Biceps tendonitis and rupture

1. Where is the most common site of biceps tendon rupture? What other shoulder condition is it associated with?
2. What are the symptoms of bicipital tendonitis? Biceps rupture.
3. What tests are done to diagnose biceps tendonitis?
4. What test is done to diagnose biceps rupture?
5. What is the treatment for biceps tendonitis/rupture?

Answers:
1. Most common site of rupture is long head of biceps proximally, often secondary to impingement syndrome or rotator cuff tears.
2. Point tenderness in bicipital groove, positive impingement signs. If there is rupture, there will be sharp pain, audible snap, ecchymosis, and visible bulge in lower arm.
3. Yergason's test (pain with supination of wrist against resistance) and Speed's test (pain with shoulder flexed, elbow extended, supination against resistance).
4. Ludington's test: deformity with flexion of biceps muscle.
5. For tendonitis, can do ROM, strengthening, modalities, or injection into tendon sheath. For rupture, reattachment isn't indicated except in young people who do heavy lifting.

Degenerative joint disease in the shoulder

1. What occurs in arthritis of the shoulder?
2. What are the symptoms and signs of shoulder arthritis?
3. What imaging should be ordered? What is seen on X-ray?
4. What is conservative treatment for shoulder arthritis?
5. What are the indications for total shoulder arthroplasty? What are the stages of recovery?
6. What is shoulder arthrodesis? What are indications for arthrodesis?

Answers:
1. Destruction of articular cartilage and narrowing of the joint space in either of the GH or AC joint.
2. Limitation and pain on AROM and PROM, worse with internal rotation, tenderness with palpation.
3. AP in internal and external rotation and 40 degrees, axillary view. Findings are irregular joint surfaces, joint space narrowing, subacromial sclerosis, osteophyte changes, flattened glenoid, cystic changes in humeral head.
4. NSAIDs, steroid injection, ROM, rotator cuff strengthening.
5. Indications for surgery are pain, avascular necrosis, neoplasm. In stage 1 (0-6 wks), avoid abduction and extension, ext rot >15 deg, NWB, sling immobilization, treat with pendulum exercises, isometrics, wall-walking. In stage 2 (6-12 wks), can start light wks, AROM. In stage 3 (>12 wks), no restrictions, start progressive resistive exercises.
6. Shoulder arthrodesis is surgical resection and fusion of shoulder joint. Indications are severe pain, loosening of arthroplasty, or joint infection.

Shoulder impingement: imaging and treatment

1. What is seen on plain film with impingement? Chronic rotator cuff tear?
2. What is the gold standard for rotator cuff tears? For labral tears?
3. What is the utility of arthrogram for rotator cuff tears?
4. What is the conservative treatment for rotator cuff injury in the acute phase (first 4 weeks)?
5. What is the conservative treatment for the first 6 months? After the first 6 months?
6. What are the indications for surgery?

Answers:
1. With impingement, there are cystic changes in the greater tuberosity. In chronic rotator cuff tear, there is superior migration of the proximal humerus, flattening of the greater tuberosity, and subacromial sclerosis.
2. MRI for rotator cuff, add gadolinium for labral assessment.
3. Can assess full thickness tears but can't tell size of tear or partial thickness tear.
4. Relative rest, pain management, modalities, reestablish nonpainful ROM, retard muscle atrophy.
5. In first 6 months, improve ROM, improve rotator cuff strength and scapular stabilizers. After the first 6 months, continue strengthening, do activity-specific training, conticosteroid injections.
6. Surgical indications include tears that fail conservative treatment. In athletes, surgical repair may be done within first 3 weeks for better return of function.

Impingement syndrome

1. What is impingement syndrome?
2. What are the three different acromion shapes? Which kinds are associated with higher risk of rotator cuff tears?
3. What are symptoms of rotator cuff tear?
4. What is the range of the painful arc?
5. What is the supraspinatus test?
6. What physical exam test indicates a complete tear of the rotator cuff?

