Brad a 37 y.o M breakdancer, presented with R knee pain, after forcefully landing on his knee with a valgus force. His knee immediately swelled and he has been unable to weightbear since the injury.

He has no other significant medical history.

Xrays in ED showed the following:

Describe the above Xray?
AP view, lateral split depression fracture - Schatzker type 2

Describe the tibial plateau classifications?
Schatzker Classification is the most commonly used

Type 1: Lateral Split - often young patient, associated with MCL injury, and lateral meniscal entrapment
Type 2: Lateral Split, Depression
Type 3: Pure Lateral Depression - often seen in the elderly
Type 4: Medial Plateau
Type 5: Bicondylar
Type 6: Metaphyseal, Diaphyseal
note: type 4-6 often associated with high velocity trauma
Below images are from orthobullets, Tibial Plateau Fractures (2016)

What factors will immediately change Brad's management?
1. Is the fracture open or closed
2. Is the knee stable - meaning is there more than 10 deg of lateral/medial movement on valgus/varus force. This may be difficult to determine due to patient's pain
3. Are there signs of compartment syndrome. (See blog below on compartment syndrome)
4. Is Brad neurovascularly intact. Any difference in pulses between Brad's two feet you should also conduct an ankle-brachial index. 'An ABI less than 0.90 has been shown to have a sensitivity exceeding 87% and a specificity exceeding 97% for identifying lower-extremity arterial injury' (Karadsheh, 2016)
Obviously an open fracture, compartment syndrome or poor perfusion requires immediate surgical intervention.

What type of tibial plateau is more likely to be associated with neurovascular injury?
Schatzker type IV are rare and commonly caused by high energy axial load, leading to medial plateau fracture pattern. At the time of the injury their is usually a momentary knee dislocation, where popliteal artery and peroneal nerve are put under tension. Thus it is this type of tibial plateau fracture that is associated with neurovascular compromise due to popliteal artery injury. 

What type(s) of tibial plateau injury is more commonly associated with compartment syndrome?
Schatzker type V and VI, is more commonly associated with compartment syndrome and 25% are associated with ACL tears (Karadsheh, 2016). 

What type of injury is associated with lateral meniscal injury?
Lateral meniscal injuries are more common than medial in terms of tibial plateau fractures. Schatzker type II injuries are associated with lateral tibial plateau fractures (Karadsheh, 2016). 


What investigations would you order?
Xrays:

• AP
• Lateral
• Oblique (good if you suspect depression)
• +/- plateau view (10 deg of caudal tilt)

CT

• important to determine depression and comminution

MRI -not routinely used

• ligament and soft tissue injury

Management:
​Initial management from ED involves:
- continue non-weightbear patients, analgesia, ice, keep nil by mouth
- calling the orthopaedic registrar on call (additional imaging/operative v non operative management)
- note: tibial plateau fractures (unless neurovascular compromise) will not be operated on for a few days
- normally you will discharge patient home in a Richard's Splint (immobilisation knee brace/backslab) and crutches and referral to orthopaedic outpatient fracture clinic

​Indication for Non-Operative Management
1. minimally  displaced lateral depression or split fractures
2. minimal trauma injuries with no varus/valgus knee instability
3. non- ambulatory patients

Non operative management involves:
Hinged knee brace, partial weight bear for 8-12 weeks and immediate passive range of movement

Indications for Operative Management (open reduction internal fixation):
1. articular step off greater than 3mm
2. bicondylar fracture
3. medial plateau fracture
4. condylar widening greater than 5mm
5. valgus/varus instability
6. open injury
7. vascular compromise, compartment syndrome

Indications for Operative Management (external fixation):
​1. severe open fracture with contamination
2. severe soft tissue injury

Post operative management:
Non or Partial weight bear for 8-12 weeks in hinged knee brace with early ROM

REFERENCES:
Karadsheh, M. (2016). Tibial Palteau Fracture. Orthobullets (3/7/16). Available from: http://www.orthobullets.com/trauma/1044/tibial-plateau-fractures Accessed: 1/4/16.Ip, D. (2006). Tibial Plateau Fractures. In Ip, D (Ed), Orthopedic Traumatology - A Resident's Guide (pp. 421-428). Berlin Heidelberg: Springer.

Nathan 38 y.o M, police officer, presented to ED with sudden onset left heel and calf pain, immediately on jumping whilst playing basketball. He reports hearing an immediate 'pop' sound.
He was unable to weight bear due to the pain and is finding it difficult to plantar flex his foot






What are the risk factors for achilles tendon rupture?
1. Steroid injections
2. Episodic athletes
3. Fluoroquinolone antibiotics: broad spectrum antibiotics (covers gram negative and positive bacteria) often used to treat hospital acquired infections, ie pneumonia, or UTIs. Examples include: ciprofloxacin, gemifloxacin, levofloxacin moxifloxacin, and norfloxacin.

Nathan denies any of the above risk factors.

​What are the main mechanisms of injury?
1. Sudden forced plantar flexion 
2. Sudden dorsiflexion from foot being in a plantar position

Describe the anatomy of the achilles tendon; origin, insertion, blood supply, innervation:
The Achilles tendon is the largest tendon in the body and is a confluence of the soleus muscle tendon and the lateral and medial gastrocnemius heads. It inserts into the middle 1/3 of the posterior calcaneal surface. Supplied by the posterior tibial artery.
Achilles tendon reflex tests S1, S2

What clinical findings would you look for?
1. Obvious deformity - Obvious calf swelling/deformity. Also ask Nathan to lie in prone position and flex both knees, if there is an increase dorsiflexion of affected side this is indicative of achilles injury (as achilles tendon plantar flexes foot). There can be calf atrophy in chronic cases of achilles tendon rupture.

