Sternoclavicular dislocation (SCD) is a rare injury (<3% of all joint dislocations) that is frequently misdiagnosed in the ED. [1-2] The critical distinction is between anterior (more common, generally benign) and posterior (less common, potentially life-threatening due to proximity to mediastinal structures). [1][3] Over one-third of posterior SCDs are missed at initial presentation. [4]
1. History
- Mechanism of injury — the single most important HPI element:
- Anterior dislocation: arm pulled posteriorly with force, or indirect force through the arm in flexion/abduction/external rotation [3][5]
- Posterior dislocation: compressive anterior-to-posterior force on the chest, or lateral compression of the shoulder (e.g., pile-on in contact sports, MVC rollover) [3][6]
- Timing of injury and any prior episodes of SC joint instability
- Pain location: anterior chest/medial clavicle, often radiating to shoulder
- Ability to move the affected arm (typically decreased active ROM) [1]
- Symptoms suggesting mediastinal compression: dyspnea, dysphagia, hoarseness, choking sensation, arm swelling [2-3]
- Mechanism energy level: high-energy (MVC, contact sports) vs. low-energy (atraumatic instability) [7-8]
2. Alarm Features
- Dyspnea or stridor → tracheal compression [1][3]
- Dysphagia or odynophagia → esophageal compression [2]
- Hoarseness → recurrent laryngeal nerve involvement [3]
- Ipsilateral upper extremity swelling, cyanosis, or venous engorgement → subclavian/brachiocephalic vein compression [2]
- Diminished or absent distal pulses → arterial compromise [1]
- Hemodynamic instability → vascular injury or hemorrhage [9]
- Palpable defect or "hollow" at the SC joint (vs. prominence in anterior dislocation) → suggests posterior dislocation [2]
- Pain-limited forward flexion — present in 83% of posterior SCDs in one pediatric series and should raise suspicion [4]
3. Medications
- Acute analgesia: IV opioids, NSAIDs, acetaminophen for pain control
- Procedural sedation: required for closed reduction attempts (propofol, ketamine, or midazolam/fentanyl per institutional protocol) [1]
- Post-reduction: oral NSAIDs, acetaminophen; short course of opioids if needed
- Avoid: Kirschner wires (K-wires) for fixation — historically associated with catastrophic migration into mediastinal structures; their use is contraindicated [2][8]
4. Diet
- If posterior dislocation with dysphagia is present, maintain NPO status pending CT evaluation and potential surgical intervention
- No specific long-term dietary considerations
- Standard hydration and nutrition for musculoskeletal healing post-reduction
5. Review of Systems
- Respiratory: dyspnea, stridor, pleuritic chest pain (pneumothorax)
- Cardiovascular: arm swelling, color changes, pulselessness
- GI: dysphagia, globus sensation
- Neurologic: paresthesias, weakness in ipsilateral upper extremity (brachial plexus) [2]
- ENT: voice changes, hoarseness
- MSK: shoulder pain, decreased ROM, prior shoulder/clavicle injuries
- Constitutional: syncope or near-syncope at time of injury (suggests vascular compromise)
6. Collateral History and Family History
- Witnesses to mechanism (especially in sports — lateral blow to shoulder vs. direct anterior chest impact) [4]
- Prior episodes of SC joint subluxation or instability
- Generalized ligamentous laxity or connective tissue disorders (Ehlers-Danlos, Marfan) — associated with atraumatic SC instability [5]
- Family history of hypermobility syndromes
- In adolescents, confirm skeletal maturity status (medial clavicular physis is the last to fuse, ~age 23–25) [2][6]
7. Risk Factors
- Contact/collision sports: football (especially offensive linemen), rugby, wrestling, hockey — most common cause (74–86% of cases in younger patients) [4][10]
- Motor vehicle collisions (especially rollover) [6-7]
- Age <25 years: physeal separation more common than true dislocation [2][6]
- Male sex: ~88–92% of cases [4][10]
- Generalized ligamentous laxity [5]
- Falls from standing height [10]
8. Differential Diagnosis
- Medial clavicle fracture — especially in patients <25 years (physeal fracture-separation mimics dislocation; MRI helps differentiate) [2][6]
- Clavicle shaft fracture with medial extension
- SC joint sprain/subluxation (grade I–II without complete dislocation)
- Sternal fracture
- Costochondritis or Tietze syndrome (atraumatic)
- SC joint septic arthritis (atraumatic, febrile, IV drug use risk factor)
- SC joint osteoarthritis (chronic, degenerative)
- Condensing osteitis of the medial clavicle
- Chest wall contusion — cannot-miss: posterior SCD masquerading as simple contusion (36% missed at initial visit) [4]
9. Past Medical History
- Prior SC joint dislocations or subluxations (recurrent instability)
- Prior clavicle fractures
- Connective tissue disorders
- Osteoporosis (affects fixation strategy if surgical) [11]
- History of chest/mediastinal surgery
- Anticoagulant use (increases hemorrhage risk with posterior dislocation)
10. Physical Exam
- Vital signs: tachycardia, hypotension (vascular compromise); tachypnea, hypoxia (airway/pneumothorax)
- Inspection:
- Anterior dislocation: visible/palpable prominence of the medial clavicle anterior to the sternum [3]
- Posterior dislocation: palpable defect or "hollow" at the SC joint; the medial clavicle is less prominent than the contralateral side [2]
- Swelling, ecchymosis over the SC joint
- Venous engorgement of the ipsilateral neck/arm
- Palpation: tenderness directly over the SC joint; compare bilaterally
- ROM: decreased active shoulder ROM, especially forward flexion and cross-body adduction [1][4]
- Neurovascular exam: distal pulses, capillary refill, sensation in the ipsilateral upper extremity [1]
- Auscultation: diminished breath sounds (pneumothorax); stridor
11. Lab Studies
- Labs are generally not diagnostic for SCD itself
