ulnar nerve palsy - Rushdan

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Ulnar Nerve Palsy

Examination

· Rule out median, radial and brachial neuritis

· Inspecting

· Wasting of the muscles of the hands, hypothenar eminence and partial clawing of the 4^th and 5^th fingers, sparing of the thenar eminence, ulnar paradox

· Proceed to tests for finger abduction and Froment’s sign (weakness of the adduction of the thumb)

· Test finger flexion of the 5^th finger for flexor digitorum profundus involvement; test for wrist flexion at the ulna side and look for the tendon of the flexor carpi ulnaris

· Rule out median nerve (thenar eminence and ext rot thumb, pen touch test and Oschner clasping test) and radial nerve

· Sensory testing in the medial 1 ½ fingers; test T1 sensory loss

· Examine the wrist and elbows (feel for thickened nerve, wide carrying angle))

· Function

· Thickened nerve (cf with Pb for radial and Acromeg etc for median)

Presentation

Sir, this patient has got a isolated left ulnar palsy as evidenced by a left ulnar claw hand with wasting of the small muscles of the hands with dorsal guttering as well as wasting of the hypothenar eminence. There is sparing of the thenar eminence.

There is weakness of finger abduction and Froment’s sign is positive. There is preservation of the flexion of the DIPJ of the 4^th and 5^th fingers; when the hand is flexed to the ulna side against resistance, the tendon of the flexor carpi ulnaris is palpable. This is associated with reduced sensation to pinprick in the medial 1/1/2 fingers. There are no associated median or radial nerve palsies and T1 involvement.

In terms of aetiology, there is a scar at the wrist associated with a marked ulnar claw hand, demonstrating the ulna paradox. I did not find any signs to suggest leprosy such as thickened nerves, hypopigmentation patches or finger resorption.

Both coarse and fine motor function of the hand is preserved.

In summary, this patient has a left ulna claw hand due to a traumatic injury to the left wrist.

Questions

What is the anatomical course of the ulnar nerve?

· It provides motor to all muscles of the hands except the LOAF; flexor carpi ulnaris and flexor digitorum profundus to the 4^th and 5^th fingers.

· Sensory to the ulna 1 ½ fingers

· Begins from the medial cord of the brachial plexus (C8 and T1)

· No branches in the arm

· Enters the forearm via the cubital tunnel (medial epicondyle and the olecranon process) and motor supply to the flexor carpi ulnaris and ulna half of the flexor digitorum profundus

· It gives off a sensory branch just above the wrist and enters Guyon’s canal and supplies the sensory medial 1½ fingers and hypothenar as well as motor to all intrinsic muscles of the hands except LOAF.

What is the level of lesions and its clinical correlation?

· Wrist – Hypothenar eminence wasting, Froment’s positive, weakness of finger abduction, pronounced claw and loss of sensation

· Elbow – less pronounced claw and loss of terminal flexion of the DIPJ and loss of flexor carpi ulnaris tendon on ulna flexion of the wrist

How do you differentiate ulnar nerve palsy vs a T1 lesion?

Motor – wasting of the thenar eminence in addition for T1

Sensory – loss in T1 dermatomal distribution

What is the ulna claw hand?

It refers to the hyperextension of the 4^th and 5^th MCPJ associated with flexion of the IPJs of the 4^th and 5^th fingers as a result of ulnar nerve palsy.

It is due to the unopposed long extensors of the 4^th and 5^th fingers in contrast to the IF and MF which are counteracted by the lumbricals which are served by the median nerve.

What is the ulnar paradox?

It means that the ulnar claw deformity is more pronounced for lesions distally e.g. at the wrist as compared to a more proximal lesion e.g. at the elbow.

This is because a more proximal lesion at the elbow also causes weakness of the ulnar half of the flexor digitorum profundus, resulting in less flexion of the IPJs of the 4^th and 5^th fingers.

What is Froment’s sign?

Patient is asked to grasp a piece of paper between the thumbs and the lateral aspect of the index finger. The affected thumb will flex as the adductor pollicis muscles are weak. (Patient is trying to compensate by using the flexor pollicis longus supplied by median nerve)

What are the causes of an ulnar nerve palsy?

