Vascular Etiologies of Musculoskeletal Pain

Audio Podcast for Vascular Etiologies of MSK Pain

Musculoskeletal pain is a very common complaint.  Vascular etiologies consist of a wide variety of pathologies included in MSK pain ranging from the benign to the life threatening.  Some of the etiologies discussed in this podcast are vasculitides, ischemia/infarction (including carpal tunnel syndrome and thoracic outlet syndrome) and coagulopathies.

•Where is the pain?
–Localized or Diffuse?
–If localized: is it joint pain (skeletal), muscular, or at the enthesis?
•Quick overview of Myalgias…
Differential Diagnosis for Localized Myalgia
Unusually strenuous exercise or overuse
Myofascial pain syndrome
Muscle infarction
Compartment syndrome
Differential Diagnosis for Diffuse Myalgia (much more variable)
Systemic rheumatic diseases
including vasculitis
•Metabolic syndromes
•Endocrinologic syndromes
•Medication side effects
•Myalgia but not myalgia
•Referral Pain
–Can present as “muscle or joint pain” when they origin is visceral or distant somatic
–“Back pain”
•Any retroperitoneal organ will refer pain to back
•Dissecting Aortic aneurysm
−Distal to Left Subclavian will refer to back and proximal to L subclavian will refer to chest
•Kidney disease
–“Arm or jaw pain”
•Vascular Causes of Musculoskeletal pain
–Compression of vessel/blockage of vessel/systemic hypotension
•Quick overview of Vasculitides
•Small vessel
–Henoch-Schonlein purpura, hypersensitivites, vasculitis secondary to viral infection (hep, HIV, parvo)
–Palpable purpura normally due to type III hypersensitivity
•Medium sized vessel (muscular arteries)
–Polyarteritis nodosa, kawasaki
–Rash, infarction, MI, swelling
•Large vessel (elastic arteries)
–Takayasu, Giant cell
–Pulselessness, stroke


•Skeletal muscle vasculitis
•Usually presents in association with systemic vasculitis or isolated peripheral nervous system vasculitis
–Major peripheral clinical manifestation is often due to associated vasculitic neuropathy
•About 55% of patients will have significant myalgias and some degree of muscle weakness
–About 20% will have parasthesia due to associated peripheral neuropathy
•Temporal Arteritis
•Elderly females
•Most Common Vasculitis; affecting medium and large arteries
•HA, Jaw CLAUDICATION, decreased vision
•50% of patients with temporal arteritis (TA) will have PMR and 15% of patients with PMR will also have TA
•Henoch-Schonlein purpura
•MC systemic vasculitis in children
–Affects small vessels of SKIN, GI and JOINTS
–Skin rash, abdominal pain, melena and ARTHRALGAS
•Follows URI
•Up to 44% in one study had a mutation in the MEFV gene, the familial Mediterranean fever gene
•IgA immune complexes


–Usually transient or migratory and typically oligoarticular
–It usually affects the lower extremity large joints (hips, knees, and ankles),
–There is usually swelling and tenderness, but normally no joint effusion, erythema, or warmth.
–Severe decreased ROM, especially in younger children
–No chronic damage, sequelae or joint deformity.
•Supportive care for all systemic issues (renal, GI…)
•NSAIDS for arthritis
-NSAIDS are NOT shown to increase GI bleeds in HSP patients
•Use of Glucocorticoids is warranted if NSAIDS fail
•Buerger’s disease
•Seen in heavy smokers
•Intermittent claudication of muscles
•Severe pain with thrombosis/infarction of arteries
–Smoking cessation
•Polyarteritis nodosa
•Immune-copmplex mediated transmural vasculitis
•Systemic symptoms due to small and medium artery inflammation
•Fever, weight loss, abdominal pain, melena, HA, nuerologic dysfunction, rash, MYALGIA, associated with Hep B
–Corticosteroids, cyclophosphamide
•Takayasu’s arteritis
•Asian females >40 years old
•“Pulseless disease” affecting medium and large arteries
•Fever, night sweats, skin nodules, dyspnea, brain and ocular involvement (carotid arteries) weak pulses in UE, ARTHRITIS AND MYALGIA
–Glucocorticoids and symptomatic treatment as they arise


•Compartment syndrome
•Due to increased pressure within a facial compartment.
–Compromises the circulation and function of the tissues within that space.
•Most commonly presents after trauma as an acute presentation (anterior leg most common)
•May also present in young athletes as Chronic exertional compartment syndrome
•Compartment syndrome’s pathophysiology is cellular anoxia
•Regardless of the mechanism, the common end point is ischemia and subsequent reperfusion injury (particularly in cases of vascular injury) to the muscles in the affected compartment.
•Two Incision Fasciotomy
•Thoracic Outlet Syndrome (TOS)
•Compression of the neurovascular bundle as it passes through anterior and middle scalene muscles in the superior thoracic outlet
•Pain, tingling and coolness in the upper extremity may be present
–Pain can also be found in the lateral neck, the pectoral area, the axilla, and the upper back
•Most patients respond to conservative treatment: stretching, posture exercises and Osteopathic manipulative treatment
•Goals of OMT
–Treat hypertonic muscles
–Release tissue adhesions
–Balance the surrounding structures
•Patients who fail conservative treatment may require more invasive procedures: cortisone or Botox injections or first rib resection and scalenectomy
•Carpal Tunnel Syndrome (CTS)
•Most common peripheral neuopathy
•Compression of a peripheral nerve induces marked changes in intraneural microcirculation and nerve fiber structure, impairment of axonal transport, and alterations in vascular permeability, with edema formation and deterioration of nerve function (Lundborg and Dahlin, 1992).
•Presents as parasthesia in the median nerve distribution with accompanying ache and occasional weakness.
–There can be sensory loss across the first three digits while sparing the thenar eminence
-palmar sensory cutaneous nerve arises proximal to the wrist and passes over, rather than through, the carpal tunnel
•TREATMENT of Carpal Tunnel Syndrome
•Conservative treatment includes splinting, glucocorticoids, yoga and osteopathic manipulative treatment (OMT).
•Surgical decompression of the median nerve is appropriate in moderate to severe CTS to prevent permanent damage to the median nerve
•OMT for CTS
•Goals of OMT in CTS
–Stretch soft tissues
–Release tissue adhesions
–Free restricted metacarpal and carpal bones, increase range of motion
–Strengthen the muscles
–Remove edematous fluid
•Results: improvement in circulation and median nerve function
•OMT has been shown to be a safe and effective method of treatment for mild to moderate CTS (Sucher 1994).