2. Squeeze test (Thompson test) - get Nathan to kneel on edge of bed/seat or move down bed so that feet unsupported and are hanging off the end. Squeeze the normal calf first and watch his foot (foot should plantar-flex then retract to neutral if achilles tendon in tact). Then squeeze calf of affected side, no movement of foot suggests complete rupture of achilles tendon - POSITIVE Thompson Test (See image below, (Stretanski, M 2015)). If there is some movement (or equivocal result), further investigations (USS or MRI) should be undertaken.

 3. Step deformity: palpate along the tendon to determine whether there is an obvious rupture/disruption

Your ED consultant conducts a quick bedside USS of the achilles tendon which demonstrates complete rupture approximately 5cm proximal from the calcaneal insertion. Why do achilles tendon's normally rupture here?
The posterior tibial artery supplies the achillies tendon, however, there is a watershed area (hypovascular region) 4-6cm from the calcaneal insertion, it is this area that is prone to rupture.
Achilles tendon injury can either be classified as complete or partial rupture.

Xrays are not diagnostic but can be useful if an associated calcaneal avulsion injury needs to be ruled out. Otherwise USS or MRI can be utilised.

What does the orthopaedic registrar need to know when you call them?
Patient information, including medical history (diabetic), occupation (athlete), smoker, risk factors
Affected side, mechanism of injury, previous achilles tendon injury
Clinical signs
Investigations: Xray, USS findings - confirmed full/partial achilles tendon rupture

Treatment Options
Conservative vs Surgical Management AGAIN!! -  Historically operative management was preferred with younger, healthier patients due to a re-rupture rate of 2% compared to 11-30% for non surgical. However, a recent meta-analysis of randomised controlled trials have demonstrated there is no significant difference between re-rupture rates in operative versus conservative management, if conservative management involves aggressive functional rehabilitation protocols (Soroceanu, et al 2012). There is however, an absolute risk increase of 15.8% associated with surgery for complications other than rupture, such as infection and wound breakdown (Soroceanu, et al 2012). These results have driven a change towards conservative management with aggressive function rehabilitation rather than surgical treatment for achilles tendon ruptures.

Conservative Management:
This is becoming the primary method of management for complete achilles tendon ruptures. There are many protocols available. They aim for aggressive functional rehabilitation. In the November 2015 Journal of Bone and Joint surgery, discussed a recent randomised controllled trial, Barford 35 al. which demonstrated there was no significant difference between the Achilles tendon Total Rupture Score (ATRS) and heel-rise strength in patients that weight bear day 1 post injury compared to a control non-weight-bearing (6 weeks).

Below is an example of two different conservative management protocols. The hospital or individual consultant you work for may have there own. The first is a more aggressive protocol, the second more conservative (Brunello R,et al, 2013). 

Surgical Management:
1. End to end achilles tendon repair: incision is made just medial to tendon to avoid sural nerve, the paratendon is incised to expose the tendon edges and heavy non-absorable sutures are used to repair the achilles tendon.
2. Minimally invasive percutaneous tendon repair: a small transverse incision is made at the level of achilles tendon rupture, and tendon ends are identified. Sutures are passed both proximally and distally to the incision, capturing the ends of the tendon. From the incision the sutures are pulled out of the skin and paratendon so that they are only through the achilles tendon. The sutures from both ends are tied, approximating both ends of the tendon. This technique's pitfulls include limited purchase of the tendon and incidental damage of the sural nerve (0 to 10.5%) in the literature (Rouvillian 2010).
There are additional surgical techniques for chronic (> 3 months old) ruptures.

Post surgical rehabilitation protocol is then instigated. Similarly to conservative management there are multiple protocols available. Here is an example of one from the University of Wisconsin Sports Medicine and Physician group (2015):

James a RHD 9 year old boy was brought into ED after getting his right ring and middle finger caught in the car door. He has sustained a subungal haematoma of his ring finger and nail bed laceration of his middle finger. He otherwise has no medical and surgical history. 
There are three main types nail bed injuries listed below. 

1. Subungal Haematoma: bleeding beneath nail
2. Nail Bed Laceration: laceration of the nail and underlying nail bed
3. Nail Bed Avulsion: avulsion of nail and underlying nail bed

​

However, it is important to first understand the underlying anatomy. See images below.

​It normally takes 3-6 months for nail to grow from the cuticle to the tip of the finger.
 
James'  ringfinger has a haemtoma under the nail, see picture below, known as a subungal haematoma.

Normally the nail is intact and there is an underlying subungal haematoma covering >50% of the nail surface area. This is managed with tetanus, antibiotic prophylaxis and nail bed repair as described in detail below. 

Nail bed avulsion injuries, as mentioned above are associated with nail and nail bed avulsion. If this is associated with significant loss of nail matrix this can be managed with nail bed matrix transfer from adjacent finger or second toe.

 
What associated injuries do you have to investigate for?
1. distal phalanx fractures or dislocations – common associated injury,
2. cuts of the nailbed and fingertip (pulp)
3. extensor of flexor tendon laceration
4. digital nerve laceration
 
Xrays were taken of James’ right hand, of his middle finger, shown below, please describe:

There is an extra-articular minimally displaced tranverse fracture of James' distal phalanx of his right middle finger. Distal phalangeal fracture reduction and healing is important to final nail formation. Poor reduction will result in irregularities of the nailbed. However, lateral views would need to be obtained to ensure no displacement of the fracture. Fixation will depend on the fracture. 

What are the basic principles of nail bed repair?

