Ortho Short Case Questions 2006/2007/2008
(Patient Station)
Victor Chong 20/11/08
Trigger Finger (Stenosing Tenovaginitis)
Q. How they present?
pain over a1 pulley site, pain may radiate down the finger or into the palm
stiffness
demostratable triggering or locking of fingers
waking up to find locked fingers at night
palpable nodule in the palm
Q. What is the cause of the nodule?
The nodular enlargement of the tendon is due to inflammation of the tendon as a result of repetitive trauma and restricted gliding of the
tendon in the constricted, inflamed, thicken and fibrosed tendon sheath
Q. Where is the nodule?
Anywhere along the tendon at the A1 pulley?
Q. What else would you look out for after diagnosing TF?
- Look for signs of RA, Gout
Q. Who gets it? (What is the profile of someone with Trigger finger?)

>40 y/o – (middle aged)

Women > Men (Female)

Idiopathic, but associated with RA, DM, gout

Occupations which require frequent gripping, pinching and vibration.
- Musicians
- Typist
- Occupations that use vibrating tools
Q. What is the commonest cause of Trigger finger?
Idiopathic
Q. What is your Differential Diagnosis?
Dupuytren's contracture – but this is usually painless
Q. Trigger Finger is associated with what medical condition?
- RA, Gout, DM
Q. What is the pathophysiology?
The cause of Trigger finger is idiopathic but it can be due to trauma and is associated with DM, Gout, RA.
It is thought to occur as a result of a discrepancy between the volume of the tunnel at the A1 pulley and the volume of the tunnel’s contents.
It is thought to be due to thickening and fibrosis of the TENDON SHEATH at the A1 pulley. This thickening of the tendon sheath constricts and
prevents the free gliding of the tendon within it. Repeated trauma to the tendon as it moves pass the constriction causes inflammation to the
tendon which forms a nodular enlargement of tendon distal to pulley.
Q. What is the treatment?
Take a quick history to assess
1. Age
2. Occupation
3. Hand Dominance
4. Affect on hand function, Work, ADL, IADL
Start with conservative treatment first.
Non surgical
Non Pharmaco
Rest with ice over inflamed area for 15 mins for pain relief
Splintage – Trigger/Buddy Splint to keep the affected finger in an extended position for up to six weeks. The splint helps to rest the
joint. Splinting also helps prevent you from curling your fingers into a fist while sleeping, which can make it painful to move your
fingers in the morning.
Lifestyle modification - Avoid activities which involve a sustained gripping, pinching, and vibration. Hold off on the use of grip
strengthening devices or exercises involving repetitive squeezing - these put stress on the irritated tendon. Or wear antivibration
gloves.
Finger exercises. Your doctor may also suggest that you perform gentle exercises with the affected finger. This can help you to
maintain mobility in your finger.
Pharmaco
1
-
Analgesia: Paracetamol, NSAIDs to relieve pain
For persistent symptoms after 6 weeks, can give H&L up to about 2 times.
Surgical
Trigger finger release by Division of the A1 pulley.
Q. How do you splint?
By buddy splint or metal finger splint in ?extension if buddy splint not tolerated well for 6 weeks. If fingers bend and lock during the night
and are painful to straighten in the morning, it may be helpful to wear a splint to keep them straight while sleeping.
Q. When is surgery indicated? What surgery is offered?
Surgery is indicated when locking and tenosynovitis persists despite two consecutive local corticosteroid injections. Percutaneous and open
surgical release of the A-1 pulley ligament is equally effective, with a recurrence rate of only 3 percent
Q. What are the grades of Trigger Finger?
Green’s Classification of Trigger Finger
Stage 1: Pre-triggering (non-demonstratable triggering): Pain at the A1 pulley site
Stage 2: Demonstratable triggering/Active Extension
Stage 3a: Locking on Passive Extension
Stage 3b: Locking on Passive Flexion
Stage 4: Fixed Flexion Deformity/Contracture
Q. What is an A1 Pulley? Where is it?
A1 Pulley = 1st Annular pulley of the finger formed by a single fibrous band that slings around the tendon, securing it to the bone and guiding
it along the finger. A1 pulley is found at the distal palmar crease at the level of the MCPJ.
There are 5 A pulleys and 3 cruciate pulleys per finger
Q. What important questions will you ask a patient who has Trigger Finger?
- Occupation?
- Handedness?
- Previous H&L injection given? How many?
- Affect on work/home, ADL, IADL
- Associated DM, Gout, RA?  do the relevant investigations: uric acid, fasting blood, hba1c, RF anti CCP
Q. Where do you inject H&L?
Done under Aseptic sterile technique
Cleaned and drapped
Mixture of Lignocaine and Triamincinolone used
H&L is injected into the tendon sheath around the tendon (NOT INTO the TENDON) at the level of the A1 pulley which is at the distal palmar
crease. (Intrasynovial but outside the tendon)
Q. How do you inject? How will you know when the needle is in the sheath? Once you reach the sheath what do you do?
The hand is placed flat with the palm up and the fingers outstretched.
The proximal volar crease of the finger or the distal palmar crease over the metacarpophalangeal (MP) joint of the thumb is
identified.
The point of entry for the finger is just proximal to the first volar crease in the midline. The point of entry for the thumb is at the
distal palmar crease in the midline.
Ethyl chloride is sprayed on the skin for anaesthesia and H&L in a syringe prepared. (lignocaine and triamincinolone)
A 5/8 inch 25 gauge needle is inserted to a depth of 1/4 to 3/8 inch for trigger finger and 1/8 to 1/4 inch for trigger thumb.
The needle is advanced down to the firm resistance of the flexor tendon, a rubbery sensation. The needle is held flush against the
tendon, utilizing just the weight of the syringe.
Without advancing the needle, 1/2 mL of lidocaine is injected for an anesthetic block for diagnostic purposes. For therapeutic
injection, 1/4 mL of methylprednisolone (80 mg/mL) is injected in addition to lidocaine. As injection is taking place, watch for the
flow of the fluid down the finger distally.
Do not inject the corticosteroid solution if there is significant resistance to injection flow, which may indicate that the needle tip is
in the tendon rather than just within the tendon sheath.
Q. Where will you make the incision for tendon sheath release?
Along the crease of the distal palmar crease.
Q. Complications of H&L injection?
Bleeding
Infection < 0.1%
Tendon Rupture  if repeated H&L and in rupture prone pp leg. RA with trigger finger
Subcutaneous Fat necrosis/atrophy
Digital Nerve Injury
Recurrence of trigger finger 40% at 3 months
Q. How does H&L Work?
It reduces inflammation and causes atrophy of the tendons, thus reducing the size of the tendon
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Q. What is the cure rate for Trigger finger after H&L?
90%
30-50% recurrence rate
Q. Complications of Tendon Sheath Release?
Bleeding
Infection
Incising A1 pulley may cause bowstringing of tendon & deviation of finger toward midline & propensity for anterior MCP
subluxation
Digital nerve injury
Recurrence of trigger finger
Q. Will you want to splint after surgery?
No.?
Dequirvain’s Tenosynovitis
Q. What is Dequirvain’s Tenosynovitis?
Inflammation of the tendon and tendon sheath (APL and EPB) of the 1st extensor compartment of the hand.
Repeatedly performing hand and thumb motions such as grasping, pinching, squeezing, or wringing may lead to the inflammation of
tenosynovitis. This inflammation can lead to swelling, which hampers the smooth gliding action of the tendons within the tunnel
Q. What Provocative test to do?
Finkelstein Test. Do the test first with thumb in. and again but thumb out. If patient experiences less pain when thumb is out, it’s a positive
Finkelstein test.
Q. What specific activity predisposes to DT?
wringing washcloths, clothes
typing on the computer keyboard
cutting with scissors
sewing or pinching
stirring food for a long period of time
opening jars
carrying babies
Q. What is the Management?
Take a quick history to assess
1. Age
2. Occupation
3. Hand Dominance
4. Affect on hand function, Work, ADL, IADL
Start with Conservative treatment first
Non surgical
Pharmaco
Paracetamol
NSAIDs
H&L injection
Non Pharmaco
Rest
Lifestyle modification
As far as possible, avoid or reduce activities that involve the thumb or wrist, such as:
o wringing washcloths, clothes
o typing on the computer keyboard
o cutting with scissors
o sewing or pinching
o stirring food for a long period of time
o opening jars
Splints
o Thumb Spica splint - This splint keeps the wrist and lower joints of the thumb from moving. The splint allows the APL and
EPB tendons to rest, giving them a chance to begin to heal.
Surgical
Surgical release of the roof of the tunnel. - Decompression of first dorsal compartment:
Q. Where do you inject the H&L?
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At the level of the radial styloid into the 1st extensor compartment distal to proximal. Inject intrasynovial but outside the tendon. Aim is to
target the point of maximal tenderness and this often corresponds to the tendon location
Q. What is the position of splint?
Neutral position or position of safe immobilization
Q. What are the boundaries of your Anatomical Snuff Box?
Radially: APL, EPB
Ulnar: EPL
Contents: Scaphoid, Radial Artery.
Q. Differential diagnosis of DQTS? (Pain over radial styloid)
Scaphoid #
Radial styloid #
Radial styloid OA
1st CMC OA
Wartenberg Syndrome- isolated neuritis of the superficial radial nerve;
Intersection syndrome - the tendons of the first compartment may cross over the tendons of the second
compartment (ECRL/B),
OA Hands
Examine this patient’s hand
Approach
Expose till shoulder, place hands on pillow, palms up.
1. Examine joints: look feel move
2. Examine other joints: CMC, PIPJ, Knees, OA
3. NV Assessment
4. Functional screen: write, unbutton shirt(for males)
Q. Describe what you see
“This is an elderly gentle. He has asymmetrical bilateral deforming polyarthropathy affecting the DIPJ”
Q. What are Heberden’s Nodes?
They are hard or bony swellings which can develop in the distal interphalangeal joints (DIP).
They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the articular (joint) cartilage
- Heberden's nodes:
- cystic swellings containing gelatinous hyaluronic acid appear on the dorsolateral aspects of DIP joints
Q. What causes these nodes?
Heberden's nodes typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset
of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a
permanent bony outgrowth that often skews the fingertip sideways.
Q. Where else will you look?
1. Bouchard's nodes may also be present; these are similar bony growths in the proximal interphalangeal(PIP) joints (middle joints of the
fingers), and are also associated with osteoarthritis.
2. CMCJ – grind test, squaring of hand or metacarpal bossing appearance.
3. signs of OA in Knees
4. Signs of OA in hips
Q. What are you differentials? What to exclude?
Gout, RA
Q. What goes against gout in HER case?
- FEMALE!!! Gout tends to occur in males.
Q. What Investigations will you do?
RA: RF, Anti CCP
Gout: Uric Acid
X ray Hand
Q. What would you like to ask in history from this patient?
Age
Handedness
Occupation
Affect on Hand function, work, ADL, IADL
Q. What is the management of OA Hands?
Take a quick history to assess
4
1.
2.
3.
4.
Age
Occupation
Hand Dominance
Affect on hand function, Work, ADL, IADL
Do a quick PE
Start with conservative treatment first
Non surgical
Pharmacological
Paracetamol, NSAIDS, opiates
Non pharmacological
Rest
PT
Lifestyle modifications
Aids/splints
Surgical
Arthroplasty
Arthrodesis
RA Hands (Refer to Ramachandran for more)
Q. Describe what you see? Examination Approach
EXPOSE PATIENT TILL SHOULDERS, LAY PALMS UP on Pillow
General inspection: Look for cushingoid facies due to treatment
Local inspection
“This patient has a bilateral symmetrical deforming polyarthropathy affecting the proximal joints of the hand, such as the PIPJ and MCPJ” On
inspection I note that there is ………..
Look
Wrist
Subluxation of the wrist joint
Radial Deviation of wrist due to subluxation of the ECRL tendons
Piano Key sign – due to subluxation of the distal radio-ulnar joint that causes the ulnar head to jut out.
Palmar erythema
Wasting of the 1st dorsal Interosseous muscles
Fingers
Z thumb
Ulnar deviation of the fingers
Boutonnière’s deformity
Swan neck deformity
Subluxation of the MCPJ
Swelling of the MCPJ
Treatment
Scars due to surgery for tendon release/tendon transfer
Say important negatives:
There is absence of pitting of the nails
Absence of any salmon pink patches with silvery scales of Psoriatic arthritis
Feel
Move
-
Swelling
Pain/Tenderness
Warmth
Decreased ROM.
REMEMBER TO LOOK FOR EXT TENDON RUPTURE – test the extension of MCPJ.
End off by wanting to
1. Examining other joints
2. Examining for extra articular manifestations
3. NV Assessment – Do a tinel’s to assess for carpal tunnel syndrome
4. Functional Assessment of Hand – writing, unbuttoning shirt
5. Look for complication of Treatment (Steroid toxicity) – BP, Slit lamp examination, 2 pinch test, h/c
Q. What are the Hand Signs of RA?
Wrist
Subluxation of the wrist joint
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Fingers
-
Radial Deviation of wrist due to subluxation of the ECRL tendons
Piano Key sign – due to subluxation of the distal radio-ulnar joint that causes the ulnar head to jut out.
Palmar erythema
Wasting of the 1st dorsal Interosseous muscles n other intrinsics
Z thumb
Ulnar deviation of the fingers
Boutonnière’s deformity
Swan neck deformity
Subluxation of the MCPJ
Swelling of the MCPJ
Q. What are the extra articular signs of RA?
Skin
Rheumatoid Nodules  Commonest extra articular manifestation
Eyes
Scleritis
Episcleritis
Keratoconjunctivitis secca
CardioPulmonary
Pulmonary fibrosis
Pleural Effusion
Pericarditis
vasculitis
Reticuloendothelial
Lymphadenopathies
Splenomegaly
Lymphoma?
Neurological
Carpel tunnel syndrome
Peripheral neuropathies
Q. What are your Differential Diagnosis?
1. Psoriatic Arthropathy – but not because of the absence of psoriatic patches
2. Gout – unlikely if its a female, and gout tends to be asymmetrical
3. Jaccound’s arthropathy – deforming arthropathy is reversible when hands are placed on a flat surface
Q. What tests can you do to confirm RA?
General: FBC, ESR, CRP
RA: RF, HLA DR3/4, Anti CCP (MORE SPECIFIC - anti-cyclic citrullinated peptide antibody)
SLE: ANA, Anti ds dna, Anti sm, C3, c4
Gout: Uric acid, X ray Hands
Q, What is the percentage of patients with RA that have a Positive RF?, HLA- DR3/4? ANA?
75% of RA patients are positive for RF
33% of RA patients are positive for HLA DR3 DR4
30% of RA patients are positive for ANA
Q. Management of RA hands?
Take a quick history to assess
1. Age
2. Occupation
3. Hand Dominance
4. Affect on hand function, Work, ADL, IADL
Diagnostic criteria of RA