Answers:
1. Narrowing of subacromial space causing compresion and inflammation of the subacromial bursa, biceps tendon, and rotator cuff tendons. These tendons then get inpinged upon under the acromion and greater tuberosity with arm abduction and internal rotation.
2. Type I is flat, type II is curved, type III is hooked. Curved and hooked have higher risk of tear.
3. Pain with repetitive overhead activities or sports (throwing ball, swimming), crepitus, clicking, weakness, nocturnal pain (sleeping on affected side), tenderness over greater tuberosity or inferior to acromion, atrophy (with tears).
4. 60-120 degrees.
5. Pain and weakness with arm in flexion, abduction, and internal rotation.
6. Drop arm test: passively abduct arm to 90 degrees and internally rotated --> positive is if patient is unable to maintain arm in abduction.

Glenoid labrum tears

1. What are common causes of labral tears?
2. What is a SLAP lesion?
3. What are the symptoms of glenoid labral tears?
4. What is a physical exam finding in a glenoid labral tear?

Answers:
1. Repetitive overhead sports or trauma.
2. Superior glenoid Labral tear in the Anterior to Posterior direction, which encompasses entire glenoid labrum.
3. Symptoms similar to shoulder instability (clicking, locking, pain).
4. Load and shift test: grasp humeral head and push into glenoid while applying anterior and posterior force. Positive test is excess translation.

Treatment of glenohumeral instability

1. What is the conservative treatment for anterior GH instability?
2. When should surgery be considered for anterior GH instability?
3. What is the conservative treatment for posterior GH instability?
4. How successful is rehab for multidirectional GH instability?

Answers:
1. Sling immobilization, strengthening and ROM of shoulder girdle complex, PROM (Pendulum-Codman's exercises).
2. After 3 dislocations or in a very active patient.
3. Immobilize in a neutral position for 3 weeks, strengthening of posterior shoulder-scapula musculature (infraspinatus, post deltoid, teres minor), rehab usually curative.
4. 80% success.

Work-up of glenohumeral instability

1. What are the symptoms of shoulder instability? How is laxity measured?
2. What are three tests for anterior GH instability?
3. What are two tests for posterior GH instability?
4. What is a test for multidirectional GH instability?
5. What imaging is done to assess GH instability? What special views are used for Bankart and Hill-Sachs lesions?

Answers:
1. Symptoms are early shoulder fatigue, pain, numbness, paresthesias. The shoulder slips out of place when in a "throwing" position. Joints are considered lax if the patient can touch the thumb against the flexor surface of the forearm.
2. The apprehension test (feeling of instability with 90 deg shoulder abduction and ext rotation), relocation test (relief of Apprehension with posterior directed force), anterior draw (passive anterior displacement).
3. The jerk test (arm in 90 flexion and int rot with elbow flexed 90 degrees --> patient jerks away when arm is passively adducted while pushing humerus posteriorly), posterior draw (posterior displacement of humerus).
4. The sulcus sign involves pulling down on the patient's arm while stabilizing scapula --> indentation between the acromion and the humeral head is a positive.
5. Routine AP, scapular Y view, axillary lateral view. The West Point lateral axillary is used for Bankart lesions and the Stryker notch view is used for Hill-Sachs.

Glenohumeral instability

1. What is the difference between shoulder instability, subluxation, and dislocation?
2. What is the most common direction of instability? What is the mechanism and complications?
3. What is the presentation and mechanism of posterior GH instability?
4. What is a Bankart lesion? What sort of instability results from this?
5. What is a Hill-Sachs lesion? What sort of instability is associated with this lesion?

