The time factor for fracture healing

The rate of repair depend upon

1. The type of bone involved - cancelous bone heals faster than corticol bone

2. The type of fracture - Transverse fracture takes longer than a spiral fracture

3. The state of blood suply- Poor circulation means slow healing

4. Patient’s general constitution-  Healthy bone heals faster

5. Patient’s age - Healing is almost twice as fast in children as in adults

spinal cord injury in bahasa melayu - cintailah bahasa melayu

KEPATAHAN TULANG SPINAL
SEJARAH ASAL
Klasifikasi fracture spine secara amnya berdasarkan stabiliti tulang itu sendiri Holdsworth`s (1963) mengklafikasi mekanisma kecederaan termasuk flexion, flexion rotation, extension dan compression.Ada dua teori tentang stabiliti spine dari Kelly dan whitesiders (1986) iaitu anterior vetebra column termasuk primary weight bearing sementara posterior neural arch column melawan tekanan, kestabilan juga berdasarkan kekukuhan atau pelekatan posterior column.

KECEDERAAN STABIL DAN TIDAK STABIL

Nicoll (1962) dan Housworth (1970) menekankan kepentingan membezakan fracture dan dislokasi yang stabil dan yang tidak stabil. Fracture dan dislokasi tidak stabil bertanggungjawab terhadap sasaran selanjutnya dan mendatangkan bahaya kecederaan saraf tunjang

Kecederaan Spina Lumbar

Kecederaan spinal lumbar boleh dikelaskan :

I. Anatomi patologi : Fracture mampatan jasad vertebra / compression,
II. Fracture letusan jasad vertebra / burst, subluksasi ekstensi, subluksasi fleksi, dislokasi.
III. Mekanisma yang menyebabkan kecederaan.

Mekanisma Kecederaan Spine

Menurut Angelo Grillo dan Robert E. O’ Connar, kecederaan spina dikategorikan mengikut mekanisma kecederaan. Dua pertiga dari kecederaan lumbar berlaku di bahagian torakolumbar. 15 % dari fracture thorakolumbar melibatkan kecederaan neurological terutama renjatan neurogenik dengan hipotensi bradikardia.

I. Hiperfleksi
II. Tekanan (Compression)
III. Hiperekstensi

JENIS KECEDERAAN
Berdasarkan gambaran CT Scan pada kecederaan thoracolumbar, Denis (1984) mengeluarkan satu lagi klasifikasi baru berdasarkan 3 column teori tulang spinal. Anatomi spine terbahagi kepada 3 column:

a. Anterior column
Anterior longitudinal ligament, 2/3 anterior annulus dan vetebra body.

b. Middle column
Posterior 1/3 vetebra body, annulus dan posterior longitudinal ligament.

c. Supraspinous ligament:
Body neural arch, interspinous, supraspinous ligament dan ligamentum flavam.

Kestabilan tulang spine memerlukan intact dua dari tiga column. Semakin intact (15 % keseluruhannya) maka semakin besar kecederaannya. Kecederaan kecil melibatkan kecederaan luar column termasuk kepatahan spinous dan transverst processes, parsintaryrartieularis dan facet articulation. Kecederaan keritikal melibatkan kecederaan keseluruhan satu column (ruang) dan terbahagi kepada compression, burst, seatbelt, dan kepatahan dislocation.

“Burst fracture” - tekanan pada anterior dan middle columns samaada berlaku atau tidak kecederaan pada posterior column.

Terdapat lima jenis Burst fracture untuk diterangkan

1. Type A : Kepatahan pada kedua-dua endplates (24%)
2. Type B : kepatahan hanya pada superior endplates (45%) dan kerap berlaku.
3. Type C : Kepatahan hanya inferior endplates (7%)
4. Type D : kecederaan jenis burst atau rotaction (15%)
5. Type E : kecederaan jenis burst atau lateral traction (15%)

Kecederaan pada bahagian spinal

Sebanyak 20 % kecederaan pada bahagian spinal yang melibatkan spinal injuri yang melibatkan neurological deficit yang melibatkan paraplegia.( J.Maheshwari 1993 )

Rawatan
Rawatan yang dilakukan ialah

1. Positioning

2. Care of the back

3. Personal hygine

4. Care of bladder

5. Physiotherapy

6. Rehabilitation
• Physical

7. Social
• economic

5 katagori yang di periksa untuk mengetahui fungsi neurologic .

I. Tahap kesedaran (level of consciousness)

II. Menitik beratkan vital sign termasuk airway dan corak pernafasan (vital sign particularly the airway dan breathing pattern)

III. Reaksi pupil (papillary reaction/ berkenaan dengan pergerakan anak mata)

IV. Ocular movement (berkenaan dengan mata)

V. Skeletal and muscle respond (respond pada muscle dan tulang)


Paraplegia

a Paralysis pada bahagian bawah portion of the body dan kadang kala melibatkan pada lower trunk.

b Paraplegia terjadi apabila kecederaan yang melibatkan thoracic, lumber dan sacral portion of spinal cord dan menyebabkan gangguan pada sensory dan hilang fungsi pada motor.