Symmetrical arthropathy

Affects small joints of hands for > 6/52

Rh +

Xray changes +

Affects > 3 joints for > 6/52

Morning stiffness > 1hr for > 6/52

Subcutaneous nodules
Do a quick PE
Start with conservative treatment first
1. Non Surgical
Pharm
Analgesia: Paracetamol, NSAIDS, Opioids, H&L
DMARDS: SSZ, HXQ, Penicillamine, Gold, MTX
Non Pharm
Rest
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Splintage
Lifestyle modifications
Assist devices
PT
2. Surgical
Soft tissue
Synovectomy and debridement
Tendon Transfer
Tendon repair
Bones
Arthroplasty
Arthrodesis
Realignment Osteotomy
Ganglion Cyst
Q. What is the definition of a ganglion cyst? Where does it arise from?
A ganglion is a cystic mucoid myxomatous degeneration of the tendon sheath or synovium of the joint capsule.
This results in herniation of synovial fluid through the areas of degeneration to for a cyst.
Majority or dorsal wrist ganglions arise from the scapholunate joint (90 to 95%)
Otherwise, ganglions can originate from the tendon sheath or the synovium of joints (Radiocarpal joint)
Q. Where are the common areas of ganglion occurrences?
Dorsal Wrist  Commonest site of occurrence
Volar Wrist
Fingers
Dorsum of Ankle
Q. What does it contain?
Synovial Fluid
Q. How do patient’s with ganglion present?
- Worried about a lump that is cancerous
- Cosmesis issue
- Ganglion affecting ROM of joints
- affecting hand function
Q. What else will you ask the patient?
How the ganglion has affect the patients life
Age
Occupation
Handedness
Whether they have noticed similar lumps elsewhere?
Q. Describe the lump
This is a ganglion as evidenced by the mass being located over the dorsal aspect of the Right Wrist. It is solitary hemispherical lump, of A by B
cm in diameter. … See below
Q. What are the characteristics of a Ganglion?
Scars: Indicate recurrent ganglion after previous excision
Solitary,
hemispherical lump
located over the dorsal/ventral wrist/hand that is
small/large in size of ____
Smooth
Hard, tense  Small OR Soft, fluctuant  large
Regular edge
Multiloculated (feel like collection of cyst)
Transilluminable brilliantly
Reducibility +/Surrounding skin is normal.
No thrill/bruits
Not warm
Non tender/Tender
Not attached to overlying skin
Non pulsatile, non expansile
No lymph nodes present
Q. What are your Differential Diagnoses?
Compound Ganglion
7
-
Lobulated Lipoma
Aneurysm (if over the wrist)
PVNS
Neuroma
Sebaceous cyst
Bursae
Q. How do you differentiate a Lipoma from a ganglion?
Lipoma
No transilluminance
Slip sign
Lobulated
Irregular edges
Not attached to underlying structures
Ganglion
Transilluminance
No slip sign
Single or multiloculated
Defined edges
Attached to underlying structures
Q. How do you confirm if it’s a ganglion by the bedside?
Transilluminate or Aspirate
Q. Will Lipomas transilluminate?
No. They do not transilluminate. But Ganglions transilluminate brilliantly
Q. What is a slip sign?
Slip sign describes the manner in which the lipoma tends to slips away from the examining finger on gentle pressure.
Note: Diagnosis is CLINICAL. X ray may be taken to exclude any joint pathology
Q. What is the Management?
Take a quick history to assess
1. Age
2. Occupation
3. Hand Dominance
4. Affect on hand function, Work, ADL, IADL
Do a quick PE
Start with conservative treatment.
Conservative
- Rest, watch and wait (expectant management is appropriate if the mass is not painful or interfering with function.) Many will regress over
months
- Aspiration
Surgical
- Surgical Excision of the ganglion at the neck
Q. Surgical complication?
- Bleeding  damage to Radial Artery
- Infection
- Recurrence of Ganglion
- May develop contractures, scars
- scapholunate dissociation (if it’s a dorsal wrist ganglion)
Q. How do you prevent complications of injury to radial artery?
- Do not use tourniquet during the operation. (Aziz)
NOTE: Hand operations USE TOURNIQUET to make the surgical site less bloody.
Q. What is the recurrence rate for Aspiration of a Ganglion?
Almost 100%
Q. What is the recurrence rate of Surgical Excision?
<10% (Prof Aziz) to 30% (standard teaching)
Q. Where to place incision?
Along the lines of Langer, perpendicular to the tendon – so that should post op contractures occur, it will not affect the finger movement
Langer’s Lines: cleavage lines, is a term used to define the direction within the human skin along which the skin has the least flexibility. These
lines correspond to the alignment of collagen fibers within the dermis
Gouty Tophi
Q. Describe what you see?
Sing the song
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Q. Common Locations of Gouty Tophi?
Finger joints
Olecranon Bursae
Pinna of the ear
Knees
1st MT
Dorsum of Foot
Achilles tendon
Q. Differential diagnosis of acute gouty arthritis?
Septic Arthritis
Pseudogout
RA
Bursitis
Monoarticular gout can look exactly like SA -- beware
Gout and SA can be differentiated by Joint aspiration. Look for birefringent crystals
Gout and Pseudogout can be differentiated by the below list
Gout and RA can be differentiated by Joint aspiration, X ray and clinical features
Q. What is the Difference between Gout and Pseudogout?
Gout
Male > female
Smaller joints
Pain is intense
Joint is inflamed
Gouty tophi seen
Hyperuricemia
Urate Crystals
Negatively birefringent crystals, needle shaped
Pseudogout
Female > Male
Larger joints
Pain moderate
Joint is swollen
Chondrocalcinosis
Normal Uric acid level
CPPD
Weakly positively birefringent, linear or rhomboid
Q. What are the Predisposing factors for acute gout attack?
- Hyperuricemia
- Obesity
- Hypertension
- Hyperlipidemia
- Alcohol
- Meat
- Fish
- Trauma
- Surgery
- Dietary indiscretion
- Starvation
- Drugs that affect uric acid levels  NOTE: Uricosuric agents/Allopurinol should NOT be given during an acute attack as they precipitate
gouty attacks.
 uric acid production