Answers:
1. Instability is translation of humeral head on glenoid fossa without separation. Subluxation is separation of humeral head from glenoid fossa with immediate reduction. Dislocation is separation of humeral head from glenoid fossa without immediate reduction.
2. Most common direction is anterior inferior, via arm abduction and external rotation. Complications include axillary nerve injury.
3. Mechanism is landing on a forward flexed adducted arm or as a result of seizure. The patient presents with an adducted, internally rotated arm.
4. Bankart lesion is a tear of the glenoid labrum off the front of the glenoid, allowing the humeral head to slip anteriorly --> anterior instability.
5. A Hill-Sachs lesion is a compression fracture of the posterolateral aspect of the humeral head caused by abutment against the anterior rim of the glenoid fossa due to recurring anterior shoulder dislocation.

Acromioclavicular joint sprains

1. What are the 3 ligaments surrounding the AC joint?
2. How do AC joint sprains usually occur?
3. What are the 6 types of AC joint sprain?
4. What sort of X-ray should be obtained for AC joint separation? What is seen?
5. What is the treatment of Type I and II AC injury?
6. What is the treatment for Type III AC injury?
7. What is the treatment for Type IV-VI AC injury?
8. What is the treatment for chronic AC joint pain?

Answers:
1. AC ligament, coracoclavicular (CC) ligament, coracoacromial ligament.
2. Direct impact to shoulder, falling on outstretched arm.
3. Type I is a partial sprain of the AC ligament with intact CC ligament. Type II involves a complete tear of the AC ligament and a partial tear of the CC ligament. Types III-VI involve complete tear of the AC and CC ligaments with varying displacement.
4. Weighted (10lb) radiographs of shoulder should be obtained. Type III injury shows 25-100% widening of clavicular-coracoid area. Type V injury may show widening >100%.
5. Rest, ice, NSAIDs, sling (comfort), avoid heavy lifting, shoulder girdle strengthening, return to play if asymptomatic with full ROM for 2 weeks if Type I, 6 weeks if Type II.
6. Controversial: surgery vs. conservative, based on need.
7. ORIF or distal clavicular resection with reconstruction of CC ligament.
8. Corticosteroid injection vs. surgery.

Glenohumeral joint

1. What is the labrum? What attaches at the labrum?
2. What is the purpose of the glenohumeral ligaments?
3. What are the three glenohumeral ligaments?
4. What are the muscles that surround the humeral head and provide dynamic stabilization?

Answers:
1. The labrum is a fibrocartilaginous fold of capsular tissue that surrounds the glenoid fossa, increasing contact between the humeral head and the glenoid. The labrum is where the glenohumeral ligaments and tendons attach and prevents humeral head dislocation.
2. To provide stability and keep the head of the humerus in the glenoid fossa.
3. Superior, middle, and inferior ligaments.
4. Rotator cuff muscles (SITS), long head of biceps tendon, deltoid, teres major.

Shoulder movement

1. What are the 4 muscles responsible for shoulder flexion?
2. What are 5 muscles responsible for shoulder extension?
3. What are 2 muscles responsible for shoulder abduction?
4. What are 7 muscles responsible for shoulder adduction?
5. What are 5 muscles responsible for internal rotation of the shoulder?
6. What are 4 muscles responsible for external rotation of the shoulder?

Answers:
1. Deltoid, pectoralis major, biceps brachii, coracobrachialis.
2. Deltoid, triceps, latissimus dorsi, teres major, pectoralis major.
3. Supraspinatus and deltoid.
4. Pectoralis major, triceps, coracobrachialis, infraspinatus, teres major, latissimus dorsi, deltoid.
5. Subscapularis, pectoralis major, latissimus dorsi, anterior deltoid, teres major. (SPLAT)
6. Infraspinatus, teres minor, deltoid, supraspinatus.

Obturator innervated muscles

1. What is the origin, insertion, and action of the adductor longus?
2. What is the origin, insertion, and action of the gracilis?
3. What is the origin, insertion, and action of the adductor brevis?
4. What is the origin, insertion, and action of the adductor magnus? What other nerve provides innervation to the adductor magnus?
5. What is the origin, insertion, and action of the obturator externus?
6. What other muscle is sometimes innervated by the obturator nerve?