•Deep Venous Thrombosis (DVT)
•Manifestation of Venous thromboembolism (VTE)
–Most commonly seen in lower extremity
•Presents as acute onset of swelling, pain, and erythema of the involved extremity
–Important to recognize risk factors for VTE
–May be administrered as LMH Heparin, fondaparinux, unfractionated heparin or adjusted-dose subcutaneous heparin
–For most patients warfarin should be started simultaneously
–Heparin can be discontinued on day 5-6
•The use of thrombolytic agents, surgical thrombectomy, or percutaneous mechanical thrombectomy must be taken in to consideration when Heparin use is not favorable (hemodynamically unstable PE)
•Subclavian Steal syndrome
•Most commonly caused by atherosclerosis in the subclavian artery but can be due to an occlusion
•If the occlusion or stenosis is proximal to the origin of the vertebral artery you will get this phenomenom
•Ischemia of the ipsilateral upper extremity can lead to exercise-induced arm pain, fatigue, coolness, paresthesias, or numbness.
•Ischemic and trophic changes are rare

•Vascular Causes of Skeletal Pain

•Osteonecrosis (Avascular necrosis)
–Localized pain exacerbated by movement
–Can be asymptomatic
–Sickle Cell
•Osteonecrosis (AVN)
•Caused by various traumatic and nontraumatic stressors that ultimately lead to decreased blood circulation within the bone
–This leads to hyperemia in adjacent areas which results in demineralization and trabecular thinning
-If the bone is then stressed it can result in collapse
•Seen commonly in adults with extensive glucocorticoid use or traumatic femoral neck fractures
•Osteonecrosis in Children
–Idiopathic AVN of hip seen in children 3-12 years old
–Presents as hip pain or limp of acute onset
–Males>Females (4:1)
–African-Americans are rarely affected
–Higher incidence in children infected with HIV
•Slipped ephiphysis
–Slipped capital femoral epiphysis (SCFE)
•Posterior slip of femoral epiphysis
•Results in limp and reduced internal rotation
•Common presentation is obese child around 10-12 years old
–Osteonecrosis is most serious complication of SCFE; occurring in up to 20% of severe slips
•TREATMENT of Osteonecrosis
•Conservative treatment:
–Rest, partial weight bearing as tolerated, NSAIDS and other analgesics
–Bisphosphonates help slow resorption of necrotic bone
•Joint preserving procedures (decompression, osteotomy, marrow grafts)
•Joint replacement

•Vasoocclusive crisis (VOC) in Sickle Cell

•Bone and joint problems are the most common manifestations of sickle cell disease
•Hypoxia-induced polymerization of abnormal Hemoglobin results in sickling of red blood cell
–Causes microvascular occlusion which presents clinically as a painful episode or crisis
•Can lead to AVN of femoral or humeral head, collapsed vertebral bodies, dactylitis, osteomyelitis and septic arthritis
•Warm packs on affected areas
•Surfactants that inhibit cell adherence and aggregation
•Analgesics (opioids)
–Special care has to be given to monitor cardiopulmonary function on opioids (incentive spirometry and ambulation)

•Overview of Osteopathic approach to musculoskeletal pain

•History and Physical
•Palpatory skills are key in differential
•Recognize pain’s impact on all aspects of life and address all components
•Work to normalize sympathetic tone

•Musculoskeletal pain of vascular origin Resources

•Lundborg G, Dahlin LB. The pathophysiology of nerve compression. Hand clin. May 1992; 8(2): 215-27
•Sucher BM. Palpatory diagnosis and manipulation management of carpal tunnel syndrome. Journal of American Osteopathic Association 1994; 94;647-663
•Jay Allan Liveson (25 September 2000). Peripheral neurology: case studies. Oxford University Press US. pp. 255–. ISBN 9780195135633. Retrieved 4 August 2010.
•Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br 2003; 85:625.
•Mankin HJ. Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 1992; 326:1473.
•Sherry, DD, Malleson, PN. Nonrheumatic musculoskeletal pain. In: Textbook of Pediatric Rheumatology, 4th ed, Cassidy, JT, Petty, RE (Eds), WB Saunders, Philadelphia 2001. p. 362.
•Platt OS, Thorington BD, Brambilla DJ, et al. Pain in sickle cell disease. Rates and risk factors. N Engl J Med 1991; 325:11.
•Kuchera, DO, Michael L. Applying Osteopathic Principles to Formulate Treatment for Patients With Chronic Pain. J Am Osteopath Assoc, Nov 2007; 107: ES28 – ES38

By Brandon Masi Parker

One Comment on “Vascular Etiologies of Musculoskeletal Pain”

  1. Devan says:

    I looked all over for the anatomic distinction between the thoracic inlet and outlet. Look no further! Thanks for the great podcast.

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