Dietary

 cellular breakdown – psoariasis, lymphoproliferative disorders

Obesity

Alcohol

Dehydration
 uric acid secretion

Renal impairment

Medications
Q. What reduces risk of Gout attacks?
- Dairy products
- Coffee Consumption
Q. What do you know about gout?
Gout: Monosodium Urate Crystal deposition disease
Gout has 3 clinical stages in its natural progressive history.
1. Acute Gouty arthritis attack
2. Interval/intercritical gout
3. Chronic Tophaceous gout.
Progression from stage 1 to 3 occurs in about 12 years if untreated. The duration of remission shortens, frequency of attacks increase,
duration of attack lengthens, initial monoarticular gout becomes polyarticular gout till Chronic tophaceous gout occurs.
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Acute Gouty Arthritis
Fever, constitutional symptoms
Joint is Pain/inflamed/Stiffness/Swelling/Erythema/Disability  1st attack: 80% Monoarticular, 20% polyarticular
With increasing no. of recurrent attacks, monoarticular gout progresses to involve other joints and become polyarticular
Signs of inflammation affecting surrounding soft tissue (dactylitis, cellulitis, tenosynovitis)
No signs of gouty tophi?
Intercritical gout
Asymptomatic
Duration of remission varies. If untreated, duration decrease and attack frequency increases
Chronic Tophaceous Gout
Characterised by collection of sodium urate crystal deposition in connective tissue.
Tophi are visible or palpable and can be present on the wars or in the soft tissues including articular structures or bone. Tophi are
typically not painful or tender
Q. Investigations?
FBC
ESR
CRP
X-ray: Acute Attack: Soft tissue swelling. Chronic Gout: “Punched out cysts”, Narrow Joint space, 2OA changes
Uric Acid
Joint aspiration – send for
- Cytology
- Biochemistry
- Microscopy for birefringent Crystals
- Gram Stain and Aerobic and anaerobic culture
- AFB Smear and AFB Culture
Q. Diagnosis of Gout?
Gold standard is: Visualisation of Na Urate crystals in joint aspirate or tophi.
If cannot visualize: base diagnosis of clinical features
Q. Management of Acute gout?
Pharmacological
Main aim is to quickly control pain and inflammation and disability
1. NSAIDS  first line drug
2. Colchicine  Used second line as it has more unpleasant side effects than NSAIDS
3. Steroids – Intraarticular or systemic
NOTE: Uricosuric agents/Allopurinol should NOT be given during an acute attack as they precipitate gouty attacks. They are used to prevent
gout, but can only be given after the attack has settled. After ~3/52
After Gout attack, can start uricosuric agents or Allopurinol.
Allopurinol is a drug used primarily to treat conditions arising from excess uric acid in blood plasma. Most notable of these conditions is
chronic gout. Allopurinol does not alleviate acute attacks of gout, but is useful in preventing recurrence.
Uricosuric medications (drugs) are substances that increase the excretion of uric acid in the urine, thus reducing the concentration of uric
acid in blood plasma. Generally, this effect is achieved by action on the proximal tubule. Uricosurics often are used in the treatment of gout,
a disease in which uric acid crystals deposit in joints. By decreasing plasma uric acid levels, uricosurics help to help to dissolve these crystals
and limit the formation of new crystals. However, by increasing urinary uric acid levels these drugs may contribute to stones (calculi) in the
kidneys and urinary system (see Uric acid nephrolithiasis). Thus use of these drugs is contraindicated in persons who already have a high
urine concentration of uric acid (hyperuricosuria). In borderline cases, hydration sufficient to produce 2 liters of urine per day may be
sufficient to permit use of an uricosuric drug.
Non Pharmacological
Stop diuretics
Stop alcohol (beer)
Stop high protein/purine diet (Red meat, legumes, bean curd, seafood)
Lose weight
Control hypertension, hyperlipidemia
Hydration: Drink plenty of liquids, especially water, to dilute and assist excretion of urates;
Q. What are the side effects of Colchicine?
GI side effects: nausea/vomiting, diarrhoea
Neutropenia
Anaemia due to bone marrow suppression
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Radial Nerve Palsy
Patient has difficulty raising his hand. Examine this mans hand.
Nerve Approach
1. Confirm Radial Nerve is involved
2. Confirm the level of lesion
3. Assess other nerves to see if it’s a Root or Nerve
4. Look for the cause
5. Assess patient’s hand function
1. Confirm Radial Nerve is involved. (What are the signs of Radial N. Palsy?)
Motor (Inspection)
Finger drop
Wrist drop
Inability to extend elbow
Wasting of extensor muscles
Sensory
(High lesion) Loss of sensation over 1st dorsal interossei
Autonomic
decreased sweating
2. Confirm the level (Where is the lesion?)
Motor
Elbow Extension
- Triceps Brachii
Long/medial  RN before groove
Lateral/medial  RN in groove
- Anconeus  RN in groove
Wrist Extension
- ECRL  RN
(Brachioradialis/Brachialis RN supply given
off here but they are not extensors)
Supply given off Above elbow
Supply given off Below elbow
- ECRB  DRN
- ECU  PIN
MCPJ Extension  by PIN
- Extensor digitorium
- Extensor indices
- Extensor pollicis brevis
- Extensor pollicis longus
- Extensor digiti minimi
- Abductor pollicis brevis
Inspection
Sensory
High (Axilla)
Brachial Plexus
injury
Saturday night palsy
Crutch Palsy
Middle
- Fracture of shaft of
humerus – radial groove
Low
- Elbow lesion  PIN
lesion (rarer)
Weak
Strong
Strong
Weak
Weak
Strong
Weak
Weak
Weak
Finger and Wrist drop
Finger and wrist drop
Finger drop
Absent
Absent
Present
Remember to test the sensation of regimental badge area: for Axillary nerve injury due to humeral neck fracture
Test abduction of the arm: Deltoid supplied by the axillary nerve
3. Screen the (Is it root or Nerve?)
Test the strength of the bicep brachii (C5, C6, Musculocutaneous N)
Test the strength of the Deltoids (C5, C6, Axillary Nerve)
Test the strength of the Brachioradialis (C5, C6, Radial Nerve)
If Bicep Brachii and deltoids normal  Isolated radial nerve palsy. C5, C6 roots not involved
If all weak  C5, C6 nerve root involved
4. Look for the cause of lesion
- look for scars at the elbow  low lesion
- Look for scars at the forearm  middle lesion ORIF of Humeral fracture
- Look for crutches  high lesion
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5. Assess Hand Function!  Very IMPT!
- Writing, unbuttoning shirt, chopsticks
Q. Where are the common sites of Radial Nerve Lesion?
Axilla
Radial Groove of humerus
Elbow
Q. What level is the lesion?
Refer above table
Q. What is the course of the radial Nerve?
Radial Nerve arises from the brachial plexus in the neck and is supplied by the C5, C6, C7,C8, T1 nerve roots
From the brachial plexus, it travels posteriorly in the axilla.
The radial nerve enters the arm behind the axillary artery/brachial artery, and it then travels posteriorly on the medial side of the arm.
After giving off branches to the long and lateral heads of the triceps brachii, it enters a groove on the humerus, the radial sulcus.
Along with the deep brachial artery, the radial nerve winds around in the groove (between the medial and lateral heads of the triceps)
towards the forearm, running laterally on the posterior aspect of the humerus.
While in the groove, it gives off a branch to the medial head of the triceps brachii.
The radial nerve emerges from the groove on the lateral aspect of the humerus.
At this point, it pierces the lateral intermuscular septum and enters the anterior compartment of the arm.
It continues its journey inferiorly between the brachialis and brachioradialis muscles.
When the radial nerve reaches the distal part of the humerus, it passes in front of the lateral epicondyle and continues in the forearm.
In forearm
In the forearm, it branches into a superficial branch (primarily sensory) and a deep branch (primarily motor).
The superficial branch of the radial nerve descends in the forearm under the brachioradialis. It eventually pierces the deep fascia near the
back of the wrist.
The deep branch of the radial nerve pierces the supinator muscle, after which it is known as the posterior interosseous nerve
Q. What is the Prognosis of Radial Nerve injury?
Seddon's classification is a scheme for describing nerve injury.
1. Neurapraxia -- temporary paralysis of a nerve caused by lack of blood flow or by pressure on the affected nerve with no loss of
structural continuity.
2. Axonotmesis -- neural tube intact, but axons are disrupted. These nerves are likely to recover.
There is disruption of the neuronal axon, but with maintenance of the myelin sheath. Mainly seen in crush injury.
3. Neurotmesis -- the neural tube is severed. These injuries are likely permanent without repair, and will likely only achieve partial
recovery at best.
Usually Neurapraxia?
Nerve grows 1mm a day
*most important factor for nerve regeneration is AGE!! > 60years, regeneration potential is poor 
Q. Management of Radial Nerve Palsy?
Take a quick history to assess
1. Age
2. Occupation
3. Hand Dominance
4. Affect on hand function, Work, ADL, IADL
Do a quick PE
Start with conservative treatment first
Non surgical
Rest
PT
Cockup splint
Surgical
- Surgical reconstruction?
Carpel Tunnel Syndrome (Median N Palsy)
Examine this man’s hand
Nerve Approach
1. Confirm Median Nerve is involved
2. Confirm the level of lesion
3. Assess other nerves to see if it’s a Root or Nerve
4. Look for the underlying cause of CTS if any.
5. Assess Hand function!!!
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1. Confirm Median Nerve is involved. (What are the signs of Median N. Palsy?)
Motor (Inspection)
Wasting of Thenar Eminence
Weakness of the APL
(Note: Clawing/Benediction sign  high Median Nerve palsy. CTS  NO BENEDICTION SIGN)
Sensory
(high lesion) Loss of sensation over the radial 3 and ½ fingers (Entire palmar aspect and dorsal aspect from PIPJ to finger tips
low lesion/CTS - Loss of sensation over the radial 3 and ½ fingers (Palmar aspect and dorsal aspect from PIPJ to finger tips – but
SPARING THE SENSATION OVER THENAR EMINENCE)
2 point discrimination (optional)
Autonomic
decreased sweating
Provocative tests
Tinels sign
Phalen’s sign
Flexion compression test
2. Confirm the level (Where is the lesion?)
1. Test the FDP of 2nd finger. (MOTOR)
 if weak  High lesion  look at the elbow for scars  cubital tunnel syndrome or tardy ulnar nerve palsy secondary to malunion of
supracondylar fracture of the humerus
 if strong  Low lesion  look at the wrist for scars  carpal tunnel
2. Test the sensation over the thenar eminence (SENSORY)
 if insensate  High Lesion
 if sensate  low lesion
3. Screen the Median Nerves (Is it root or Nerve?)
Test the strength of the Interossei
} If normal  Isolated median nerve palsy