Answers:
1. Adductor longus
Origin: Pubic tubercle
Insertion: Linea aspera of femur
Action: Adduct, flex thigh
2. Gracilis
Origin: Inferior ramus of pubis, ramus of ischium
Insertion: Proximal tibia
Action: Adduct thigh, flex leg, medial rotation of leg
3. Adductor brevis
Origin: Inferior ramus of pubis
Insertion: Pectineal line, proximal linea aspera
Action: Adduct, flex thigh
4. Adductor magnus
Origin: Inferior ramus of pubis, ramus of ischium, ischial tuberosity
Insertion: linea aspera, adductor tubercle of femur
Action: Adduct, flex thigh, extend thigh.
Other innervation: Sciatic nerve (posterior fibers)
5. Obturator externus
Origin: Obturator membrane
Insertion: Trochanteric fossa of femur
Action: Lateral rotation of thigh
6. Pectineus, which flexes and adducts hip.

Sacral plexus

1. From what portion of which nerve roots is the superior gluteal nerve formed?
2. From what nerve roots is the inferior gluteal nerve formed?
3. The nerve to what muscle comes directly off the posterior part of S2?
4. How is the tibial portion of the sciatic nerve formed? How does it run in comparison to the peroneal portion?
5. How is the peroneal portion of the sciatic nerve formed?
6. From what nerve roots is the pudendal nerve formed?

Answers:
1. The superior gluteal nerve is formed from the posterior part of the lumbosacral trunk (L4 and L5) and S1.
2. The posterior part of L5, S1, S2.
3. Piriformis.
4. The anterior branches of the ventral rami of L4-S3 form the tibial portion, which lies medially to the peroneal portion.
5. The posterior branches of L4-S2 joint to form the common peroneal portion of the sciatic nerve.
6. The anterior portions of S2 and S3 and part of S4.

Lumbar plexus

1. What 2 branches does L1 give off? What nerves arise from the upper branch? The lower branch?
2. What nerve roots come together to form the obturator nerve? Where does the accessory obturator nerve come off?
3. What nerve roots join together to form the lateral cutaneous nerve of the thigh?
4. What nerve roots joint to form the femoral nerve?
5. What happens to the rest of L4?

Answers:
1. The lower branch goins with a branch from L2 to from the genitofemoral nerve to the scrotum. The upper branch gives off the iliohypogastric and ilioinguinal nerves to the lower abdominal wall.
2. The anterior branch of L2-L4 form the obturator nerve while branches from L3 and L4 may form the accessory obturator nerve (10% people).
3. The ventral rami of L2 and L3 form the lateral cutaneous nerve of the thigh.
4. The posterior rami of L2 and L3 and part of L4 form the femoral nerve.
5. The rest of L4 joins the sacral plexus.

Incomplete SCI syndromes

1. What symptoms are seen in central cord syndrome?
2. What are the symptoms of Brown-Sequard syndrome?
3. What is anterior cord syndrome and how does it occur?
4. What are the symptoms of anterior cord syndrome?
5. What are the symptoms of posterior cord syndrome?

Answers:
1. Sacral sensory sparing, motor weakness greater in upper limbs than lower, urinary retension.
2. Ipsilateral motor and proprioception deficits, contralateral pain and temperature deficits.
3. Anterior cord syndrome involves the anterior 2/3 of the spinal cord and preserves the posterior columns. It results from anterior spinal artery lesions, direct injury to the anterior cord, bone fragments, retropulsed disc, polyarteritis nodosa, angioplasty, aortic and cardiac surgery, embolism.
4. Loss of motor function (variable), loss of pain and temperature sensation. Preserved proprioception and light touch.
5. Loss of proprioception with variable preservation of motor function.

Reflexes following SCI

1. What is spinal shock? How long does it usually last?
2. What are the first reflexes to return, signaling the end of spinal shock?
3. What does the return of the bulbocavernosus reflex mean for bowel and bladder?
4. What are signs of increased reflex activity?