Spinal shock

a Kehilangan fungsi reflex yang sementara bawah pada kecederaan yang dialami dan ianya dikenali sebagai(areflexia)

b Ia adalah respond yang biasa terjadi jika terdapat kecederaan pada spinal cord.

c Respon ini berlaku dalam kadar yang segera selepas complete transaction pada spinal cord terganggu dan cord tidak berfungsi dengan baik.

d Respon juga terjadi (walaupun dalam varging degrees) selepas partial transaction berlaku dengan segera selepas spinal cord contusion,compression dan ischemic.

e Sebab terjadinya spinal shock masih tidak diketahui walau bagaimanapun ianya diketahui melibatkan motor pathways dengan kehilangan fungsi motor, tendon reflex dan fungsi autonomic.


Manifestasi acute spinal shock.

I. bradycardia

II. hypotension

III. flaccid paralysis of skeletal muscle

IV. loss of sensation of pain , touch, tempreture,dan blood pressure.

V. absence of viseral and somatic sensations .

VI. bowel and bladder disfunction.

VII. loss of Ability to perspine

VIII. loss of muscle aktiviti.


PRINSIP UMUM

Pemilihan pesakit untuk menjalani pembedahan pada kecederaan pada thoracolumbar spine mesti berdasarkan matlamat perawatan secara spesifik. Tidak ada jalam mudah untuk masalah pada spinal canal atau yang mempunyai ganguan neurology. Mereka perlu dibetulkan dengan decompression atau sebarang cara lain untuk membetulkan kecacatan atau ganguan tersebut. Kecederaan tulang spine yang ketara perlu diperbetulkan. Ketidak stabilan spinal column mesti dikembalikan kestabilannya dengan menggunakan cara “ instrumentation and fusion” dalam banyak kes yang melibatkan anterior, posterior atau gabungan mungkin memerlukan pembedahan.

Masa tiap-tiap satu pembedahan kecederaan thoracolumbar spine tidak dapat dijelaskan. Ada diantara lapan hingga dua belas jam selepas kecederaan pesakit yang memerlukan pembedahan perlu menerima rawatan. Dipecayai lagi cepat pesakit menerima rawatan decompression dan stabilization adalah lebih baik. Ini kerana untuk mencegah spinal cord dari lain-lain kecederaan.

Terdapat dua situasi yang memerlukan surgical intevention dengan segera

1. Mempunyai kecederaan neurological yang teruk
2. Kecederaan “incomplete neurologic” berserta irreducible discloction



KECEDERAAN YANG MEMERLUKAN PEMBEDAHAN

Rawatan yang tidak memerlukan pembedahan adalah untuk mereka yang tahap kecederaannya stabil dengan sedikit potensi kecacatan. Satu kecederaan column termasuk kepatahan “ wedge compression” dan kepatahan posterior aligment dikira stabil. Kepatahan boleh sembuh dengan imbolisasi yang sempurna iaitu plaster kas atau orthotic untuk ambulasi awal

Jenis external immobilasi mesti melindungi kecederaan ulangan, untuk kecederaan atas dari T7 adalah seperti occipitocervicothoracis orthocis boleh digunakan. Penyembuhan dalam jangka masa lapan hingga 12 minggu. Manakala Thoracolumbosacral orthosis digunakan untuk kecederaan T7 kebawah dan penyembuhan memakan masa 12 hingga 16 minggu. Kecederaan di bawah paras lumber kas atau orthosis termasuk bahagian peha memerlukan penyembuhan 6 hingga 12 minggu untuk stabilkan tulang pelvic. Non operative juga perlu untuk sesetengah kecederaan yang stabil dan tidak ada ganguan neurologi.

RAWATAN PEMBEDAHAN

Pembedahan atau rawatan kecederaan spine perlu untuk kes-kes

1. Tidak stabil berdasarkan kepada neurological status

2. Pesakit dengan incomplete spinal cord injury dan spinal canal compromise dan cord compression

3. Fracture dislocation memerlukan realignmen

4. Complete neurologic injury pada cauda dan beserta pencuaran yang berterusan


Walaupun dalam pesakit yang mempunyai gangguan kecederaan neurologi yang teruk, surgical stabilization perlu untuk mobility dan rehabilatasi ke atas pesakit.

Terdapat kontroversi berkaitan dengan rawatan pembedahan untuk kecederaan yang tidak stabil ini. Kebiasaannya rawatan konservertif adalah yang terbaik difikirkan. Jika terdapat kecederaan neurologi kecacatan tulang dan kestabilan boleh diperbetulkan jika berlaku.