Test the sensation over the little finger } if not normal  likely C8, T1 Nerve root problem.
4. Look for the cause of lesion
- look for scars, or mass over the Carpel canal
- Look for scars over the elbow/forearm  possible pronator syndrome (rare), AIN Syndrome (rare).
- Examine the neck!!!
5. Assess Hand Function!  Very IMPT!
- Writing, unbuttoning shirt, chopsticks
Q. What are the causes of CTS?
Primary:
Idiopathic  Commonest cause of CTS
Secondary:
Anatomical – Colles fracture, compression by ganglion, lipoma
Physiological States
DM, Gout, RA
Hypothyroidism, Acromegaly
Pregnancy, Menopause
Amyloidosis, Renal Failure, Nephrotic Syndrome
Q. What is a typical History of CTS?
Pain, numbness, tingling, burning sensation in the radial 3 and ½ fingers
Woken up in the middle of the night due to pain
Pain relieved by shaking the affected hand
Q. Differential diagnosis?
- Cervical Root Lesion (Thoracic outlet obstruction or Cervical Spondylosis)
- High Median Nerve root lesion
Q. Investigations to order to confirm diagnosis?
NCS
Q. What will you look out for on NCS?
Decreased conduction velocity along the nerve (increased latency)
But a negative result does not rule out CTS.
Q. Management of CTS?
Take a quick history to assess
1. Age
2. Occupation
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3.
4.
Hand Dominance
Affect on hand function, Work, ADL, IADL
Do a quick PE
Start with conservative treatment first
Non Surgical
TREAT UNDERLYING CONDITION
Pharm
Paracetamol
NSAIDS
H&L – Injected proximal to the tunnel!!!
Non Pharm
Rest
PT
Night Splintage – Wrist splint
Lifestyle modification
Surgical
Carpel Tunnel Decompression
Q. Complications of Carpel Tunnel Decompression?
Bleeding
Wound infection
Wound Scar
Recurrence of symptoms
Nerve injury
Q. What are the muscles in the thenar eminence?
Opponens pollicis
Abductor pollicis
Flexor Pollicis brevis
Ulnar Nerve Palsy (Claw Hand) *Always think of cubitus valgus as a cause!*
Examine this man’s hand
Nerve Approach
1. Confirm Ulnar Nerve is involved
2. Confirm the level of lesion
3. Assess other nerves to see if it’s a Root or Nerve
4. Look for the cause  Look at the wrist, elbow and NECK - Look for Cubitus VALGUS! Which causes tardy ulnar nerve palsy
5. Assess Hand function!!!
1. Confirm Ulnar Nerve is involved. (What are the signs of Ulnar N. Palsy?)
Motor (Inspection)
Clawing
Wasting of Hypothenar Eminence
Guttering of the hand
Wasting of the 1st dorsal interossei
Weakness of intrinsic muscles: Froment’s Sign Positive
Sensory
(High lesion) Loss of sensation over the ulnar 1 and ½ fingers (Entire palmar aspect and dorsal aspect)
(Low Lesion) Loss of sensation over the ulnar 1 and ½ fingers (Entire palmar aspect and dorsal aspect from PIPJ to finger tips
Autonomic
decreased sweating
2. Confirm the level (Where is the lesion?)
1. Test the FDP of little finger. (MOTOR)
 if weak  High lesion  look at the elbow for scars  cubital tunnel syndrome or tardy ulnar nerve palsy secondary to malunion of
supracondylar fracture of the humerus
 if strong  Low lesion  look at the wrist for scars  Guyons’ canal.
2. Test the sensation over the dorsal ulnar aspect of hand (SENSORY)
 if insensate  High Lesion
 if sensate  low lesion
3. Screen the Median Nerves (Is it root or Nerve?)
Test the strength of the APL
} If normal  Isolated ulnar nerve palsy
Test the sensation over the index finger } if not normal  likely C8, T1 Nerve root problem
4. Look for the cause of lesion
- look for scars, or mass over the guyon’s canal
- Look for scars over the medial epicondyle  possible ulnar nerve decompression/anterior transposition of ulnar nerve or medial
epicondyletomy.
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- Look at the elbow for scars due to previous surgery for a lateral condyle fracture of humerus.
- Examine the Elbow for Cubitus Valgus and signs of Non union of lateral condyle fracture of humerus.
- Examine the neck!!!
5. Assess Hand Function!  Very IMPT!
- Writing, unbuttoning shirt, chopsticks
Q. What is the Guyon’s canal?
The ulnar canal, also called Guyon's canal, is a potential space at the wrist between the pisiform bone and the hamate bone through which
the ulnar artery and the ulnar nerve travel into the hand.
Q. Anywhere else you want to examine?
- Look for scars, or mass over the guyon’s canal
- Look for scars over the medial epicondyle  possible ulnar nerve decompression/anterior transposition of ulnar nerve or medial
epicondyletomy.
- Examine the Elbow for Cubitus Valgus and signs of Non union of lateral condyle fracture of humerus.
- Examine the neck!!!
- Assess Hand Function!  Very IMPT!
Q. Is the ulnar Nerve palsy a HIGH or LOW Lesion?
Confirm the level (Where is the lesion?)
1. Test the FDP of little finger.
 if weak  High lesion  look at the elbow for scars  cubital tunnel syndrome or tardy ulnar nerve palsy secondary to malunion of
supracondylar fracture of the humerus
 if strong  Low lesion  look at the wrist for scars  Guyons’ canal.
2. Test the sensation over the dorsal ulnar aspect of hand
 if insensate  High Lesion
 if sensate  low lesion
Q. What do you think is the CAUSE of the ulnar nerve palsy?
Look for scars!!!
Very High lesions (rarer)
- Pancoast tumour
- Cervical lesions affecting nerve roots
High Lesions
- Cubital Tunnel Syndrome
- Non union of a lateral condyle fracture of the humerus resulting cubitus valgus and subsequent Tardy ulnar nerve palsy
Low lesions
- Ganglion over Guyon’s canal
Q. Why does ulnar nerve palsy causes clawing of the little and ring finger?
The Ulnar nerve supplies innervations to the intrinsic muscles of the hand such as the palmar, dorsal interossei and 3 rd and 4th lumbricals,
hypothenar eminence and adductor pollicis.
The interosseus and 3rd and 4th lumbrical muscles supplied by the ulnar nerve are responsible for causing flexion of the MCPJ and extension
of the interphalangeal joints. However with ulnar nerve palsy there is paralysis of these muscles, the MCPJ goes into hyperextension and
there is flexion of the interphalageal joints of the little and ring finger which causes the claw hand. The radial 3 fingers are unaffected as the
1st and 2nd lumbricals are supplied by the median nerve.
Q. What muscles of the thumb does the ulnar nerve supply?
Adductor pollicis
Q. What prognosis is the recovery for this patient?
Seddon's classification is a scheme for describing nerve injury.
1. Neurapraxia -- temporary paralysis of a nerve caused by lack of blood flow or by pressure on the affected nerve with no loss of
structural continuity.
2. Axonotmesis -- neural tube intact, but axons are disrupted. These nerves are likely to recover.
There is disruption of the neuronal axon, but with maintenance of the myelin sheath. Mainly seen in crush injury.
3. Neurotmesis -- the neural tube is severed. These injuries are likely permanent without repair, and will likely only achieve partial
recovery at best.
Q. What are the differentials of an ulnar claw hand?
Ulnar Nerve palsy
Trigger Finger
Dupuytren's Contracture
Cubitus Valgus  *think of Tardy Ulnar N Palsy*
Q. Examine this man’s elbow and describe what you see
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Elbow Examination
Start with patient placing arms touching the side of the body with palms facing anteriorly. (Anatomical position)
Look
Note the carrying angle
Look for hyperextension, and fixed flexion deformity
Feel
Assess the isosceles triangle
Tenderness
Crepitus
Warmth
Move
Flexion/Extension
Supination/Pronation
Look for scars
NV Examination  assess Ulnar Nerve
Assess function of hand
Q. What causes a cubitus valgus deformity?
Non union of fracture of the lateral humeral condyle due to pull of muscles attached to it?
Fracture causes damage and premature growth arrest of lateral condyle causing the medial condyle to grow relatively more than
the lateral condyle causing the elbow to progressively develop into a cubitus valgus;
Q. What else will you examine for? What associated injuries are there?
Tardy Ulnar Nerve Palsy (TARDY = late onset/sign!!! Many years. First sign is neuritis)
Signs of Tardy Ulnar Nerve Palsy
Non promiment clawing  ulnar paradox
Wasting of Hypothenar eminence
Wasting of 1st dorsal interossei
Guttering of dorsum of hand
Weakness of FDP(U)
Weakness of Interossei
Froment’s sign Positive
Loss of sensation over ulnar 1 and ½ fingers dorsal and palmar aspect
Diminished 2 point discrimination
Loss of sweating
Ulnar paradox = distal lesion leads to imbalance between the intrinsic and extrinsic muscles, resulting in a more severe claw hand compared
with a proximal lesion which affects both the intrinsic (interossei and lumbricals) and extrinsic muscles (flexor digitorum profundus and
superficialis).
Q. What are the muscles of the hypothenar and thenar eminence?
Thenar Eminence
Opponens pollicis
Abductor pollicis
Flexor Pollicis brevis
Hypothenar Eminence
Flexor digiti minimi
Opponens digiti minimi
Abductor digiti minimi
Q. Treatment?
The deformity of elbow is corrected by opening wedge osteotomy of distal humerus w/ graft wedge & ulnar nerve is transposed anteriorly;
- osteotomy may be indicated for cubitus valgus more than 20 deg;
Cubitus Varus
Q. What do you see?
SAY: GUNSTOCK DEFORMITY!
Q. Test the ROM?
Elbow Examination
Start with patient placing arms touching the side of the body with palms facing anteriorly. (Anatomical position)
Look
Note the carrying angle
Look for hyperextension, and fixed flexion deformity
SAY: GUNSTOCK DEFORMITY!
Feel
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Assess the isosceles triangle
Tenderness
Crepitus
Warmth
Move
Flexion/Extension
Supination/Pronation
Look for scars
Assess NV Status  Test Median Nerve, Feel for Brachial Pulses and distal pulses
Assess Hand function
Q. Landmark of the elbow?
The isosceles triangle between the Medial and lateral epicondyle and tip of olecranon process
Q. What is the cause of Cubitus Varus?
Malunion of a supracondylar fracture
originally, aetiology of cubitus varus was thought to occur because of growth disturbance of distal humeral epiphysis; - this may be true but is
uncommon;
- current thinking is that it stems from malreduction of frx, with medial displacement, internal rotation, and extension of the distal
fragment; - this then permits distal fragment to tilt into varus;
Q. What are the associated injuries in Supracondylar fracture? (What nerve lesion?)
Brachial artery injury
Median Nerve Injury
Q. What else would you like the examine for?
Examine the peripheral BRACHIAL pulses and capillary refill
Examine the hand neurologically for the presence of median nerve palsy.
Q. What would you offer her?
Corrective osteotomy of the humerus and either internal or external fixation of the bone until union
Q. What kind of disability do you think this man will have?
