will be normal and bone scan or MRI will be negative for stress fractures. Classic findings of acute compartment syndrome such as pain with passive toe dorsiflexion and sensory loss in the first web space, are typically absent.

Following diagnosis, treatment consists of the surgical release of affected compartments. During lateral compartment release, the superficial peroneal nerve, which pierces the fascia 10cm to 12cm proximal to the tip of the lateral malleolus, must be avoided. Surgical fasciotomy is usually successful but with a relatively high recurrence rate of approximately 20%. Recurrence typically occurs around two years following the initial procedure and is due to fibrosis within the compartment, causing return of symptoms and potential nerve entrapment. Additional causes of recurrences are inadequate release, failure to recognize and release all compartments, and misdiagnosis.

The differential diagnosis for CECS is large with overlap of symptoms. A common example is medial tibial stress syndrome. With this condition, bony tenderness along the posteromedial tibia will be present. Popliteal artery entrapment, a dynamic exercise related vascular phenomenon, is another condition in the differential. CECS can be distinguished by its predictable exercise related onset, relief of symptoms at rest and by being present for a long time.

Nerve Injury Positions of the Hands and Fingers

Nerve Injury Positions of the Hands and Fingers

Written by: Alec Bryson with Dr. Nabil Ebraheim

 The presentation of a patient’s hand may provide insight to which nerve is damaged and the approximate location of the damage. When presenting with ulnar n. damage, a patient may show a claw hand, Wartenberg’s sign, or Froment’s sign. Claw hand will present with clawing of the fourth and fifth digits due to the inability to extend the fingers specifically at the interphalangeal joints. This presentation is due to the lack of innervation to the intrinsic muscles of the hands, and the unopposed action of the flexor digitorum profundus m. (Moore et al., 2018). This indicates damage near the distal end of the ulnar n., below the elbow, and potentially near the wrist. Wartenberg’s sign will be seen as the inability to adduct the fifth digit when extended as well as an inability to cross the second and third digit. This is due to ulnar n. injury leading to wasting of the fifth interosseous m. This causes the fifth digit to rest in a more abducted position due to the unbalanced action of the extensor digiti minimi m. (Ebraheim, 2021). There will also be loss of function of the lumbrical m. in the fourth and fifth digits. A Froment’s test will detect palsy of the ulnar n. resulting from compression in the cubital tunnel. When asking the patient to pinch a piece of paper between their thumb and second digit, a positive Froment’s Sign will show as the patient flexing their thumb’s interphalangeal joint to grip the paper as the paper is pulled away (Attum, 2021). This will result from a weak adductor pollicis m. due to ulnar n. palsy. 

Depending on the location of a lesion to the median n., the patient will present with one of three signs. A positive Benedictine sign will be caused by proximal median n. damage. It will be seen as paralysis of the first and second digit, with weakness to the third digit. A proximal lesion would lead to paralysis of several muscles (FDS, FPL, FPB, and the radial half of FDP), leaving the ulnar half of the flexor digitorum profundus m. as the only remaining flexor (Ebraheim, 2021). When the patient is asked to make a fist, the hand will resemble the similar position taken during a blessing. A positive Benedict sign will also resemble the ulnar claw hand. However, the Benedict sign will present when the patient is flexing, not extending the fingers (Ebraheim, 2021). A median n. injury affecting the anterior interosseous n. branch will present as an inability to do the OK sign. This occurs due to paralysis of the flexor pollicus longus m. and the lateral part of the flexor digitorum m. (Moore et al., 2018). A positive Ape hand (Simian hand) is caused by paralysis of only the thenar m. from damage to the recurrent branch of the median n. to the thenar m. The thumb will be seen in the same plane as the other digits due the thumb being pulled more dorsal by the action of the adductor pollicis m., which is innervated by the ulnar n. (Moore et al., 2018). 