· Compression or entrapment (Cubital tunnel at the elbow and Guyon’s canal at the wrist)

· Trauma (Fractures or dislocation – cubitus valgus leads to tardive ulnar nerve palsy)

· Surgical

· Mononeuritis multiplex

· Infection – leprosy

· Ischaemia – Vasculitis

· Inflammatory - CIDP

How would you investigate?

· Blood Ix to rule out DM if no obvious cause

· X-rays of the elbow and wrist (both must be done to rule out double crush syndrome) (KIV C-spine and CXR)

· EMG(axonal degeneration for chronic) and NCT(motor and sensory conduction velocities useful for recent entrapment as well as chronic) to locate level and monitor

How would you manage?

· Education and avoidance of resting on elbow

· OT, PT

· Medical – NSAIDs and Vit B6

· Surgical decompression with anterior transposition of the nerve

NB: LOAF – lateral 2 lumbricals, opponens pollicis, abductor pollicis brevis and flexor pollicis brevis

mr. Amin grand ward round on 21 september 2010

picture:

1. vac dressing
2. vac dressing
3. mottling appearance
4. mottling appearance
5. delta frame (external fixator)

This is merely simple point of what being told by the doctor. Pls do ur own reading regarding those points.

Vac dressing

• · Advantage

1. 1) Closure à prevent infection
2. 2) Suck the blood
3. 3) Shrink the wound

• · Complication à puncture the artery à Kalau balang die banyak darah à stop the vac

External fixator à delta fixator

How to manage external fixator

- Pin side

-Avoid weight bearing (that patient has K-wire insertion, thus he is prohibited to walk using his foot which has external fixator)

-Use crutches à axillary or forarem (mr.amin lebih prefer forarm sebab less axillary injury & more force)

Humified à wet gangrene

Mottling appearance in gangrene.

Ischaemic pain

Sepsis or borderline sepsis gives 2 drips

What do you want to give for patient yg ade sepsis?

-3^rd generation chepalosporin, ceftazidine (broad spectrum)

Sliding scale

- -Infuse insulin hourly dextrose

- - Complication à hypoglycemic attack

- - Not more than 8 hour

Mass swelling more than 6 cm à consider malignant until proven otherwise.

Terrible triad!!!!!

"What is Terrible triad of the elbow?"
aritu Mr.Amin ada tanya waktu ward round on-call

Terrible triad of the elbow :
- Posterior dislocation of the elbow joint with fracture of both the radial head and coronoid process

(Kenneth , Joseph D.,Handbook of Fractures, 3rd Edition)

- the socalled ‘terrible triad’, is a complex and difficult-to-treat injury.


(Terrible triad of the elbow—role of the..coronoid process: a case report,R Seijas, N Joshi, A Hernández, JM Catalán, X Flores, Orthopaedic and Trauma Surgery Unit, Hospital de Traumatología Vall d’Hebron, Barcelona, Spain)
http://www.josonline.org/pdf/v13i3p296.pdf

Common fractures of the forearm

Monteggia Fracture-dislocation

Defined as fracture shaft of ulnar, together with disruption of the proximal radioulnar joint and dislocation of radiocapitallar joint..
nowadays the term includes fracture of olecranon with radial head dislocation.

The mechanism of injury is usually fall on an out-stretched hand with hyper-pronation of the forearm.

Clinical features

The deformity over the site of fracture is usually obvious.
However, the dislocated radial head can be obscured by the presence of swelling.

Pain and tenderness over the lateral aspect of elbow joint is suggestive.

It can be complicated as a radial nerve injury, causing wrist drop or injury to it's branch, the posterior interosseous nerve, causing finger drop.

Radiological features

An AP view of the elbow joint usually shows clearly the fractured shaft of ulna, and the head of radius no longer pointing towards the capitulum..if it dislocated, it lies in a plane anterior to capitulum..



Complications

1) Nerve injury
Usually caused by over-enthusiastic surgical manipulation of the dislocated radial head
However, it's a neuropraxic injury, where recovery is expected within months

2) Mal-union
Caused by imperfect reduction of the fracture, where the radial head remains dislocated.
Restricted flexion of elbow joint.
Requires open reduction and internal fixation, with excision of radial head with or without prosthetic replacement.