None. cubitus varus deformity is more cosmetic than limiting of any function
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OA Knees (Refer to long case questions for more)
Examine this man’s knee
Q. What are the signs of OA knees?
1. KNEE Articular signs
Inspection
- Genu varum
- FFD of knee
- Lateral thrust/antalgic/stiff knee gait
- Baker’s cyst – associated with degenerative joint disease
- Quadriceps wasting
Palpation
- Effusion (bulge test, cross fluctuation, patellar tap)
- Crepitus
TFOA - On Flexion and extension
PFOA – Patellar Grind Test +ve
- Tenderness
Joint line tenderness
Movement
Decreased ROM, with FFD
Positive on valgus stress test (From collapsed medial compartment to neutral position)?
2. OTHER peripheral signs of OA of other joints
- Heberden’s and Bouchard’s nodes!!!  Remember to look for these in the whole patient!
- Examine to rule out RA and gouty tophi!
Q. How much Fluid is needed for Bulge test to be positive?
Most sensitive test – 10 cc
Q. What is the management of OA knees?
Non Surgical
Non Pharmacological
Rest
PT
Lifestyle modification
Walking aids
Splints/braces
Weight loss
Pharmacological
Paracetamol
NSAIDs
H&L
Hyaluronic Acid
Glucosamine sulphate and chondroitin sulphate (chondroitin not proven to be useful in patients with OA; glucosamine use is EBM
for hip and knee OA, not thumb etc OA)
Surgical
Arthroscopic washout and debridement
Total Knee Arthroplasty
Unicompartmental Knee Arthroplasty
Arthodesis
Patellectomy
High Tibial Osteotomy
Q. Investigations for OA knees?
Diagnosis
- X- rays (WEIGHT BEARING or STANDING AP/Lateral, Skyline views)
Preop Assessment:
FBC, U/E/Cr, CXR, ECG, PT/PTT, GXM, UFEME
Q. What are the causes of OA knees?
Primary OA
Secondary OA – from trauma, intraarticular fractures
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Baker’s Cyst
Q. What is a Baker’s Cyst?
It is a posterior herniation of the knee joint capsule.
Q. Differential diagnosis
PVNS
Ganglion
Lipoma
Aneurysm
Saphena varix of SFJ
Q. How to differentiate PVNS and Baker’s cyst?
On flexion, Baker’s Cyst disappears
ACL Tear
REMEMBER TO CHECK FOR POSTERIOR SAG BEFORE ANT. DRAWER
Q. Mechanism of Injury?
Running or jumping athlete who suddenly decelerates and changes direction (eg, cutting) or twists/pivots causing rotation or lateral bending
(ie, valgus stress) of the knee, tearing the ACL.
Q. What are the symptoms of ACL tear?
Often occurring in the context of sport, but can also occur in non contact sport
Associated with a deceleration or rotational/twisting stress/valgus stress to the knee
Patient feels a pop sound in the knee, a sudden feeling of instability and giving way
Pain over the medial joint line
Patient is often unable to bear weight post trauma
Swelling of the knee is noted to occur immediately over hours due to Hemarthrosis
-
Often after the initial swelling has improved, patients are able to bear weight but complain of instability. Movements such as
squatting, pivoting, and stepping laterally, and activities such as walking down stairs, in which the entire body weight is placed on
the affected leg, most often elicit such instability.
Q. Why does the patient feel unstable?
Patient feels unstable due to the abnormal anterior displacement of the tibia wrt the femur
Q. Why does the patient feel pain?
Q. Why is there such a displacement in an ACL tear?
This is because the ACL originates from the posteromedial aspect of the lateral femoral condyle to be attached to the anterolateral aspect of
medial tibial plateau. With the rupture of the ACL, the tibia is allowed to displace forward.
Q. In ACL tear, why is the Anterior Drawer positive?
This is because, the rupture of the ACL allows the tibia to translate forward with respect to the femur.
Q. What is the course/function/anatomy of the ACL?
ACL Course
The ACL originates from the posteromedial aspect of the lateral femoral condyle to be attached to the anterolateral aspect of medial tibial
plateau.
It is Intraarticular but extrasynovial
Consists of 2 bundles. Anteromedial which is taut in flexion, lax in extension, and posterolateral which is taut in extension and lax in flexion.
ACL function
1. Offers AP stability preventing anterior movement of the tibia wrt to femur.
2. It also offers rotational stability preventing tibial rotation
3. and valus valgus angulation stability preventing varus valgus stress.
Q. Which activites/movements will most often elicit knee instability in an ACL tear?
Squatting
Pivoting, turning corners abruptly
Stepping laterally
Sudden deceleration
Walking downstairs with entire body weight on affected leg
Q. How do you test for ACL Tear?
Anterior Drawer
Lachman Test  more specific as the knee is flexed at 30 degrees and overcomes the hamstrings
Pivot shift
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Q. Which test is more specific? Why?
- Lachman test is more specific as the knee is flexed at 30 degrees and overcomes the pull of the hamstrings
Q. What causes False Positive Anterior Drawer?
Presence of a PCL tear
Q. What causes a False Negative Anterior Drawer?
Partial ACL Tear
Tight/Tense hamstrings
Q. How to overcome False Negative?
Relax the hamstrings, or perform the lachmann’s test
Q. What Investigations will you do for ACL tear?
X ray: To look for avulsion fractures of the tibial spine
MRI: to confirm diagnosis of ACL tear
Q. What investigations can Confirm ACL tear?
MRI knee
Arthroscopy knee
Q. How would you manage this patient?
Non Surgical (Grade 1 n 2)
Non Pharmacological
Aggressive Hamstring PT
Splint/Aids
Lifestyle modification
Pharmacological
Analgesia: Paracetamol (500mg), NSAIDs, opioids
Surgical (Grade 3 n 4)
Intra articular
ACL Reconstruction by using a autologous hamstring tendon graft or bone-patella tendon-bone graft
Extra articular
Macintosh Tenodesis
Q. Which muscles will you strengthen in a patient with ACL tear?
Hamstrings. As they prevent the forward displacement of the tibia wrt the femur. } x 6 months
Quadriceps, however mainly aggressive hamstring PT. (say this only if they ask for more}
6 to 12 months is the rough time frame for recovery with ongoing aggressive PT
The outcomes of PT is described by Noyes rule of 1/3s. 1/3 improve to normal physical function to play sport. 1/3 has reduced physical
activity, 1/3 have poor instability with sport or ADL and need surgery
Q. When do you want to repair? And why do you want to repair ACL tears?
Decision to surgically repair ACL is dependent on
Age, level of activities, functional demands, and presence of associated injury to other meniscus or ligaments
When patient complains that instability affecting ADL, IADL
When the patient is young and active individual affecting his ability to play sport or engage in activities
When conservative treatment such as PT fails to relieve symptoms of instability.
When there are multiple injuries to knee structures such as concomitant MM or MCL tear or PCL or capsule tear
ACL tears are often repaired because ACL offers AP and rotational stability to the knee. If left unrepaired will lead to abnormal movements of
the knee predisposing to injury to the menisci, MCL and lead to secondary knee OA.
Q. Grafts commonly used for ACL tears?
Autologous hamstring tendons (Semitendinosus, semimembranosus)
Patella Tendon
Allograft
Quadriceps tendon
Q, What are the associated injuries with ACL tear?
MM tear, Lateral CL tear, premature OA secondary to abnormal knee movement
Q. What is triad of O'Donahue?
A sports injury that includes ACL, MCL and MM tear.
PCL Tear
Q. What are the symptoms of a PCL injury?
The most common symptoms of a PCL tear are quite similar to the symptoms of an ACL tear.
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Q. What are the Signs of PCL tear and how do you test to confirm PCL Tear?
Posterior sag sign
Posterior Drawer
Also feel for the “hill-valley-hill” formation
Q. Any other test you can do to show Posterior Sag sign?
- Lift both LL flexed at 90 degrees at the hip and the knees to allow gravity to cause the tibia to fall down in a PCL tear. Look at the tibial
tuberosities from the side to see which leg has posterior sagging.
Q. What do you look for to compare for posterior sag sign?
- Look at the Tibial tuberosity and feel for widened joint space
Q. How to measure Quadriceps wasting?
- Measure at the point 10cm from the superior pole of the patella.
- measure from the medial joint line, 5cm above this point
Q. What is the mechanism of injury for PCL tears/ cause of tears?
This occurs when the knee is bent, and an object forcefully strikes the shin backwards.
Dashboard Injury: It is called a 'dashboard injury' because this can be seen in car collisions when the shin forcefully strikes the
dashboard.
The other common mechanism of injury is a sports injury when an athlete falls on the front of their knee. In this injury, the knee is
hyperflexed (bent all the way back), with the foot held pointing downwards.
These types of injuries stress the PCL, and if the force is high enough, a PCL tear will result.
Q. What investigations will you do to confirm diagnosis?
- MRI
- Arthroscopy?
- x ray to exclude avulsion fracture
Q. How do you manage PCL Tears?
Conservative
Non pharmacological
Rest
Aggressive Quadriceps PT (cf hamstring PT in ACL tears)
Pharmacological
Analgesics (Paracetamol, NSAIDs)
Surgical
PCL Reconstruction with patellar tendon or hamstring tendon (semitendinosis)
Q. Why are most PCL tears treated conservatively?
PCL reconstruction is controversial, complex and results after reconstruction are not good. Surgery is advocated for grade 3 PCL
injuries. (ie. Posterior sag > 15mm) and in patients who are very active and young.
Generally, surgical PCL reconstruction is reserved for patients who have injured several major knee ligaments, or for those who
cannot do their usual activities because of persistent knee instability.
Q. Attachments of the PCL?
Originates from the lateral aspect of the medial femoral condyle to be inserted in a depression 1 cm inferior to the articular surface on the
posterolateral aspect between the medial and lateral tibial plateaus
Osgood Schlatter’s Disease
Q. What are the Features of OSD?
OSD: also known as Osteonecrosis of tibial tuberosity. (Traction apophysitis)
Features
Benign self limiting condition.
Pain increasing gradually over time.
Exacerbated by direct trauma, running, jumping, or kneeling and is relieved by rest.
Tenderness over tibial tubercle with soft tissue swelling
Pain can be reproduced by resisted knee extension
ROM not affected, PF stable
Q. What are the predisposing factors to OSD?
Young man or women
Avid Sportsmen that are involved in jumping sports like basketball and gymnastics, because jumping places great stress on the tibial
tuberosities through repetitive contraction of the quadriceps.