Answers:
1. During spinal shock, muscles are flaccid and hyporeflexic, with atonic paralysis of the bowel and bladder, with gastric atony. Autonomic function is also impaired. It lasts 24hrs to 3mo (avg of 3 wks).
2. Bulbocavernosus reflex and anal wink.
3. Reflex B/B function is intact.
4. Reflexes becomes stronger, starting distally and proceeding proximally. Babinski sign, followed by Achilles, followed by patellar reflex. Bladder will start to contract at irregular intervals.

Autonomic dysreflexia

1. What is the cause of AD?
2. What are the symptoms of AD?
3. What are the most common causes of AD?
4. How is AD treated?
5. What are potential complications of AD?

Answer:
1. A noxious stimulus below the level of the lesion (T6 or higher) causing massive unbalanced sympathetic discharge. There is also reflex bradycardia as a vagal response to the HTN.
2. Headache, flushing, piloerection, sweating, blurry vision, nasal congestion.
3. Full bladder, fecal impaction, pressure ulcers, ingrown toenails, UTI, bladder stones, gastric ulcers, labor, abdominal emergency, fractures, orgasm, epididymitis, cholecystitis.
4. Identify and remove noxious stimulus, sit patient up, remove TEDs/binder, NTG, procardia, hydralazine, clonidine.
5. Retinal hemorrhage, CVA, SAH, a-fib, seizure, death.

Orthostatic hypotension in SCI

1. Why does reflex depression of BP occur in SCI? What levels are at risk for this and why?
2. What is the response in a SCI patient to being placed upright?
3. How is orthostatic hypotension treated in SCI patients?

Answers:
1. Low BP is caused by lack of sympathetic outflow (which would usually cause vasoconstriction) when patient is >60 degrees upright. This occurs at lesions T6 or above, due to the heart and blood vessels being supplied by T1-T7.
2. Hypotension and tachycardia (due to inhibition of parasympathetics).
3. Repositioning (Trendelenberg, tilt table), elastic stockings, abdominal binder, ACE wrap LEs, salt tabs, florinef, ephidrine, fluids.

Thoracolumbar fractures

1. What is a Chance fracture? Are they associated with neurological compromise?
2. What is a vertebral body compression fracture? Is this fracture stable?
3. What is the result of multiple compression fractures?
4. How does spinal cord injury without radiological abnormality (SCIWORA) occur in children? What factors predispose to SCIWORA?
5. How does SCIWORA occur in the elderly? What is the treatment?

Answers:
1. Chance is a transverse fracture of the lumbar spine through body and pedicles, posterior elements, commonly associated with lapbelts. They are seldom associated with neurological compromise.
2. This is an anterior wedge fracture caused by axial compression and is stable if it occurs spontaneously.
3. Thoracic kyphosis (Dowager hump).
4. Mechanism is traction in a breech delivery or violent hyperextension or flexion. Predisposing factors include large head to neck ratio, elasticity of fibrocartilaginous spine, and horizonal orientation of the planes of the cervical facet joints.
5. Mechanism is a forward fall with a blow to the head causing central cord syndrome. Due to bulging of the ligamentum flavum, there may be narrowing of the canal by up to 50%. It is treated with 24 hr cervical collar and repeat films.

Cervical fractures

1. What is a Jefferson fracture?
2. What is the mechanism of a Jefferson fracture? What are the usual neurologic findings if the patient survives?
3. What is a Hangman fracture?
4. How does a Hangman fracture occur? What are the usual neurologic findings if the patient survives?
5. What is an odontoid fracture? How does it occur and what are the neurological findings?

Answers:
1. Burst fx of C1 ring.
2. Occurs by axial loading, causing fractures of the anterior and posterior parts of the atlas. There are usually no neurological findings.
3. C2 burst fx.
4. Occurs when the body separates from the posterior element. There are usually only transient neurological findings.
5. C2 odontoid fractured off at its base, resulting from trauma. There are usually only transient neurological findings.