3) Non-union
Requires open bone grafting and internal fixation with excision of radial head.

Treatment

Close reduction is attempted first under general anesthesia.
For the next 3-4 weeks, X ray is done to check the progress of healing.
If unsatisfactory or re-displacement occurs, open reduction and internal fixation is done.


Galeazzi Fracture-dislocation


This condition is more common than it's counterpart (Monteggia F)
Defined as fracture of the distal third of radius with dislocation or subluxation of distal radio-ulnar joint.

Mechanism of injury : Fall on out-stretched hand

Clinical features

Prominence and tenderness over the ulnar styloid process.

Piano-key sign : The distal third of radius is ballotable

Instability of the distal radio-ulnar joint can be made prominent by supination and pronation of forearm.

Can be complicated as ulnar nerve injury (resulting in Ulnar claw hand)

Radiological features

Transverse of oblique fracture of the distal third of radius.
Dorsal displacement of the distal ulna or the distal radio-ulnar joint.


Complications

Main complication is mal-union, which limits supination and pronation of the forearm.

Treatment

Close reduction is not done (unless in children), since this fracture is unstable.
Instead, open reduction and internal fixation is done.


Colles' fracture

defined as transverse fracture of the distal radius just above the wrist at the level of cortico-cancellous junction, with dorsal displacement of distal fragment.

Mechanism of injury : fall on out-stretch hand

It is the most common osteoporotic-related fracture in the upper limb.
Hence, it is common among post-menopausal women.



Clinical features

Pain, swelling, deformity.
Palpation over distal radius : tenderness and irregularity.
Dinner fork deformity.
Radial styloid being leveled or situated proximal to the ulnar styloid.

Complications

1) Joint stiffness

Involving the fingers, wrist, elbow and shoulder.

2) Mal-union

Occurs usually unnoticed within the immobilisation cast.

3) Subluxation of the distal radio-ulnar joint

Resulting shortening of the radius, which made the ulnar styloid more prominent.
Hence, any movement of the wrist joint involving pronation/supination or ulnar deviation is restricted or is painful.

4) Carpal tunnel syndrome
5) Ruptured tendon of extensor policis longus
6) Sudeck's osteodystrophy

Colles' fracture is the commonest cause of this condition in the upper limb.
Characterised by pain, swelling of wrist, hand and fingers, and deformity.
There's diffuse tenderness, and the skin over it appears glazed, stretched.
Treated by physiotherapy.

Treatment

1) Undisplaced

Cast immobilisation for 6 weeks, applied below elbow towards the neck of metacarpals.
Hand is immobilised in functional position, with slight palmar flexion and ulnar deviation.

2) Displaced (with dinner fork deformity)

First, close manipulative reduction is done under anesthesia.
Ask your assistant to apply traction over the wrist joint by holding the patient's hand, and counter traction at the elbow joint.
Press over the dorsal aspect of deformity, at the same time try palmar-flexing, ulnar deviation, and pronating the hand.
After reduction, confirm that it's properly done by X ray.
Apply colles' cast.

3) Comminuted

Requires open reduction and internal fixation.

Mr.Shuk selalu tanya pasal scaphoid fracture..

Mr.Shuk selalu tanya pasal scaphoid fracture..

Apa yg special pasal scaphoid fracture ni?

Scaphoid bone has a retrograde blood supply.

So, blood flow comes from a small vessel that enters the most distant part of the bone and flows back through the bone to give nutrition to the bone cells..sbb die ada end-blood supply kan?

The interesting thing about scaphoid fracture, it can cut this blood flow and stop the delivery of necessary oxygen and nutrients to the bone cells.

When this occurs, healing can be slow, and the scaphoid fracture may not heal at all..sbb tu increase risk utk non-union..

yg lain2 bleh baca kat appleys..yg kat bawah ni utk mudah copy paste untuk case write up..huhu..

Introduction

Scaphoid fracture accounts for about 75% of carpal bone injury.Common among young adults, rare in elderly and children.