1. Minimal debridement
2. Preservation of as much tissue as possible
3. Atraumatic wound care
4. Splinting with the nail

 
Nail bed repair

1. Always give antibiotics and tetanus
2. A digital block of 1% lidocaine hydrochloride without adrenaline (Children may require procedural sedation and analgesia)
3. The hand should be prepared with povidone-iodine (Betadine) and covered with sterile drapes.
4. Exsanguinate the injured finger, in a distal to proximal direction, a tourniquet will provide a blood-free field
5. The nail is elevated using the blades of fine scissors, blunt dissecting technique should be used, the blades being placed under then nail bed until they reach the nail fold. Specific care is necessary to not injure the nail bed or nail fold.
6. Once nail is separated from nail bed, it is gently removed and placed in Betadine
7. Repair nailbed using 6-0 or smaller absorbable sutures. Ensure minimal debridement or tension on repair as this can result in scaring. 
8. Careful inspection of the nail is important. Only outer and dorsal surfaces of the nail should be cleaned, any nailbed fragments should be preserved for use as a graft.  If tissue is not available and the defect is small enough, the area will heal effectively by secondary intention.
   1. The proximal nail should be reinserted into the nail fold. Why?                                                                - Keeps nail fold open for new nail growth                                                                                             - Protective cover for nail bed                                                                                                            - Template for new nail to follow as it grows                                                                                        - Rigid split for any associated underlying fracture                                                                               - Reduces postoperative discomfort and improves function
9. Before replacement place a small hole in the nail, to allow drainage and thus prevent any developing haematoma that could separate the nail from the nailbed.
10. The nail is then placed back in the nail fold as a stent and held in position by 5-0 or smaller nylon     sutures or with adhesive, such as Dermabond. Nail fragments may be repaired together first with adhesive.
11. If there is no nail available for splinting, alluminium or nonadherent guaze can be used.
12. Dress the injured finger with nonadherent gauze and 2-inch gauze roll then splint the finger.
13. Avulsion injury with nail bed matrix injury may require nail matrix transfer from adjacent injured finger or nail matrix transfer from second toe.

REFERENCES
Sutijono, D Mills, TJ (2015) Nailbed Injuries Treatment & Management. Accessed 4 Oct 2015. Available from: http://emedicine.medscape.com/article/827104-treatment

American Society for Surgery of the Hand (2006) Nail bed injuries, Chicago. Accessed 4 Oct 2015. Available from: http://www.assh.org/handcare/hand-arm-injuries/Nail-Bed-Injury#prettyPhoto

​Jones, T. (2014) Nail Bed Injury. Orthobullets. Accessed 4 Oct 2015. Available from: http://www.orthobullets.com/hand/6109/nail-bed-injury

Hamish a 28 y.o male, right hand dominant, presented to his GP with bilateral pain in his wrists and paraesthesia on the palmer aspects of his hands. The symptoms are worse in his right hand, involve all fingers except his little finger, and it wakes him from his sleep. He never has symptoms during the day. His GP suspects carpal tunnel syndrome (CTS).

What are the risk factors for Carpal Tunnel Syndrome (McKean, J 2015)?

1. Female gender
2. Obesity
3. Inflammatory conditions: Rheumatoid arthritis, gout, pseudogout 
4. Endocrinopathies: Hypothyroidism, acromegaly, diabetes, pregnancy, OCP
5. Advanced age
6. Alcoholism
7. Chronic renal failure
8. Repetitive wrist movements
9. Smoking
10. Mucolipidosis
11. Mucopolysaccharidosis

Other aetiologies include; tumours, trauma, any cause of tenosynovitis of the flexor tendons, amyloidosis. 

The GP has taken a thorough history but Hamish has no risk factors for CTS. He has never been exposed to work involved with repetitive movement or vibrations but does love playing tennis. This is the only aggravating factor identified.

What are other symptoms associated with carpal tunnel syndrome?

• Paraesthesia, numbness often effects middle finger first, then thumb and index
• Clumsiness, dropping objects
• Pain should only radiate to the elbow

What structures are within the carpal tunnel? See below
9 flexor tendons: 4 x flexor digitorum superficialis, 4 x flexor digitorum profundus, flexor pollicis longus
median nerve.
The carpal tunnel is narrowest at level of hook of hamate.

What are the borders of the carpal tunnel? See below
The scaphoid and trapezium tubercle radially, triquetral, hook of hamate and pisiform ulnarly.
The floor is made up of carpal bones and the roof, carpal tunnel ligament. 

Remember to always approach physical examination systematically: inspect, palpate, neurological tests and finally specialised tests.

Inspect:  remember to look for signs of underlying cause. For example, signs of hypothyroidism, acromegaly, previous scars, etc. Specifically:

• Thenar atrophy (see image above) - late sign
  

Palpate:

• Compare muscle bulk from R to L

Neurological Tests:

• Thumb power: abduction, opposition and flexion (compare to contralateral side)
• Sensation: median nerve (palmer surface: thumb, index, middle and radial half of ring finger). Sensation over thenar eminence is supplied by the palmer branch of the median nerve, which enters the palm superficial to retinaculum. 

Specialised Tests:

1. Durkan's Test positive (carpal tunnel compression test): most sensitive test, involves using your thumbs to apply pressure on patient's carpal tunnel. Positive test if numbness or pain along median nerve distribution is elicited within 30 seconds. 
2. Phalen's Test: volar flexion of wrists (60 degrees). Less sensitive than Durkan's. Positive if symptoms elicited within 60 seconds
3. Tinel's Test: provocation test, repetitive tapping over median nerve on volar aspect over carpal tunnel
   

Why does Hamish only have symptoms at night?
There are multiple factors that cause night symptoms of carpal tunnel syndrome:

1. Horizontal positioning redistributes fluid (blood flow) to upper limbs. Hence why shaking arms alleviates symptoms (redistributes fluid away from carpal tunnel - decompressing nerve)
2. Drainage of fluid from muscle milking/pumping is reduced
3. Tendency towards wrist flexion at night
4. Blood pressure drops during night, resulting in reduced perfusion pressure

The GP referred Hamish for nerve conduction studies. 
What would you expect nerve conduction velocities (NCV) to demonstrate:
1. Increased latency (slowing) of NCV

• distal sensory latency of 3.2ms
• motor latencies >4.3ms

2. Decreased conduction velocities (less specific than latency)

• velocity < 52m/s is abnormal

The main benefit of electrodiagnostics is to provide objective evidence for the diagnosis. 
Diagnosis is usually clinical and criteria include:

• numbness and tingling in the median nerve distribution
• nocturnal numbness
• weakness and/or atrophy of the thenar musculature
• positive Tinel sign
• positive Phalen test
• loss of two point discrimination

Management:
Once again.. always break up into non-operative and operative management.