Young man + knee pain  DDx: Osteochondritis dessicans
Young woman + knee pain  CMP (chondromalacia patellae)
Q. What are your differential diagnosis?
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Stress fracture of proximal tibia
Peripatellar tendonitis
Quadriceps tendon avulsion
Bone tumors very rarely occur and cause pain
All these differentials can be differentiated easily as OSD always has characteristic tenderness over tibial tubercle.
Q. How do you manage?
Conservative treatment is the mainstay of therapy. Symptoms typically resolve over 6 to 18 months.
Complete avoidance of sport is not necessary. Sporting activity is encouraged even with pain.
1. Rehabilitation with strengthening of quads and hamstrings
2. Osgood Schlatter Pad
3. Ice over involved area
4. Paracetamol, NSAIDS
Casts and crutches are rarely needed. Cast causes atrophy of quads and hamstrings.
Hereditary Multiple Exostosis
Q. Describe what you see
Hard, non tender, smooth surface, narrow base, point away from joint, hemispherical
Solitary or Multiple bony lumps
Move the adjacent joint while palpating the lump and assessing the relationship with adjacent muscles and tendons, and degree of
interference with joint movement
Q. What do you know about HME?
Hereditary, AD condition characterized by multiple exostosis particularly in the limb bones.
All bones that ossify in cartilage can be affected except spine and skull.
Small incidence of sarcomatous change/malignant potential, particularly if subjected to trauma
Q. What will make you suspect malignant change?
If it becomes painful and rapid increase in size
Q. What is the Histology?
Osteochondrosarcoma
It is a lump of cancellous bone covered by cortical bone and a cartilaginous cap
Q. What will you tell the patient?
Look out for signs of malignancy and if any to urgently seek medical treatment
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Shoulder Dislocation (Short case or X ray)
Q. Examine this man’s shoulder
Look: scars, sinus, skin changes, wasting, asymmetry
Feel: warmth, tenderness, shoulder U. Biceps tendon, supraspinatus
Move : Abduction, Adduction, Flexion, Extension, Internal Rotation, External Rotation.
REMEMBER TO TEST Glenohumeral and scaphalothoracic movements of Abduction!
Special Test
Apprehension Test (anterior dislocation)
Sulcus sign (inferior joint dislocation)
Posterior traction sign (posterior dislocation)
Joint laxity, especially in multidirectional dislocations  assess using Brighton’s score for hypermobility syndrome
Test for each muscle’s strength
Supraspinatus: Abduction
Subscapularis: Internal rotation
TM, Infraspinatus: External Rotation
Impingement Test
Check for NV assessment
Check for other joint laxity
Check for complications of Shoulder Dislocation
Q. What are the complications of Shoulder dislocation?
Axillary Artery
Axillary Nerve  usually neuraprexia (regimental badge sensory loss, weakness of deltoid muscles)
Recurrent dislocation
Rotator cuff tear
Fracture dislocation of humerus
Q. Which muscle must you work on during PT of a person with Shoulder Dislocation
- Supraspinatus
Q. What investigations will you do?
X ray: AP, Lateral, Y scapular View, Axillary view (best view to see if post or ant d/l)
MRI Shoulder
Q. What do expect to see?
MRI: Bankart’s lesion  anterior-inferior tear of the glenoid labrum
Hill-Sach’s lesion  posterolateral depression fracture of the head of the humerus.
“TUBS and AMBRI”
Traumatic
Unilateral
Bankart lesion
Surgery
Atraumatic
Multidirectional
Bilateral
Rehab
Inferior capsular shift surgery if surgery is indicated
= generalized ligamentous laxity
Rotator Cuff Tendinitis
Q. Examine this man’s shoulder
Steps refer to Ramachandran
Show that Impingement Test positive  Inverted beer bottle sign/or arm flexion to 90 & internally rotated
Show the painful arc at 60 to 120
Q. How do you differentiate this from Frozen shoulder and Rotator cuff tear?
Rotator Cuff Tendinitis
Rotator Cuff Tear
Frozen Shoulder
AROM
PROM
Characteristics
Unaffected
Unaffected
Painful arc 60 to 120 degrees on
abduction
Absence of pain on abduction with
arm at external rotation
Limited in abduction
Unaffected
Abduction paradox
Limited in all direction
Limited in all direction
External rotation is most
commonly limited
Drop Arm Sign
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Pain over anterior edge of acromion
Pain on abduction
Impingement test positive 
DEMONSTRATE IT!
Q. What investigations will you do?
X ray AP, Lateral
MRI shoulder (Sagittal and axial)
+/- ultrasound shoulder: cheap, non-invasive
Q. What are you looking for on X ray?
Osteophytes
Calcification of the supraspinatous tendon
Q. What is the Management?
Non surgical
Pharmacological
Paracetamol, NSAIDS, Opiates
H&L into the subacromial space.
Non Pharmacological
Rest
PT
Lifestyle Modification
Surgical
Open or arthroscopic Subacromial Decompression
Differential diagnosis: Subacromial bursitis
Frozen Shoulder
- Refer to Ramachandram Questions.
Winging of Scapula (refer to ramachandran)
Differentiate between Long thoracic Nerve, Brachial Plexus, Root lesion
Q. What are the causes?
1. Long thoracic Nerve injury
2. C5, C6, C7 Nerve root injury
3. Faciioscaphalohumeral dystrophy
4. Viral infection of C5, C6, C7
Q. How do you treat?
Non surgical – PT/OT
Surgical – Tendon Transfer
Ruptured Extensor tendon of 4th digit
Q. What are the differentials of an ulnar claw hand?
Ulnar Nerve palsy
Trigger Finger
Dupuytren's Contracture
Q. What are the components of a claw hand?
Hyperextension of the MCPJ
Flexion of the interphalangeal joints.
Tennis Elbow
Refer to books
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Foot Drop
Examine this patient’s foot
Proceed to localize the lesion of the foot drop using the flow chart written.
Q. Causes of Foot Drop
- UMN
- L5 root lesion
- Sciatic nerve injury
- Common Peroneal injury
Q. What caused the sciatic nerve injury in RTA?
- Posterior dislocation of Hip
Q. What is the course of the common peroneal nerve?
Begins at the lumbosacral plexus at L4, L5, S1, S2, S3. Runs together with the tibial nerve in the sciatic nerve under the piriformis muscle and
down the thigh.
Divides away from the tibial nerve about 1 hands breadth above the knee joint. Runs downward through the popliteal fossa closely following
the medial border of the biceps muscles
It leaves the fossa by crossing superficially the lateral head of the gastrocnemius muscle. It passes behind the head of the fibula and winds
laterally around the neck of the bone, pierces the peroneus longus muscle and divides into 2 terminal branches: superficial and deep
peroneal nerve.
Q. What device can be used to help patients ambulate?
Ankle Foot Orthosis
Hallux Valgus
Refer to Ramachandran
Q. Describe what you see?
Sing the song for the characteristics of Hallux valgus
On examination I notice that ….
On palpation …
I would like to end of my examination by
- testing gait
- looking at the shoes
- testing the ROM of the foot joints
Characteristics
1. Often bilateral, in a LADY
2. Lateral Deviation of the great toe at the 1st MTPJ
3. Subluxation, supination of the great toes such that nail faces laterally.
4. Overriding of the lesser toes
5. Hypertrophy/Exostosis of the 1st MT head
6. Inflammation of the overlying bursa
7. 8 + 9 = Bunion formation
8. Callosities seen
9. Widened forefoot
10. May have co-existing secondary OA of 1st MTPJ therefore always examine ROM of 1st MTPJ
11.
12.
13.
14.
Hereditary
Environmental
Women > men
Associated with RA but often Idiopathic.
Q. What are the causes of Hallux Valgus?
Commonest cause: Idiopathic
However, it is often associated with conditions like
1. RA
2. Metatarsus primus varus (Widened Forefoot)
Q. What Investigations will you do?
1. WEIGHT BEARING X ray AP Lateral of Foot
Look for
1. OA changes of 1st MTPJ
2. IMA of 1st and 2nd MT  look for metatarsus primus varus
3. Severity of valgus deformity
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Remember to
Walk the patient
Look at the shoes
ROM of other joints
Hx of how its affecting her life
Q. What are the angles that you would like to look for on an AP Xray of the foot?
Inter-metatarsal Angle
Hallux valgus angle
Interphalangeal angle
Distal Metatarsal articulation angle
Q. What causes the pain over the 1st MTPJ head in Hallux valgus?
Inflammation of the overlying bursa of the 1st MTPJ
OA of the 1st MTPJ
Q. How to manage?
Non surgical
Non pharmacological
Rest
PT
Lifestyle modification
o Use shoes with wide toe boxes
o Use protective padding over prominences
Pharmacological
Paracetamol, NSAIDS, opiates
Surgical
Bunionectomy
Excision Arthroplasty
Arthroplasty
Arthodesis
Realignment osteotomy
Arthritic
Active patient  1st MTP arthrodesis or Arthroplasty
Low demand patient  Keller’s procedure (Excision arthroplasty)
Non arthritic – Do realignment osteotomy
IMA < 15  Chevron osteotomy
IMA > 15  Scarf Osteotomy
Q. What is a bunionette?
Tailor's bunion, or Bunionette, is a condition caused as a result of inflammation of the fifth metatarsal bone at the base of the little toe. It is
mostly similar to a bunion (the same type of ailment affecting the big toe). It is called Tailor's Bunion because it was thought centuries ago
that tailors sat crosslegged and caused this protrusion on the outside aspect of the foot. It is usually characterized by inflammation, pain and
redness of the little toe.
Metatarsal Lump
Q. What is your differential diagnosis?
Bunion
Bursa
Ganglion
Cyst
Q. What is a bunion?
Bunion = hypertrophy of head of 1st MT with inflammation of the overlying bursa
Charcot Marie Tooth Disease
Examine this man’s foot or examine this man’s upper limb
Q. What are the Clinical Features? Describe the deformity, What else do you want to look out for?
UL
Hypothenar, thenar, interossei muscle wasting of the hands – Median and Ulnar component
LL
Look
Atrophy of the intrinsic hand and foot muscles
o Pes Cavus
o Hammer toe and other deformities of the lesser toe
Distal calf muscle atrophy often occurs
o causing the classic "stork leg deformity."
o Or Inverted champagne bottle appearance
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Foot drop
General
Palpable enlargement of the peripheral nerves may occur secondary to nerve hypertrophy
LMN signs – Areflexia
Sensory loss – Vibration and proprioception
Scoliosis and kyphosis
HMSN/CMT 1 — HMSN type 1, also known as Charcot-Marie-Tooth type 1 (CMT1) disease, is a demyelinating disorder of peripheral nerves. It
has been subdivided on the basis of genetic markers into types 1A, 1B, and 1C, with type 1A being most common [4] , although the clinical
manifestations are similar. Affected patients typically present in the first or early second decade, but infants may be symptomatic [5] .
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