Finally, proximal radial n. damage will be seen as wrist drop. This is usually caused by fractures of the distal third of the humeral shaft (Holstein-Lewis Fracture) and caused paralysis of the wrist and fingers extensors (Ebraheim, 2010). Lower radial n. injury will present in the patient as the ability to extend the wrist, but the loss of finger extension. There will be no wrist drop, but the patient would not be able to make a hitchhiking sign.

Reference List

1. Attum B. Physical exam of the hand [Internet]. Orthobullets. Lineage Medical, Inc.; 2021 [cited 2021Oct21]. Available from: https://www.orthobullets.com/hand/6008/physical-exam-of-the-hand

2. Ebraheim N. Anterior Interosseous Nerve Injury - Everything You Need To Know - Dr. Nabil Ebraheim [Internet]. YouTube. 2021 [cited 2021Oct21]. Available from: https://www.youtube.com/watch?v=M9y-iDKLDPE

3. Ebraheim N. Claw Hand, Ulnar Claw Hand - Everything You Need To Know - Dr. Nabil Ebraheim [Internet]. YouTube. 2017 [cited 2021Oct21]. Available from: https://www.youtube.com/watch?v=GyqaKGg3HmM

4. Ebraheim N. Nerve Injury Position of the Hand & Fingers - Everything You Need To Know - Dr. Nabil Ebraheim [Internet]. YouTube. 2021 [cited 2021Oct21]. Available from: https://www.youtube.com/watch?v=nwd1h0Dfo5o

5. Ebraheim N. Radial Nerve Palsy, injury - WRIST DROP . Everything You Need To Know - Dr. Nabil Ebraheim [Internet]. YouTube. 2010 [cited 2021Oct21]. Available from: https://www.youtube.com/watch?v=_Cu6ttAhe8Y

6. Moore KL, Dalley AF, Agur A. Clinically Oriented Anatomy. 8th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2018.

 

Tennis Elbow - Everything You Need to Know

Tennis Elbow

Written by Devon Patel with Dr. Ebraheim

Lateral epicondylitis, also known as tennis elbow, is an overuse injury that results in inflammation, tendinosis, and lateral elbow pain. It is the most common cause of pain in the lateral elbow, affecting between 1 and 3% of the general population (1). The primary structure impacted in tennis elbow is the extensor carpi radialis brevis, which originates at the lateral epicondyle (2). This condition is primarily seen in middle-aged individuals, especially those between the ages of 40 and 50 (3). Tennis players (up to 50% of regular players) and workers who engage in heavy lifting or repetitive gripping are more likely to develop tennis elbow (2). Other conditions, such as rotator cuff pathology or De Quervain’s diseases, and lifestyle factors, such as smoking, are associated risk factors for lateral epicondylitis (4). Rotator cuff pathology could be a risk factor because lateral epicondylitis can also be caused by biomechanical stress, but it is unclear exactly why it and other conditions are associated with each other (4). In terms of histology, disorganized collagen, dense fibroblasts, and vascular hyperplasia are primarily seen (2). Immature fibroblastic and vascular infiltration of the origin of the extensor carpi radialis brevis has consistently been identified during surgery (5). A physical exam and history are typically used to diagnose this condition. Clinical tests to assist in diagnosis include grip strength, Cozen’s, Maudsley’s, and Mill’s tests (3). Lateral epicondylitis is indicated if the previous tests are positive along with reduced grip strength or reproduced pain (3). If necessary, diagnostic scans can be obtained. Majority of patients show altered signal around the lateral epicondyle on MRI scans and hot focus on infrared thermography (6, 7). Radial tunnel syndrome is a differential diagnosis of tennis elbow. This syndrome is seen in 5% of patients who have compression of the posterior interosseous nerve. The pain associated with radial tunnel syndrome is approximately 3-4 cm distal and anterior to the lateral epicondyle, which differentiates it from tennis elbow.