Non-operative
1. Lifestyle changes: try to minimise the precipitating factor/aggravating factors and limit the risk factors mentioned above, ie lose weight, treat hypothyroidism, stop smoking/drinking. 
2. Night splints:
To reduce nocturnal wrist flexion. This would be one of the first steps for Hamish as this is the only time he gets symptoms.
3. NSAIDS
4. Corticosteroid Injection: 80% of patients have transient improvement of symptoms, 22% remain asymptomatic at 1 year. 22 gauge needle is introduced between FCR and PL, angles 45 degrees down and distally to floor of tunnel and withdraw 5mm.

Hamish attempts the above non-operative management options but 2 years later is still experiencing symptoms. Consequently has opted for operative management.

Operative
For patient's in which conservative manaegment has failed or space occupying lesion, or acute carpal tunnel syndrome was sustained post distal radial ORIF. Temporary relief from a steroid injection is a good prognostic factor that operative management will likely give a good result for the patient.

Operative pointers:

Mark out palmaris longus tendon. 
Incision is made ulnar to palmaris longus. This is in line of the fourth ray. From the level of the distal palmer crease to the level of the outstretched thumb (Do not extend past Kaplan's line - the superficial palmer arch would be found distal to Kaplan's line). Blunt dissection down flexor retinaculum, incise retinaculum from distal to proximal releasing nerve.

Pinch strength should return by 6 weeks and complete grip strength by 12 weeks. 

REFERENCES
McKean, J. (2015). Carpal Tunnel Syndrome. OrthoBullets. Accessed 9/9/15. Available from http://www.orthobullets.com/hand/6018/carpal-tunnel-syndrome

Clifford R (2013). Anatomy of Carpal Tunnel. Wheeless' Textbook of Orthopaedics. Accessed 10/9/15. Available from: http://www.wheelessonline.com/ortho/anatomy_of_carpal_tunnel

Dophotoshop. (2011) Accessed 12/9/15. Available from: http://dophotoshop.com/carpal-unnel-exercises.php  

You are an orthopaedic registrar and an ED intern calls you with the following  case:

60 y.o M, Jo, BMI 35, presented to ED with a 2 day history of Atraumatic pain in his right hip, subjective rigors, inability to weight bear over the last day.  He previously had a right total hip replacement 10 years ago, with no complaints since. He denies any other focal infective symptoms (ie no cough, dysuria, wounds, etc)


What risk factors are associated with septic arthritis, or what other questions would you ask the patient?

Risk factors for septic arthritis can be broke up into how the organism would have spread to the infected joint, (that is how I like to break it up in my mind). You would ask Jo the following:

Contiguous Spread:
·      Skin infection – Jo denies

Direct inoculation:
·      Previous intra-articular injection
·      Prosthetic joint – which you know he has, look at timing, operative notes, infection at the time – 10 years ago, nil complication
·      Recent joint surgery – denies

Haematogenous Spread/Immunocompramised
·      Diabetes – yes T2DM, managed with oral medication only
·      Immunocompromised – Jo denies any Hx of auto-immune diseases, HIV, imunosuprpressive medication
·      IV drug user – denies
·      Other causes of sepsis – septic screen done by ED has been negative

Other questions:
·      Injury to hip/ trauma - denies
·      Hx of gout - denies
·      Osteoarthritis- yes


Risk factors for the development of prosthetic joint infections include previous fracture, seropositive rheumatoid arthritis, high body mass index, revision arthroplasty, and surgical site infections. Jo's only risk factor is his high body mass index. Septic arthritis in prosthetic joints after 24 months are normally caused by haematogenous spread (Barilla-LaBarca, M. Horowitz, D. Horowitz, S. 2011)

What investigations would you have expected the intern to have ordered?

1. Bloods, which revealed:
WCC 11.4
CRP 40
ESR 10 (note ESR is often normal in early infection, rises after 2 days, returns to normal after 3-4 weeks)
Remainder of bloods - NAD
 
2. Full septic screen
Blood cultures – pending
CXRAY
Urine

3. Imaging: Hip Xray – AP and lateral view: this is to determine if there is any obvious joint effusion, peri-prosthetic fracture, dislocation, etc.

You called the radiology registrar on call, to discuss additional imaging as you knew a CT would have significant artifact due to the patient’s right total hip replacement.

He consequently had an ultrasound guided joint aspirate of his right hip. The synovial fluid aspirated was purulent in appearance, indicative of an infective arthritis. 

NOTE: Commonly doctors will disregard a CRP of 40 and WCC 11.4, as it is not indicative of septic arthritis, orthopaedic registrars would expect a CRP much higher. However, it is important to assess the patient clinically and if uncertain an aspirate is definitive.  It is also important to remember that patients with a prosthetic joint that intraarticular WCC cutoffs may be as low as 1,1000 per mm3, making diagnosis problematic (Barilla-LaBarcam M 2001)

Jo's repeat CRP the next day was 289...

Hip aspirate was taken under ultrasound guidance. What would you put on the pathology form?

1. Gram stain
2. Cell count with differential
3. Crystal analysis
4. Microscopy, culture and sensitivities
5. Glucose analysis: in bacterial infection or tuberculosis, the synovial fluid glucose will be less than half the serum value. Occasionally, low values may be seen in RA.

(PCR testing may help isolate less common organisms, such as Borelia species and if gonococcal infection suspected).

Interpret the following results:
WCC: 75,000
PMN (polymorphnuclear) 90%
Crystals: negative
Gram stain: Gram-positive cocci
Culture: positive

Remember.. even if crystals are positive, a patient can have a crystal arthropathy and septic arthritis at one time.

What are the most common microorganism causing septic arthritis? 
Majority 80% of septic arthritis is caused by nongonococcal pathogens (most commonly Staphylococcus species (Barilla-LaBarcam M, et al 2010).