Early complaints may include frequent sprained ankles caused by distal muscle weakness or difficulty running and keeping up with
peers. The only obvious physical findings may be loss of reflexes, pes cavus foot deformity, and hammer toes.
Distal calf muscle atrophy often occurs, causing the classic "stork leg deformity." Walking often is clumsy because of both muscle
weakness and sensory loss. Sensory loss is gradual and mainly involves proprioception and vibration.
Later changes include atrophy of the intrinsic hand and foot muscles. Palpable enlargement of the peripheral nerves may occur
secondary to nerve hypertrophy. In addition, kyphosis or scoliosis often develop.
Ambulation is variable but usually is maintained through life. Life expectancy is not affected.
Disease exacerbation can occur in pregnancy, an effect that may be mediated by increased plasma progesterone [
Q. What are the Differential diagnosis of CMT?
Q. What is the management of CMT?
Treatment is supportive. Daily stretching exercises early in the course of the disease may help delay ankle contractures. Ankle orthotics often
are used to help stabilize the ankles. Orthopedic foot surgery often is required by the time the patient reaches adolescence to treat the pes
cavus deformity and hammer toes.
Specific therapy for CMT1 is not available. Animal models of CMT1A have been produced by introducing extra copies of the PMP22 gene,
resulting in overexpression of the protein; these models were then used to test different therapies:
Progesterone can increase PMP22 expression and studies in humans have suggested disease exacerbation in pregnancy, a setting in which
plasma progesterone increases up to 10-fold [6] . Observations in an animal model were consistent with these findings as the administration
of progesterone resulted in a more progressive neuropathy, while a progesterone antagonist reduced overexpression of PMP22 and slowed
disease progression [27] .