Abduction pillow

Abduction pillow (AP) is used to immobilize legs after total hip replacement surgery to accelerate the recovery and healing process.

Post-operative management of patients having undergone total hip arthroplasty or hemiarthroplasty is to prevent early dislocation of the hip.

AP is used to prevent adduction. Adduction generally increases the risk of dislocation of the hip. Pillows are used to immobilize the legs after surgery to facilitate and accelerate the healing process.

Wound closure

◙ Primary closure

• Suturing the wound few hours following the injury less than 6 hours

• Can be done provided:

– Cut wound with sharp objects
– Minimal injury to structure inside
– No infection , no contamination
• Methods : sutures, staples & adhesive tapes

◙Delayed primary closure
• Surgical closure of a wound within 5 days of the wound having been made
• Primary suture within 6 hours is not done because :
– gross edema
– increased tissue tension
– hematoma
– contamination with bacteria

◙2^nd closure
• Closure of the wound after granulation tissue is firmly established ( 7-10 days )

◙Left open
• Wound is left open without suturing & dressing is applied. Antibiotic is started
• Wound is reexamine 4-6 days later
• Heals by 2^nd intention

Reconstruction ladder
- Suturing
- Skin graft
- Local flap
- Distant flap
- Free flap

Different between skin graft and flaps?
- Skin graft (requires vascular bed as it has no blood supply of its own)
- Flaps (bring own blood supply to new site)

1. skin graft - in short case, check for the site where the skin is harvest (for example- patient's thigh)

other common site for skin graft?

2. skin flap

different between local and distant flap - A local flap implies that the tissue is adjacent to the open wound in need of coverage, whereas in a distant flap, the tissue is brought from an area away from the open wound.

local flap - uses a piece of skin and underlying tissue that lie near to the wound. The flap remains attached at one end so that it continues to be nourished by its original blood supply and is repositioned over the wounded area.

Distant flap - uses a section of tissue thatis attached by a specific blood vessel. When the flap is lifted, it needs only a very narrow attachment to the original site to receive its nourishing blood supply from the artery and vein.

Free flap reconstruction also involves the transfer of living tissue from one part of the body to another, along with the blood vessel that keeps it alive. A free flap is a further modification of flap transfer where the flap is entirely disconnected from its original blood supply and then reconnected using microsurgery in the recipient site.

Why damage to posterior interosseus nerve (PIN) does not cause wrist drop?

1. PIN arises from radial nerve. Radial nerve pulak arises from posterior cord of the brachial plexus
2. It passes posterior to the axillary artery between long and media heads of triceps muscle, to lie in the spiral groove between medial & lateral heads of triceps muscle.
3. Here it is accompanied by the profunda brachii artery before it pierces it lateral intermuscular septum of the lower third humerus to run between brachialis & brachioradialis
4. At the lateral of epicondyle humerus, it gives rises to PIN & superficial radial nerve
5. Radial nerve supply all the extensor muscle of forearm & arm
6. However it also supply brachioradialis, which is flexor of elbow when forearm pronated
7. Damage to the nerve in the spiral groove causes wrist drop but no loss of elbow extension, as fibres of triceps remain intact proximal to this site
8. Only damage in the axilla will causes loss of elbow extension & wrist drop
9. Damage to posterior interosseus nerve (PIN) does not cause wrist drop because extensor carpi radialis longus receives its innervation from the main radial nerve
10. Pin only cause unable to extend metacarpophalangeal joint à finger drop.

Why children’s fractures different?

1. In very young children à bone ends are largely cartilaginous & therefore do not show in x-ray è Fracture at these sites are difficult to diagnose
2. Children bone less brittle à more liable to plastic deformity compare to adult. Incomplete fractures – torus fracture (buckling of the cortex)& greenstick fractures are common in children compare to adult
3. Periosteum is thicker than in adult bones; this may explain why fracture displacement is more controlled
4. Cellular activity of periosteum is more active, which is why children’s fracture heal more rapidly than adult (the younger the quicker rate of union)
5. Non-union is very unusual
6. Bone growth involves modeling & remodeling à fracture deformity can be reshape to normal over time (except rotational deformity)
7. Damage to growth plate can have serious effect compare to adult

Why femoral neck fracture have a poor capacity of healing?

The femoral head obtains its blood supply from three sources:

1. Intramedullary vessels in the femoral neck

2. Ascending cervical branches of medial & lateral circumflex

3. Vessels of ligamentum artery

Why femoral neck fracture has high risk of avn?

Blood supply is interrupted due to tearing of capsular blood vessel

They have a poor capacity of healing because:

1. Main blood supply is interrupted due to tearing of capsular blood vessel

2. Difficult for callus formation à because intra- articular bone has only flimsy periosteum and has no contact with soft tissue

3. synovial fluid prevent blood clot for haematoma formation

ulnar nerve palsy - Rushdan

aku jpe kt internt.post la kt blog..smart jgok

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.