Non-Gonoccocal
Gram-positive staphylococci

• Associated with: drug abuse, cellulitis, abscesses, endocarditis, and chronic osteomyelitis

• Staphylococcus aureus: most common in developed countries 

• Methicillin-resistant S. aureus (MRSA): 5-25%, associated with older population, often involves the shoulder joint and health care (nursing home) patients
  

Gram-positive streptococci 

• Streptococcus species: second most common

Gram-negative bacilli: 14 to 19%

• Associated with: urinary tract infections, intravenous drug use, older age, compromised immune system, and skin infections.
• Pseudomonas aeruginosa and Escherichia coli (most common)

Gonoccocal:
Gram negative cocci: neisseria gonorrhea

• most common organism in otherwise healthy sexually active adolescents and young adults
• knee most commonly involved
• cultures should be taken from mucosal sites (e.g., urethra, rectum, pharynx, cervix)

Others:

• salmonella: associated with sickle cell disease
• pseudomonas aeruginosa: associated with history of IV drug abuse
• pasteurella multocida: associated with dog or cat bite
• eikenella corrodens: associated with human bite
• organism found in immunocompromised host can include fungal, and candida common pathogens

(Abassi, D. 2015)


Management:
Gram stain results should direct initial antibiotic treatment: See table below for appropriate cover. 

How was Jo's septic arthritic hip managed?

Jo was managed by an urgent washout and tissue sample in theatre. He will most likely require a repeat washout and removal/replacement of metalwork. 
Emperic intravenous antibiotics were commenced once gram stain was available. Microbiology and infectious disease was contacted to determine ideal antibiotic therapy and duration for Jo. Jo was initially managed with vancomycin. He required 4 weeks of intravenous cover and then was changed to oral antibiotics, based on microbiology and clinical response.

REFERENCES:
Abassi, D. (2015). Septic Arthritis - Adult. Orthobullets. Accessed 7/8/15. Available from: http://www.orthobullets.com/trauma/1058/septic-arthritis--adult. 

Mandell, G. Bennett, J. Dolin, R. (2010). Infectious arthritis of native joints. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, Pa.: Churchill Livingstone; 2010:1443–1456.

Ghanem E, Parvizi J, Burnett RS, et al. Cell count and differential of aspirated fluid in the diagnosis of infection at the site of total knee arthroplasty. J Bone Joint Surg Am. 2008;90(8):1637–1643.

Barilla-LaBarca, M. Horowitz, D. Horowitz, S. (2011) Approach to Septic Arthritis. Am Fam Physician. 2011 Sep 15;84(6):653-660. Accessed 8/8/15. Available from: http://www.aafp.org/afp/2011/0915/p653.html

Ella a 4 y.o girl RHD presented to the local ED department with R elbow pain, swelling and reduced range of movement.

True AP and Lateral Xrays of Ella’s elbow are below, please describe them and how you would approach an elbow Xray:

First ensure correct film, views, and the films are technically adequate, assessment should include:

Lateral view: demonstrates an obvious fracture line on the anterior supracondylar region of the humerus, less than 1/3 of the capitellum is anterior to the anterior humeral line. There is also raised posterior and anterior fat bad and surrounding soft tissue swelling. 
AP view: There is a visible supracondylar fracture line over the medial aspect of the humerus, no apparent intra-articular involvement, rotation, angulation or displacement in this view. 

Visible fracture line

1. Location and especially presence of articular involvement
   
2. Angulation (use the Anterior humeral line: passes through middle 1/3 of capitellum - see image below on left. If there is a displaced supracondylar fracture this line will pass in front of capitellum, right image below )
3. Alignment of the radius and ulnar with the distal humerus (use Radio-capitellar line: line drawn down neck of radius on AP film, should pass through the center of the capitellum. Assesses for radial dislocation) 

Baumann’s angle AKA humeral-capitellar angle: angle between the long axis of the humerus and the capitellar physis (line through growth plate of the capitellum) – see diagram. Normal angle 70-75 degrees (but always compare to the carrying angle of the uninjured side – a deviation of more that 5 degrees compared to other side should not be accepted) 

Tear drop (AKA hour glass sign): dense line representative of the capitellum and posterior margin of coronoid fossa – indicates true lateral of elbow

You should always get an xray of the ipsilateral wrist (distal radius/ulnar fracture) and shoulder (proximal humerus fracture)

Remember to consider other elbow trauma: radial head dislocation, epicondylar fractures can mimic an undisplaced supracondylar fracture

Remember ossification centres, CRITOE

Classify Ella’s fracture according to Gartland’s Classification (Sheth, U. Taylor, B 2015)
Ella has a Type 1 Gartland's fracture.
Gartland's Classification:

Type 1: Non displaced
Type 2: Displaced, posterior cortex in tact. The anterior humeral line does not intersect the capitellum. This can be further subdivided into 

• 2a: minimally displaced no rotation
  
• 2b rotational deformity
  

Type 3: Completely displaced
Type 4: (not in original Gartland’s classification): complete periosteal disruption with instability in flexion and extension

Ella cannot pronate or supernate her arm, explain why she cannot do this using biomechanics of the elbow.

The elbow has two functionally independent articulations that share a synovial compartment. They are:
1.     ulnotrochlear articulation directs flexion and extension
2.     radiocapitellar joint governs forearm rotation


Approximately 7 % of supracondylar fractures are associated with nerve injury, what nerves would most likely be effected and how would you test these?