- If hemodynamic compromise or suspected vascular injury:
- CBC, type and screen/crossmatch
- Lactate, BMP
- Coagulation studies if on anticoagulants or if surgical intervention anticipated
- Pre-operative labs as indicated
12. Imaging
- Plain radiographs: often miss the diagnosis; standard AP chest X-ray has poor sensitivity for SCD [1][4][12]
- Serendipity viewJAAOS + 1[2][13]
- CT of the chest (with or without contrast): gold standard for diagnosis and evaluation of mediastinal complications [1][3][14]
- Axial cuts clearly demonstrate anterior vs. posterior displacement
- Evaluates for pneumothorax, hematoma, vascular compression
- CT angiography (CTA): warranted when vascular injury is suspected (hemodynamic instability, pulse deficit, arm swelling) [9][14]
- MRI: useful in patients <23 years to differentiate physeal fracture-separation from true dislocation; also defines soft-tissue/ligamentous injury [2][14]
13. Special Tests
- No validated scoring systems specific to SCD
- Point-of-care ultrasound (POCUS): may identify joint asymmetry or effusion at the bedside, but CT remains the definitive study
- Bedside swallow assessment: if dysphagia is present, to assess esophageal compression
- In patients <25 years, consider MRI to evaluate physeal status [2]
14. ECG
- ECG is not routinely indicated for isolated SCD
- Obtain if:
- High-energy mechanism with concern for cardiac contusion (blunt chest trauma)
- Hemodynamic instability
- Chest pain atypical for musculoskeletal etiology
- No specific ECG pattern associated with SCD
15. Assessment
Classification: [1-2]
- Direction: Anterior (more common, ~80%) vs. Posterior (~20%, more dangerous)
- Severity: Sprain (grade I–II) vs. Subluxation vs. Complete dislocation (grade III)
- Timing: Acute (<3 weeks) vs. Chronic
- Age consideration: In patients <23–25 years, many "dislocations" are actually Salter-Harris physeal fracture-separations [6]
Key clinical pearl: Anterior SCD is generally a benign injury with good outcomes even without reduction. Posterior SCD is a potential surgical emergency due to proximity of the brachiocephalic veins, subclavian vessels, trachea, and esophagus. [1][3] However, recent large series suggest the actual incidence of clinically significant vascular injury is lower than historically reported — no vascular injuries requiring intervention were found in a multicenter series of 125 posterior SCDs, and a national database study of 140 posterior SCDs found zero vascular injuries. [10][15] Nonetheless, the potential for catastrophic hemorrhage mandates a cautious approach. [9][14]
16. Treatment Plan
Anterior SCD: [1][11]
- Closed reduction in the ED with procedural sedation: patient supine with a bolster between the scapulae; apply traction to the arm in abduction and extension, then direct posterior pressure on the medial clavicle
- High recurrence rate after reduction, but most patients remain minimally symptomatic [11]
- Sling immobilization for comfort, typically 4–6 weeks
- Surgical stabilization reserved for persistently symptomatic recurrent instability
Posterior SCD: [1][9][16]
- Emergent closed reduction if airway, hemodynamic, or vascular compromise is present
- Technique: patient supine with interscapular bolster; traction on the abducted arm; the medial clavicle may need to be grasped with a towel clip to pull it anteriorly
- Closed reduction is most successful within 48 hours (56% success vs. 31% after 48 hours) [17]
- Can be attempted up to 10 days post-injury [9]
- If no acute compromise, obtain CT first, then plan reduction in a controlled setting
- Orthopedic consultation is required for all posterior SCDs [1]
- Cardiothoracic/vascular surgery notification recommended, particularly for open reduction — though recent data suggest routine CT/vascular backup may be sufficient rather than mandatory CT surgeon presence in all cases [10][15]
- Open reduction and stabilization (ligament reconstruction, plate fixation) for failed closed reduction or chronic/locked dislocations [11][14][18]
Medications:
- NSAIDs (ibuprofen 600–800 mg TID or ketorolac 15–30 mg IV) and acetaminophen
- Short-course opioids for severe pain
- Procedural sedation agents for reduction
17. Disposition
Admit: [1]
- All posterior SCDs — for monitoring, CT evaluation, and orthopedic/surgical consultation
- Any SCD with signs of mediastinal compression, vascular compromise, or airway symptoms
- Failed closed reduction requiring operative management
- Polytrauma patients
Discharge (with close follow-up):
- Uncomplicated anterior SCD after successful closed reduction or if managed conservatively
- Sling, ice, analgesia, and orthopedic follow-up within 1 week
Observation:
Consult triggers: [1]
- Orthopedics: all posterior SCDs, complicated anterior SCDs (with fracture), failed reductions
- Cardiothoracic/vascular surgery: posterior SCD with any mediastinal symptoms, planned open reduction of posterior SCD
- Thoracic surgery: if pneumothorax or esophageal injury suspected
18. Follow Up / Return Precautions
- Orthopedic follow-up within 5–7 days for all SCDs [1]
- Return to ED immediately for:
- New or worsening shortness of breath, difficulty swallowing, voice changes
- Arm swelling, color changes, or numbness
- Increasing pain despite medications
- Feeling of the joint "popping out" again
- Expected recovery:
- Anterior SCD: sling for 4–6 weeks; gradual return to activity; may have residual cosmetic prominence [3]
- Posterior SCD (after successful closed reduction): mean return to sports ~3.1 months (range 1–6 months); 74% full return to sport [19]
- Patient counseling: recurrent instability is common after anterior SCD but usually minimally symptomatic; posterior SCD recurrence is less common but warrants closer surveillance [11]
- Avoid contact sports until cleared by orthopedics
References
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