Cervical bracing

1. What is the most restrictive cervical brace? What are less restrictive braces?
2. What sorts of injuries are most likely to result in a complete SCI?
3. What sorts of injuries are most likely to result in an incomplete SCI?

Answers:
1. In order of most restrictive to least restrictive: Halo, Minerva, four poster, SOMI, Philadelphia collar, soft collar.
2. Bilateral cervical facet dislocations, TL flex-rot injuries, transcanal GSW.
3. Cervial spondylosis, unilateral facet jt dislocations, noncanal penetrating GSW.

Pressure ulcers

1. How long would a pressure of 70mmHg take to cause tissue damage?
2. Is muscle or skin more susceptible to pressure ischemia?
3. What are three factors involved in the pathogenesis of a pressure ulcer?
4. What are common locations of pressure ulcers in the acute period? In the chronic period?
5. What are risk factors for pressure ulcers?
6. How can pressure ulcers be prevented?
7. What are 2 common complications of pressure ulcers?

Answers:
1. 2 hrs.
2. Muscle.
3. Ischemia, pressure, friction.
4. Acute period: Sacrum followed by heels. Chronic period: 1) ischium, 2) greater trochanter, 3) sacrum, 4) heels.
5. Immobility, incontinence, lack of sensation, ALOC.
6. Minimize pressure, maceration, and pressure, turn patient every 2 hrs, pressure relief q30min when sitting, proper cushioning of WC, WC pushups.
7. Osteomyelitis, dehydration.

Pain in SCI

1. What are common causes of UE pain in SCI?
2. What is syringomyelia? When does it usually occur post-injury? How does it present?
3. What is the diagnosis and treatment of syringomyelia?
4. What is a Charcot joint?

Answers:
1. CTS, rotator cuff tendonitis, rotator cuff tears, subacromial bursitis, cervical radiculopathy, lateral epicondylitis, medial epicondylitis, myofascial pain.
2. Syringomyelia is posttraumatic cystic myelopathy, including cavity formation in the spinal cord progressing in a cephalad direction. It usually occurs 2-34 months post injury, presenting as pain and numbness.
3. It is diagnosed by MRI and treated by surgical drainage with shunt to the subarachnoid space or peritoneum.
4. Charcot joint refers to the destruction of an insensate joint due to minor trauma that goes unrecognized.

Pulmonary embolism in SCI

1. What are the symptoms of PE?
2. How is PE diagnosed?
3. What is the treatment for PE?

Answers:
1. Pleuritic chest pain, dyspnea, fever, hemoptysis, tachycardia, hypoxemia
2. EKG (R axis deviation, tachycardia, RBBB), ABG, CXR (wedge shaped opacity, fluid, vascularity), VQ scan, pulmonary arteriogram (gold standard).
3. O2, heparin, vasopressor (for shock), and possible embolectomy.

DVT in SCI

1. What are predisposing factors to DVT?
2. When are DVTs most commonly seen in the SCI?
3. What are methods of DVT diagnosis?
4. How can DVT be prevented in the SCI population?
5. How is DVT treated?

Answers:
1. Virchow's triad (venous stasis, intimal injury, hypercoag), LE fx, obesity, previous DVT, DM, arterial vascular disease, immobility, malignancy.
2. Most common in first 2 weeks and incidence decreases 8-12 weeks post injury.
3. Venogram is the gold standard, dopplers are used for screening.
4. SCDs (do duplex if delayed >72 hrs), LMWH, TEDS, coumadin, unfractionated heparin, IVC filter.
5. Heparin drip or Lovenox 1mg/kg sq bid until coumadin therapeutic. Give 3 months of coumadin for DVT, 3-6 months for PE. No ROM in involved extremity. IVC filter if no anticoagulation.