• Anterior interosseus nerve (branch of median nerve): Ella would be unable to make A-OK sign (cannot flex interphalangeal joint of this thumb and DIPJ of  her index finger.
• Radial nerve: Ella would be unable extend her wrist or digits
  

How would you manage Ella’s supracondylar fracture?
Always ensure patient is neurovascularly intact
Ella was managed with a closed reduction, which involved traction followed by flexion of elbow with slight anterior pressure of the posterior displaced segment and placed in a long arm posterior splint (or collar and cuff) at > 90 degrees of flexion for three to four weeks.
Repeat radiographs were taken to ensure adequate reduction and she was referred to fracture clinic in 5-7 days with repeat X-ray.
Note: Without support, the weight of the cast applies an extension torque to the distal humerus and can lead to posterior fracture displacement

How would you manage other supracondylar fractures?
Non-Operative Long arm posterior splint then long arm casting with up to 90 degrees of elbow flexion:

• Indication: Type 1, Type 2a fractures that has no medial comminution, minimal swelling and anterior humeral line intersects the anterior half of the capitellum
• Repeat radiographs at 3-7 days and immobalisation for 3-4 weeks +/- additional time with removal posterior long arm posterior splint.

Operative
Immediate closed reduction and percutaneous pinning (K-wires)

• Indications: vascular compromise (pale, cool hand), floating elbow
• Technique: check vascular status after reduction

 
Closed reduction and percutaneous pinning

• Indications: Type 2b (not meeting the above criteria) and Type 3

Open reduction with percutaneous pinning

• Indication: when closed reduction was not successful, more likely if a flexion type fracture

REFERENCES
Kids Health WA. Supracondylar Fractures (2015).Available from: http://kidshealthwa.com/wp-content/uploads/2013/12/Supracondylar.jpg
Accessed: 30/8/15

Radiology Masterclass. Trauma Xrays Upper Limb. (2015). Available from: http://www.radiologymasterclass.co.uk/gallery/trauma
Accessed: 2/8/15

Sheth, U. Taylor, B. (2015) Supracondylar Fractures -Pediatric. Orthobullets. Available from: http://www.orthobullets.com/pediatrics/4007/supracondylar-fracture--pediatric Accessed: 1/8/15

Dan, an orthopaedic consultant, and avid wrestler presented to the ED department with right sided shoulder pain and deformity post falling onto his right shoulder during a wrestling match. He suspects he has an AC joint disruption and as you are a junior doctor in ED he starts questioning your knowledge. 




"What ligaments stabilise AC joint?"

As you have read junior bones you keenly answer, "the ACJ stabalised by the..:
1.     Acromioclavicular ligament: provides horizontal stability, has 4 components (superior, inferior, anterior and posterior component)
2.     Coricoclavicular ligaments: provides vertical stability, this is comprised of:

1. Trapezoid ligament: located 3 cm from the lateral end of the clavicle
   
2. Conoid ligament: located 4.5cm from the lateral end of the clavicle
   

Dr Dan's Xray is below, please interpret..

Remember to go back to basic principles: identify patient, date, view and see if there are previous Xrays and additional views. Also ensure you have imaging of the contralateral ACJ for comparison.

The above AP Xray demonstrates widening of the right coricoclavicular distance, the right clavicle is superiorly displaced 100% (normally compared to other side), suggestive of a type 3 acromioclavicular distance, however, additional views would be required to confirm this.

Note: to visualize the AC ligament you can ask for imaging at 1/3 penetration

What other imaging (views) would you order?

• Axillary lateral: required to diagnose type 4
  
• Zanca view: tilt the Xray 10-15deg towards cephalic direction and using only 50% of the standard AP penetration strength

Describe Rockwell Classification of AC Joint Injuries:

What are the management options for Dr Dan's Grade 3 ACJ injury?
Remember: conservative vs operative
And the 4 basic principles: reduce, fix, wait, rehabilitate

Conservative Management
Indication: Types 1, 2, 3 (not in labourers, elite athletes)
ICE, rest and sling for 3 weeks
Rehabilitation: early ROM, regain functional movement by 6 weeks and return to normal activity by 12 weeks
Complications : ACJ arthritis, chronic subluxation and instability

vs

Operative Management: ORIF or ligament reconstruction
Indication: Types 3 (labourers, athletes), 4, 5, 6
Contraindications: poor compliance with post operative rehabilitation, skin problems over surgical site
Rehabilitation: sling, with no abduction for 6 weeks, no shoulder ROM for 6 weeks, return to normal activity at 6 months

ORIF with hook plate:

• Approach: exposure of middle and distal clavicle, hook plate positioned over superior distal clavicle and ‘hooked’ under the acromian.
  
• Pros and cons: rigid fixation, often requires removal of plate, high rate of acromial wea.
  

ORIF with CC suture fixation:

• Approach: proximal aspect of anterolateral approach to the shoulder
  
• Technique: suture placed around/through clavicle and around the base of the coracoid (+/- suture anchors for coracoid fixation)
  
• Pros and cons: requires careful suture passage inferior to coracoid. Minimal risk of hardware failure or migration, suture not as strong as screw fixation.
  

ORIF with screw fixation:

• Approach: proximal aspect of the anteriorlateral approach to the shoulder
  
• Technique: screw from distal clavicle into coracoid
  
• Pros and cons: rigid fixation, danger of screw damaging critical structure below coracoid, complicated by hardware irritation or failure.
  

CC Ligament reconstruction: with free tendon graft OR Modified Weaver-Dunn (transfer of coracoacromial ligament to the distal clavicle to recreate CC ligament)

• Approach: proximal aspect of the anteriorlateral approach to the shoulder +/-  harvest site (hamstring/Palmaris tendon)
  
• Pros and cons: coracoacromial ligament not as strong as normal CC ligament vs graft which recreates strength of native CC ligament but standard risk of graft use.

 

Above is Dr Dan's post operative Xray. He was managed with corico-clavicular suture fixation. 


REFERENCES:

Abbasi, D. Badylak, J. 2015. Acromio-Clavicular Injuries (AC Seperation). Orthobullets. Accessed: 15/7/15

Caribbean Sports Orthopaedic Clinic, 2010. ACJ Reconstruction. Available from: https://www.c-soc.com/surgical/treatments/shoulder/acj-reconstruction/ Accessed: 20/7/15

Sinnerton, R. ACJ (Hook Plate, Surgilig) Available from: http://www.lu-lu.co.uk/operations/acromio-clavicular-joint/ Accessed: 17/7/15.