The most common part of scaphoid bone fractured is the waist, which is the narrowest part.

The most common complication associated with scaphoid fracture is non-union and avascular necrosis.Both of these complications are more common is case of fracture of scaphoid involving the proximal part.
Since the arterial supply of the scaphoid diminishes as it approaches the proximal part.

Note that 1% of distal fracture, 20% of mid-fracture and 40% of proximal fracture complicates as AVN and non-union.

Mechanism of injury

The mechanism of injury here is fall on an outstretched hand.

The primary forces causing scaphoid fracture is dorsiflexion of the wrist joint and radial deviation.Such forces are transmitted through the two rows of carpal bones, and since scaphoid being part of both rows, it fractures through the waist, and rarely involves the tuberosity.

Clinical features

In an adult, if there is a history of trauma as stated above, and later the patient complains of pain and swelling over the radial aspect of the wrist, especially over the anatomical snuff box (scaphoid fossa), together with tenderness of the scaphoid fossa, the diagnosis of scaphoid fracture is likely.

However, tenderness over the anatomical snuff box can be due to wrist sprain as well. Hence to differentiate, palpate over the dorsal aspect of the scaphoid bone, and try eliciting tenderness over this region.In wrist sprain, there'll be no tenderness over this region.

Radiological featuresAP, lateral and 2 oblique views of the wrist joint is required for scaphoid fracture.The first few days after the fracture, the fracture line may not be visible.The patient should be asked for a follow up 2 weeks later, as X ray is taken again.

After 2 weeks, the break in the scaphoid bone should appear.

Complications

1. Avascular necrosis of scaphoid bone2-3 months later, X ray of the wrist joint reveals increased bony density over the proximal part of scaphoid.Such feature is pathognomic of AVN of the scaphoid bone.

Operative intervention needs to be done to prevent secondary degenerative osteoarthritis of the wrist joint.Either by doing surgical removal of the scaphoid bone and fusion of the proximal row to the distal row of the carpal bone, or by removing the proximal row of the scaphoid bone.

2. Non-union of scaphoid fracture

3 months later, X ray wrist taken and if there's no signs of union, a firm diagnosis of non-union of scaphoid fracture can be made. Usually, bone grafting is attempted to prevent secondary osteoarthritis.

3. Secondary osteoarthritis due to AVN and non-unionManagement

At first, if the clinical features are suggestive of a scaphoid fracture, but X ray is normal. Then is wise to ask the patient to come back after 2 weeks for another X ray to be taken.

Mean time, cast immobilisation is applied from the upper forearm to the metacarpals, including the proximal phalanx of the thumb.The hand is immobilised in a way where the wrist is dorsiflexed, and the fingers in a glass-holding position.2 weeks later, if a fracture of confirmed, further treatment will depends on the type of scaphoid fracture.

a) If it's a fracture involving the scaphoid's tuberosity, treatment is conservative which is similar to that of wrist sprain. Crepe bandage is applied to the wrist and allow early mobilisation.

b) If it's a undisplaced fracture involving the waist, then the cast is maintained for another 8 weeks. 8 weeks later, if both clinical and radiologically, there is evidence of union, then the cast can be removed and wrist is allowed for mobilisation.If beyond the 8 weeks, there's no clinical or radiological evidence of union, cast should be re-applied and wait for another 6 weeks. However, if at that time there're signs of delayed union, internal fixation and bone grafting hastens the healing process.

c) If it's a displaced fracture of the waist of scaphoid, treatment is ORIF using compression screws.

Gout (apley page 37)

Gout is one of the disease involving presence of the crystal around the joint, bursae and tendons.

Here are the disease similar to gout and their crystal composition

• Gout - Urate crystal depostion disorder


• Peudogout - Calcium pyrophosphate dihydrate (CPPD) deposition disease


• Calcium hydroxyapatite (HA) depostion disorder - Calcium hydroxyapatite

There are 3 main courses of these disease:
1) Become inert and assymptomatic.
2) Acute inflammatory rxn.
3) Slow destruction of t/s.