The efficacy of ascorbic acid (vitamin C), which is known to promote myelination, was tested in another animal model of CMT1A
[28] . Ascorbic acid therapy given once weekly at a dose of 57 mg/kg, which is similar to the maximum approved dose for the
treatment of ascorbic acid deficiency in humans, reduced the expression of PMP22 to a level below that required to induce the
disease. This change was associated with remyelination, substantial amelioration of the CMT1A phenotype, and prolonged lifespan.

Neurotrophin-3 (NT3) improved axonal regeneration and associated myelination in both a xenograft model of Schwann cells with a
PMP22 duplication and in a mouse model with a PMP22 point mutation [29] . In the same report, a single-blinded pilot clinical trial
involving eight patients with CMT1A found that NT3 treatment for six months was associated with improved sural nerve
myelinated fiber regeneration compared with placebo treatment.
Tendo-Achilles Rupture
Examine this man’s LL. Get patient to kneel on a chair
Q. Describe what you see
A visible gap of the tendoachilles is noted with the foot of that leg being more in a plantarflexed position then the contralateral foot. There is
a prominent gap in the tendoachilles about 4 cm from the heel.
Simmonds Test: squeezing the calf muscles of the affected side while the patient lies prone, face down, with his feet hanging loose results in
no movement (no passive planter flexion) of the foot, while movement is expected with an intact Achilles tendon and should be observable
upon manipulation of the uninvolved calf.
Q. How is it Diagnosed?
Diagnosis is made by clinical history
typically people say it feels like being kicked or shot behind the ankle.
PE
Upon examination a gap may be felt just above the heel unless swelling has filled the gap and the Simmonds' test will be positive
MRI or U/S can be used to clarify or confirm the diagnosis for cases of partial tear
Q. How to manage?
Non surgical
Rest
PT
29
Lifestyle modification
Placed in a cast with foot in equines position for 6 to 8 weeks
Surgical
- TA Reconstruction – less risk of rerupture
Lump over elbow
Q. Differential diagnosis of lumps over elbow
Olecranon bursitis
Gouty tophi
Rheumatoid nodules
Flexion Contracture of the elbow
Q. What systemic diseases will you be thinking of?
Gout
Q. How does gout present?
Refer to section on Gout
rachial plexopathy
LOOK

Flail UL

Wasting of muscles

Ptosis (lesion is close to sympathetic pathways, hence poor prognosis as unresectable)

Comment on posture – elevated ipsilateral shoulder

Limitations in movements on removal of shirt

Scars – primary from trauma or secondary from tendon transfers, skin grafts etc
FEEL

Sensory deficits over C5,6,7,8,T1

Thenar/hypothenar wasting
MOVE

Assess ROM

Power:
C5 – shoulder abduction (deltoids)
C6 – elbow flexion (biceps)
C7 – elbow extension (triceps), wrist extension (wrist extensors)
C8 – hand grip (intrinsic muscles)
T1 – abduction of finger (interossei)

Long thoracic nerve  winging of scapula (close shoulders in)

Rhomboid  shoulders stick out

Suprascapularis  supplies both suprascapular and infrascapular muscles

3 types of brachial plexus injury
1. Complete injury affecting all trunks
2. Upper injury affecting C5,6,7
3. Lower injury affecting C7,8,T1 (rare)
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