The Physio Lounge, 2014. Skiing Injuries. Available at http://www.physiolounge.co.uk/skiing-injuries/. Accessed: 14/7/15

You are on night ward call and a nurse calls you to review a post operative patient for worsening leg pain. James, a 25 year old male, is day 1 post right intramedullary tibial nail. You have been called multiple times about James for pain relief. He has low pain tolerance and is suspected to use regular recreational drugs.

What questions would you ask the nurse?

1. Neurovascular observations - including capillary refill
2. Amount of analgesia used
3. Background

also consider:

• known bleeding disorder
• does he have a cast in situ

REMEMBER: compartment syndrome can occur wherever skeletal muscle is surrounded by fascia, including leg (similar to this case), forearm, hand, foot, thigh, buttocks, shoulder, etc
     
Pathophysiology of compartment syndrome

1. trauma/ soft tissue destruction
   
2. bleeding and oedema
3. increased interstitial pressure
4. vascular occlusion
5. myoneural compromise

Majority of cases are secondary to fractures

What are the 6 P's of Compartment Syndrome and what are late and early signs? Hint: think of the pathophysiology above (Stracciolini, Hammerberg 2015)

1. Pain on passive stress - early sign - most sensitive
2. Palpable swelling - woodlike
3. Paraesthesia -reduced sensation secondary to ischaemic nerve dysfunction
   
4. Poikilothermia 
5. Pallor - unusual finding
   
6. Peripheral pulses absent - late finding
   

Realistically the patient will complain of pain out of proportion, described as a deep ache or burning pain, deep ache or burning pain and potentially paraesthesia and muscle weakness (onset is usually 30minutes to 2 hours of acute compartment syndrome).

Interpreting Clinical Findings:

• Capillary refill becomes compromised if compartment pressure reaches 25-30mmHg of mean arterial pressure
• Pain develops with compartment pressure of 20-30mmHg
• Ischaemia occurs if compartment pressure reaches diastolic pressure

What are the 4 compartments of the leg and define what structures are within them?
1. Anterior Compartment:

• Function: dorsifllexion of foot and ankle
• Muscles within compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, peroneus tertius

2. Lateral Compartment

• Function: plantarflexion and eversion of foot
• Muscles within compartment: peroneus (fibularis) longus, peroneus brevis
• Nerve: isolated lateral compartment syndrome would affect superficial peroneal nerve

3. Deep Posterior Compartment

• Function: plantarflexion and inversion of foot
• Muscles: tibialis posterior, felxor digitorum longus, flexor hallucis longus

4. Superfical Posterior Compartment

• Function: plantarflexion of foot and ankle
• Muscles: gastrocnemius, soleus, plantaris

REMEMBER: you will never get told off for removing a cast if you suspect compartment syndrome
How to measure compartment pressures?

How do I measure compartments?
3 methods are used frequently:
1. A handheld manometer (eg, Stryker device)
2. A simple needle manometer system, and
3. The wick or slit catheter technique
Both manometer methods involve injecting a small quantity of saline into a closed compartment and measuring the resistance from tissue pressure

The normal pressure of a tissue compartment falls between 0 and 8 mmHg (Klenerman L, 2007)

Procedure:
Should aim to measure pressures within 5cm of fracture site.

• Anterior Compartment: enter perpendicular to skin 1cm lateral to anterior border of tibia
• Deep Posterior Compartment: enter perpendicular to skin, just posterior to the medial border of tibia
• Superficial Posterior Compartment: enter middle of calf
• Lateral Compartment: enter just anterior to posterior border of fibula

Treatment:
Non-operative:
1. Bi-Valve James' cast
2. Observe: if not consistent with compartment syndrome
3. Hyperbaric oxygen therapy: increases oxygen diffusion gradient

Operative: Emergent fasciotomy of all four compartments
Indications:

• Compartment pressures of 30-45mmHg
• Clinical presentation with compartment syndrome
• Compartment pressures within 30mmHg of diastolic BP

Procedure
1. Dual (2 incisions) medial and lateral incision: 2 x 15 cm incisions

2. Single lateral incision from head of fibula to ankle along line of fibula

REFERENCES
Karadsheh, M. 2015 Leg Compartment Syndrome. Orthobullets. Available from: http://www.orthobullets.com/trauma/1001/leg-compartment-syndrome. Accessed 10/7/15.

Klenerman L. The evolution of the compartment syndrome since 1948 as recorded in the JBJS (B). J Bone Joint Surg Br 2007; 89:1280.

Stracciolini, A., Hammerberg, E. 2014. Up To Date. Acute Compartment Syndrome available from: http://www.uptodate.com/contents/acute-compartment-syndrome-of-the-extremities#H8 Accessed 1/7/15

Melissa a 26 year old female, RHD, presented to her local GP with ongoing pain and swelling on the ulnar aspect of the base of her right thumb. 2 weeks ago, whilst on a 1 month cycling trip around Europe she fell off her bike and her thumb was forcefully abducted, caught on the bike handle. She had immediate pain but continued her tour. This is the first management she has sought for her thumb. 

What is Gamekeepers Thumb?
Avulsion or rupture of the ulnar collateral ligament (UCL) - see image below


Mechanism of injury: hyper abduction or extension of MCP joint of thumb

Epidemiology: gamekeepers repetitively stressed the UCL ligament and MCP joint of their thumb when breaking rabbits necks (chronic injury). Today more commonly seen in skiers, also known as 'Skiers Thumb,' occurs when the stock or stock strap forcefully abduct the skiers thumb when falling or aggressively planting the pole (acute injury). 

Stener Lesion: UCL ligament avulsed above the adductor aponeurosis. Adductor aponeurosis and adductor pollicis muscle now lying between ligament and proximal phalanx, will not heal without surgical repair.