Generally - disorder of purine metabolism

Characterized by:
1) Hyperuricaemia
2) Deposition of monosodium monohydrate crystal in joint and periarticular t/s.
3) Recurrent attacks of acute synovitis.

Classification
Primary:
- 95%
- Without apparent cause
- d/t under-excretion (majority) and over-production of urate.
Secondary:
- 5%
- Results from prolonged hyperuricemia d/t acquired disorders such as myeloproliferative diseases, administration of diuretics or renal failure.

Sequlae
1) Cartilage degeneration.
2) Renal dysfunction.
3) Uric acid kidney stone.

Epid
- Men:women = 20:1
- Usuallt men >30 y/o
- Often have family h/x of gout.
- Rarely seen before menapause in female.

Pathophysiology
1) Urate crystal deposited in minute clumps in the connective t/s and articular cartilage (commonest sites are the small joints of the hands and feet)
2) They can remain inert for month or years.
3) Possibly as a result of local trauma, the crystal can disperse into the joints and surrounding t/s which excite inflammatory rxn.
4) Clumps or tophi vary in size. It may destroy cartilage and periarticular bone and penetrate the skin.

Common sites
Type of t/s:
- Joints
- Periarticular t/s
- Tendons
- Bursae
Sites:
- Metatarsophalengeal joints of big toe (ada sorang pt hari tu ada swelling and discharge at both feet)
- Finger joints
- Ankle
- Achilles tendon
- Olecranon bursae
- Pinnae of ears

c/f
Acute attack:
- Sudden onset of joint pain which last a week or 2 is typical.
- Maybe spontaneous or aggravated by alcohol, minor trauma, operation, unaccustomed exercise.
- Commonest sites are metatarsophalengeal joints of big toe, ankle, finger joints and olecranon bursa.
- There will be swelling, redness and shiny skin.
- The joint become extreme tender and warm suggesting cellulitis or septic arthritis.
- Sometimes, pt just present with acute pain and tenderness in the heel or the sole of the foot.
Chronic gout:
- Recurrent attack may produce polyarticular gout.
- Tophi may appear around joint, pinna, olecranon. The large one can ulcerate the skin and discharge chalky white material.
- Joint erosion cause stiffness, deformity and chronic pain.
- May present with calculi and renal parenchymal disease.

x-rays
- Acute attack: show soft t/s swelling.
- Chronic attack: asymmetrical, punch out ‘cyst’ in the juxtaarticular bone, joint space narrowing and secondary OA.

Ddx
Psudogout:
- Affect large rather than small joint
- Affect women>men
- Articular calcification on x-ray
- Demonstrating crystal in synovial fluid to confirm dx.
Infxn:
- Cellulitis, septic bursitis, infected bunion.
- Aspiration and synovial fluid exam.
RA:
- Polyarticular gout affecting finger maybe confuse with RA and elbow tophi for rheumatoid nodules.
- Biopsy establish dx.

Rx:
Acute attack:
- Resting joint
- Large dose NSAIDs
- In severe cases, give colchicine
Between attacks:
- Lose wt, cut alcohol, stop diuretics
- Asymptomatic hyperuricemia need no rx.
- Uricosuric (probenecid or sulphinpyrazone) can be used if renal fxn normal.
- Allopurinol usually preferred.
- ! never use these drug in acute attackas it can precipitate the attack.
- ! always use these drug with anti-inflammatory preparation or colchicine.

Hyperuricaemia
- Uric acid in the blood is saturated at 6.4-6.8 mg/dL at ambient conditions, with the upper limit of solubility placed at 7 mg/dL
- Uric acid biosyntesis (refer pic)
- 70% of uric acid from endogenous source while 30% from diet.
- Excreted by the kidey and gut.

link: http://emedicine.medscape.com/article/241767-overview

How is gout treated? (ARTHRITIS FOUNDATION MALAYSIA)
a. For the acute attack

• Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used to control both the pain and the swelling. They are usually taken in moderate to full doses over a short period of time and are generally efficacious within 2 days. COX II inhibitors are the newer anti-inflammatory drugs which are effective to treat an acute gouty attack. It has less adverse effects to the stomach as compared to the conventional NSAIDs.