Non-surgical treatments are the primary mode of treatment and there is a 95% success rate with treatments to relieve pain. The most frequently used treatment is corticosteroid injection (2). Oral or topical non-steroidal anti-inflammatory drugs (NSAIDs) can also be prescribed, but their effectiveness is variable (8). Patients can also undergo physical therapy to relieve their symptoms. Eccentric exercises have been shown to be especially effective in pain management (9). Using an inelastic, nonarticular proximal forearm brace could also be recommended (10). Two relatively newer treatments for tennis elbow are ultrasonic (US) and extracorporeal shock wave therapy (ESWT). There are minimal side effects to US and ESWT, thus making them preferable for patients and clinicians (11). Even though there is no difference between US and ESWT in elbow function evaluation scores, ESWT has been shown to have greater efficacy in pain relief (12). Surgical procedures are a last resort for treatment of tennis elbow and only indicated if patients are unresponsive to conservative treatments after an extended period of time. Debridement is the most common surgical intervention, but it can result in injury of the lateral collateral ligament and subsequent posterolateral rotary instability of the elbow.

           

References

1.         Shiri R, Viikari-Juntura E, Varonen H, Heliovaara M. Prevalence and Determinants of Lateral and Medial Epicondylitis: A Population Study. American Journal of Epidemiology. 2006;164(11):1065-74. doi: 10.1093/aje/kwj325.

2.         Cutts S, Gangoo S, Modi N, Pasapula C. Tennis elbow: A clinical review article. Journal of Orthopaedics. 2020;17:203-7. doi: 10.1016/j.jor.2019.08.005.

3.         Speers CJ, Bhogal GS, Collins R. Lateral elbow tendinosis: a review of diagnosis and management in general practice. British Journal of General Practice. 2018;68(676):548-9. doi: 10.3399/bjgp18x699725.

4.         Titchener AG, Fakis A, Tambe AA, Smith C, Hubbard RB, Clark DI. Risk factors in lateral epicondylitis (tennis elbow): a case-control study. Journal of Hand Surgery (European Volume). 2013;38(2):159-64. doi: 10.1177/1753193412442464.

5.         Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. The Journal of bone and joint surgery American volume. 1979;61(6A):832-9. PubMed PMID: 479229.

6.         Steinborn M, Heuck A, Jessel C, Bonel H, Reiser M. Magnetic resonance imaging of lateral epicondylitis of the elbow with a 0.2-T dedicated system. European Radiology. 1999;9(7):1376-80. doi: 10.1007/s003300050851.

7.         Thomas D, Siahamis G, Marion M, Boyle C. Computerised infrared thermography and isotopic bone scanning in tennis elbow. Annals of the Rheumatic Diseases. 1992;51(1):103. doi: 10.1136/ard.51.1.103.

8.         Pattanittum P, Turner T, Green S, Buchbinder R. Non‐steroidal anti‐inflammatory drugs (NSAIDs) for treating lateral elbow pain in adults. Cochrane Database of Systematic Reviews. 2013(5). doi: 10.1002/14651858.CD003686.pub2. PubMed PMID: CD003686.

9.         Croisier J-L, Foidart-Dessalle M, Tinant F, Crielaard J-M, Forthomme B. An isokinetic eccentric programme for the management of chronic lateral epicondylar tendinopathy. British Journal of Sports Medicine. 2007;41(4):269. doi: 10.1136/bjsm.2006.033324.

10.       Johnson GW, Cadwallader K, Scheffel SB, Epperly TD. Treatment of lateral epicondylitis. Am Fam Physician. 2007;76(6):843-8. Epub 2007/10/04. PubMed PMID: 17910298.

11.       Coombes BK, Connelly L, Bisset L, Vicenzino B. Economic evaluation favours physiotherapy but not corticosteroid injection as a first-line intervention for chronic lateral epicondylalgia: evidence from a randomised clinical trial. British Journal of Sports Medicine. 2016;50(22):1400-5. doi: 10.1136/bjsports-2015-094729.

12.       Yan C, Xiong Y, Chen L, Endo Y, Hu L, Liu M, et al. A comparative study of the efficacy of ultrasonics and extracorporeal shock wave in the treatment of tennis elbow: a meta-analysis of randomized controlled trials. Journal of Orthopaedic Surgery and Research. 2019;14(1). doi: 10.1186/s13018-019-1290-y.