What imaging would you order?
1. X-rays: AP, lateral, oblique - can show bony avulsion
If there is no bony avulsion, look for ulnar side of the MCP joint, if it appears widened this is suggestive of UCL injury. Stress views were previously undertaken in this situation, however, now there is believed risk of worsening the injury and creating a Stener lesion.

2. Ultrasound scan: to identify tear and Stener lesion, however, operator dependent. 

3. MRI: gold standard in identifying; discontinuity of ligament and or joint capsule, boney oedema and Stener lesion. 

Describe Mel's AP X-ray (image to left):
Always ensure you identify patient and search for old X-rays for comparison, and all views available
There is a minimally displaced intra-articular avulsion fracture of the ulnar aspect of the proximal phalanx of the right thumb.
Always ensure you look for additional fractures, soft tissue swellings, etc. Remember here could be more than one injury.


Treatment Options: Non Operative vs Operative 
Non-operative: Immobilise in cast for 4-6 weeks
Indication: partial tears (<20 degrees of side to side variation). (McKean, J. 2014)

Operative:
1. Ligament Repair: using sutures, anchors, screws
2. Ligament Reconstruction: tendon graft
3. MCP Fusion: for chronic injury and pain, often if the above methods have failed 
Indication:

1. Acute injury with >20 degrees of varus/valgus instability 
2. >35 degrees of opening
3. Stener lesion: as described and depicted above

References: 
Dawes, L., Weerakkody, Y et al. Gamekeepers Thumb. Radiopaedia. Retrieved 27 June 2015 from http://radiopaedia.org/articles/gamekeeper-thumb

Gaillard, F. (2009). Gamekeepers Thumb. Radiopaedia. Retrieved 27 June 2015 from http://radiopaedia.org/articles/gamekeeper-thumb

McKean, J. (2014) Thumb Collateral Ligament Injuries. Orthobullets. Retrieved 27 June 2015 from http://www.orthobullets.com/hand/6040/thumb-collateral-ligament-injury

24 y.o male has been referred to fracture clinic query a right foot, Lisfranc injury, He presented to ED 2 days ago with inability to weightbear, forefoot pain and swelling after a tackle in a rugby game.

What is the Lisfranc ligament and why is it important?

It is a ligament (depicted above in yellow) from medial cuneiform (under 1st metatarsal) to the base of the 2nd metatarsal on the plantar surface. It tightens with abduction and pronation of the forefoot.
It is integral in maintaining the midfoot arch and stabalising the 2nd metatarsal. As there is no ligament directly connecting the 1st and 2nd metatarsal. 

What is the mechanism of injury usually?
Injury usually includes fall from height, motor vehicle accident or athletic injury like in this case.

Hyperplantar flexed forefoot, compression (axial load) and abduction (indirect rotational force) transmitted to the tarso-metotarsal articulation – causing metatarsals to be displace in a dorsal/lateral direction, as depicted below.

Assessing the patient:
1. Assess foot circulation

• The anterior tibial artery has the first dorsal and first plantar metatarsal artery that supplies the medial foot, disruption of this astemosis can cause signficiant haemorrhage and compartment syndrome
  
• Compartment syndrome
  

2. Assess soft tissue

• Stellate bruising over midfoot plantar area
  
• Swelling, prominence of medial tarsal bones, shortening of forefoot

3. Assess associated injury

• Abduction mechanism of injury – compression fracture of cuboid, MTPJ dislocations, TMTJ fractures/dislocations, metatarsal fractures
  

Instability test: grasp metatarsal heads and apply dorsal force to forefoot while other hand palpates the TMT joints dorsal subluxation suggests instability

• If 1st and 2nd  metatarsals can be displaced medially and laterally, global instability is present and surgery is required
  
• No dorsal subluxation = plantar ligaments are intact, injury may be treated non-operatively
  

Provocative tests may reproduce pain with pronation and abduction of forefoot


What imaging would you order?
Xrays: AP, lateral, oblique 30 degrees, If possible -AP Weight bearing Xrays: comparison can be made to other side
Stress radiograph: if non-weight bearing Xrays normal but clinically high suspicion for Lisfranc stress views may be helpful to show instability
CT scan: for diagnosis and preoperative planning
MRI: diagnose pure ligamentous injury

 
Below are his Xrays, describe the deformity.

What are the 5 critical radiographic signs of midfoot instability?
AP view:
1. The medial base of the 2nd metatarsal does not align with the medial side of the middle cuneiform.
2. Widening of the interval between the first and second ray

Oblique view:
3. Medial side of  4th metatarsal base does not line up with medial side of cuboid

Lateral view:
4. Dorsal displacement of metatarsal base
5. Disruption of the medial column line (line tangential to the medial aspect of the navicular and the medial cuneiform)

Flec sign (on AP view): may see bony fragment  in 1st intermetatarsal space (avulsion of Lisfanc ligament from base of 2nd metatarsal) 

Treatment
Non-operative: immobilization for 8 weeks Vs Operative

Indications for non-operative management?
Non-displaced on weight-bearing and stress radiographs and no evidence of bony injury on CT. OR:

• Non-ambulatory patients
  
• Severe vascular disease
  
• Severe peripheral neuropathy
  
• Instability in only the transverse plane

What are the different operative options:
1.    Open reduction and rigid internal fixation:
Indication: Any instability (> 2mm shift) and or fracture dislocations, rather than pure ligamentous injuries

2.    Primary athrodesis of the 1st, 2nd and 3rd metatarsal joints
Indication: pure ligamentous injury

3.    Midfoot athrodesis
Indication: unstable midfoot architecture with progressive arch collapse and forefoot abduction, chronic lisfranc injuries that have led to midfoot arthrosis and failed conservative management

Reference:
[1] Blomberg, J (2015)  Lisfranc Injury (Tarsometatarsal fracture-dislocation). Orthobullets. Retrieved 20 June 2015 from http://www.orthobullets.com
[2] And Rabou, A., Gaillard, F et al. (2015) Lisfranc Injury. Radiopaeidia. Retrieved 20 June 2014 from http://radiopaedia.org/articles/lisfranc-injury