• Colchicine has been used for more than 100 years to treat the inflammation caused by gout. Up to six tablets over a 24-hour period usually settle an attack. It is seldom used nowadays to treat acute gout as NSAIDs/COX II inhibitors are more efficacious to settle an attack. Lower doses over a longer period are sometimes prescribed as a preventive measure to reduce the frequency of gout attack when a patient is on uric acid lowering drug.


• Corticosteroids, usually injected directly into the inflamed joint, are used and can control an acute episode efficaciously.


• Each attack should be treated promptly to achieve the best results. If possible tablets should be taken at the very beginning of an attack - if attacks recur - the doctor may give you tablets to keep so you do not have to wait until he/she arrives, or the chemist opens. By following your doctor's instructions carefully and promptly, your attack of gout can be controlled quickly and satisfactorily.
  RememberAlways be on the look-out for the early signs of an attack, because the earlier you start the treatment, the better.

b)Long term To remove contributing factors that raise uric acid level:• Weight control. Being overweight interferes with the body's ability to get rid of uric acid.

• Avoid excessive alcohol. More than one glass of wine or one can of beer a day can raise uric acid levels.

• Diets. Special diets used to be prescribed, but since the effective treatment has been found, most sufferers can eat or drink anything they like. However, certain foods can cause increased uric acid levels. It is sensible to avoid them or reduce the intake. These include liver, brains, kidneys, sweetbreads (pancreas), anchovies, leguminous vegetables, roe, yeast, broths, gravies and sardines. Avoid periods of sudden strict starvation because this can start an attack of gout. Increased consumption of low- fat dairy products can help to reduce uric acid levels.

Remember

• Help yourself by modifying your lifestyle to reduce uric acid • Drink plenty of water

Uric acid lowering drugs
The drugs given to relieve an acute attack have little effect on uric acid levels in the blood. They can do little to prevent further attacks, or stop uric acid being laid down in the joints. Should your attacks become more frequent, or if blood tests show you are accumulating too much uric acid, your doctor may decide to prescribe one of the drugs that reduce the quantity of uric acid in the blood. These have to be taken everyday, whether you have an attack or not, as a preventive measure.

There are now several drugs available that will lower the uric acid level, but it must be appreciated that you may have to persist with the daily treatment for the rest of your life. Should you stop, uric acid will begin to accumulate again.

These tablets are prescribed to be taken regularly. Taken consistently over a period, the treatment ensures that you maintain a normal blood level of uric acid.

The most commonly prescribed tablet is Allopurinol. It reduces the amount of uric acid made by the body. It is well tolerated even when taken for years; the only side-effect that occurs frequently is a rash, which disappears when the tablets are stopped. Occasionally, people may be allergic and have more severe skin rashes.

Sometimes acute attacks of gout may become more common when Allopurinol is started, so it may be necessary to take Colchicine or an NSAID as well. Whichever drug proves right for you, drinking plenty of fluid will help to get rid of uric acid through the kidneys.

Remember

• Allopuritol is not a painkiller • Allopuritol once prescribed means life-time treatment • Do not stop or change the dose of Allopuritol yourself when you have an acute attack.

hand examination (with hemangioma case) by 'Aliah

salam

this case was discussed 2 times, 1st during grand ward round, the other one was during Mr Amin's teaching with his mentee, di mane aku sibuk2 nak join jgk. sy tukang tulis blk je di sini, smg kite sume dpt manfaat bersame. it happened at ward 2A.

c/o: 40 years old Malay lady presented with painful swelling of right ring finger. please examine her.

1) Position

Mr Amin said the most important for hand examination is to position both hands correctly. put the hands on top of a pillow with the patient in sitting position. ask the patient to abduct the fingers as maximum as she can because from this position, we can already detect any neurological disorder related to the hands, specifically motor disorder.

2) Inspection (look)

inspection is divided into 2, towards the pathology (mass) itself, as well as towards the hand as a whole. 1st, compare both hands, don't take too much time doing this, just inspect surfacely because the examiner can be annoyed if korang sibuk2 nak pegang2 ke, angkat2 ke, or give excessive attention to the normal hand.

then, check for any signs of wasting or skin discoloration, or any obvious changes related to the hand.

for the mass or swelling, inspect it just like you inspect any lump and bump in surgery. do not forget to include the edge, border, size, site, character of the mass (fungating, etc), surface, and any discharge noted. for the site, describe precisely where is the origin of the mass. don't forget to check fo any associated deformity, such as nail deformity or finger deformity.

3) Palpation (feel)

begin with soft palpation, in order to detect any tenderness associated with the mass, xkesahlah at the mass itself or the area surrounding the mass. then, don't forget to check for circulatory status, i.e. CRT and pulse, as well as the sensation whether it is intact or not.

4) Movement (move)

for movement, just test for active movement first and examine the ROM. assess the ROM of all fingers of the hand, not just the affected finger, because others can be affected too. for example, ring finger share the same tendon with the little finger, so, if one is affected, the other might be affected too.

5) Ending

complete your examination by checking the lymph node, other features of malignancy, or any relevant examination related to your differentials.

now, let's go to the case:

c/o: 40 years old Malay lady presented with painful swelling of right ring finger. please examine her.

presentation:

on general inspection, the patient is alert and concious. she is not ill neither in pain.

on inspection, there is a mass arises beneath the nail of the right ring finger. the mass is fungating in nature with an irregular edge and uncircumscribed border. the margin is raised and the surface and consistency are hard. there is no discharge or blood or pus seen. it is associated with skin discoloration around it, nail deformity of the same finger, and also wasting of dorsal interossei m/s of the same hand. on palpation, the mass is warm and tender. upon movement, there is reduced ROM of both ring and little finger of the same hand.

i want to complete my examination with checking the related lymph nodes as well as to examine the other features of malignancy.

the ddx:
1) wartz
2) Squamous cell ca the finger
3) infected melanoma
4)TB of the phalanx
5) severe fungal infection
6) melanic features of leukaemia

hmwork mr. amin by Saifuddin

1. First muscle start wasting ?

Vmo - vastus medialis obliquus

The vastus medialis oblique muscle (VMO) is most commonly the weakest of the quadriceps group and appears to be the first muscle to atrophy and the last to rehabilitate.

2. Swelling at the back of the knee?

• semimembranous bursa,popliteal cyst,popliteal aneurysm (appley)
• Bakers Cyst
• Sebaceous cyst
• Varicose vein
• Deep vein thrombosis
• Haematoma




3. Normal synovial fluid volume of knee? How much volume we expect if patella tap positive?

- Normal synovial fluid contains 0.5 ml (last anatomy)

- Small to moderate effusion <>

- Large effusion > 100 ml

4. Position of Suprapatella pouch?

Lies beneath the quadriceps muscle and communicates with the join cavity.

5. Test for patella effusion

a. Cross-fluctuation

- Applicable only in large join effusion

- Left hand compresses and empties the suprepatella pouch while the right hand straddles the front of the join bellow the patella; by squeezing which each hand alternately, a fluid impulse is transmitted across the join

b. The patellar tap

- suprepatella pouch is compressed with the left hand

- while the index finger of the right hand pushes the patellar sharply backward

- positive – patella can be felt striking the femur and bounce off again

c. The bulge test

- Useful when little fluid is present

- Medial compartment is emptied by pressing on that side of the joint

- At the same time the suprepatellar pouch is kept closed by the other hand

- The first hand is lifted away from the medial side and move to the lateral side

- Which is then sharply compressed – a distinct ripple is seen on the flattened medial surface

d. The patellar hollow test

- When normal knee flexed - a hollow appears lateral to the patellar ligament and disappear with further flexion

- with excess fluid – the hollow fills and disappears at lesser angle of flexion

6. Normal extension of the knee?

Extend 0 to 5-15° (Netter)

7. Special test of knee?

bleh tengok kat buku....

Lain-lain soalan..

a. how to differentiate open fracture wound with other wound?

in open fracture wound there will be altered bleeding, so we will see the blood become dark in colour..because the blood mix with the fat globule..in open fracture juga biasanya ade active bleeding..