keep on walking !

life is motion..........................

Rheumatoid Arthritis Medical treatment

RHEUMATOID ARTHRITIS

It is a chronic inflammatory systemic disease of young or middle aged adult
chatact by – destructive & proliferative changes in the synovial membrane
periarticular structure, skeletak muscle& perineural sheath.
Eventually joints are deformed and ankylosed

Etilogy –

Exact cause unknown
Theories
(1) Infection – haemolytic /nonhaemolytic streptococci have been isolated from
joint & regional lymph node
(2) Endocinal - suggested by response to adrenocortical steroid
(3) Allergies – exhibit various allergic manifestations. Eosinophilia +
(4) Metabolic
(5) Immune overactivity –
- +nt of antibody immunoglobulin – RA factor
- Infilteration of synivial tissue by immunologically competent cells eg
plasma cell , lymphocytes
- +nt of Ag-Ab complexes with leucocytesbin synivialfluid & blood
- Lowered complement level in synovial fluid
(6) Genetic factors – tendancy for aggregating in family
(7) Vascular changes – alteration of peripheral vascular bed , perhaps by
autonomic influxes
Age – young & middle age ( mean age of onset – 40 years)
Sex – Women > Men (3 :1)

Pathogenesis –

Most widely accepted theory – immunological response in synovial tissue
Exogenous antigen (Ag)
↓ entry
Defender cell (WBC – T lymphocyte) + Ag
Transform in to ↓
Plasma cell
↓
Ab + Ag → Ag-Ab complexes ← phagocytes engulf
↓
Lysosomal enzyme releases (proteases)
↓
Inflammation → destruction of tissues (synovium & cartilages)
↓
Pannus – is a granulomatous mass that grows over & destroys cartilage, tendon,
ligament
Under electron microscope,the lining consist of thee types of synovial cells
Type A – phagocytic .Take up Ag-Ab complexes & particulate matter from
synovial fluids
Type B – resembles fibroblast & are belived to synthesis protein & hyaluronic acid
which are +nt in synivial effusion
Type C – Undifferentiated . can become type A or B
In response to human immunoglobulin IgG autoantibodies are synthesized in
rheumatoid synovial tissue (RA factor - RF). It not only reacts with human IgG but
also with IgG of no.of other anomal species making it feasible to test for RF with
sheep cells coated with rabbit IgG. Patient with high titer of Rf have a poor
prognosis.
Standard test for RF determines - only IgM RF (most rapidly measured)
Elevated RF seen in
- RA
- SLE
- Scleroderma
- Polymyositis & dermatomyositis
- Sarcoidosis
- Chronic bacterial endocarditis
- TB
- Chronic hepatitis
- S’jogren syndrome
- Haemochromatosis
- Haemophilic arthritis

Medical management –

• Disease suppressing drugs
• Disease midifying drugs
• Immunosuppressant
(A) Disease suppressing drugs
1. Salicyclates –
Eg – acetylsalicyclate (Aspirin) ,Mg salicayclate, Mg choline
Antiinflammatory ,antipyretic & analgesics
Serum salicyclates level should be monitored. Non therapeutics anti-inflammatory
level are 20-30 mg/dl
Metabolized in Liver & excreted by kidney
C/I – Asthama (Bronchoconstriction)
Bleeding tendencies (platelet inhibition)
Hyperurecemia (Urate retention)
Acute renal/hepatic failure
Side effect – GIT – dyspepsia, nausea,vomiting,occult bleed
CNS – titnitus ,deafness, convulsion
Hy50-75 mg bid/tdspersensitivity reaction
2. NSAID’s –
Reversible PG synthetase inhibitor - Antiinflammatory ,antipyretic & analgesics
Side effect – GI irritation, platelet inhibition, headache,dizziness, ARF,nephritic
syndrome, GN, Steven –Johnson syn,aplastic anaemia
Indomethacine – most potent NSAID Dose – 25 mg bid/tds , Max-150 mg/day
Diclofenac Na - 50-75 mg bid/tds ,Max – 200 mg/day
Ibuprofen – 400 mg tds/qid ,Max 3200 mg/day
Phenylbutazone – 100 mg tds
(B)Disease modifying agents
1.Gold salts –
More effective than NSAID’s
Retards progession of bony erosions & cartilage loss – alter natural course of RA
Reuires close clinical & lab monitoring
Used in Juvenile RA, Psoriatic arthritis, Felty’s syndrome
Indication – patient with acute synovitis who does not respond to conservative
management with NSAID, Sylicyclates
- patient with rapidly progressive erosive arthritis
Metabolism -

Back, Bladder and Bowel Care

Back, Bladder and Bowel Care

BACK CARE

Patients in Orthopedics are usually bed ridden so they have problems in proper bladder and bowel care. These makes them prone to development of pressure sores and poor function of bladder and bowel.

BACK CARE

Spinal injury patients especially with neurological deficit are more prone to develop various bladder and bowel dysfunctions, which affects their physical and mental wellbeing leading to poor recovery of functions.

Why back care???

  

PROLONGED BED RIDDEN

1Multiple fractures.

2Spinal injury with neurological involvement.

3Poor general condition.

4Secondary complication like muscle weakness, deformity and muscle contractures etc.

 Back care 

AIMS-

1.Avoid pressure sores.

2.To prevent secondary complication.

3.Maximize functional recovery.

The EPUAP Guide to Pressure Ulcer Grading

Pressure sore

     Found during autopsies on Egyptian mummies, pressure sores are an ancient medical problem.

The sites of occurrence include the

1.ischium (28%),

2.sacrum (17-27%),

3.trochanter (12-19%), and

4.heel (9-18%).

Pressure sore

HIGH RISK GROUP

1.Patients with fractures treated by conventional method like prolonged traction.

2.Elderly patients.

3.Patients with spinal cord injury.

Pressure sore - Management

Remove all clothing.

Use pressure relieving mattress ( Water bed, Air mattress)

Lift or log roll the body hourly

Examine skin for marking or damage

Posturing

Support injured spine in alignment

Maintains limbs and joints in functional position to avoid contractures.

In paraplegic patients sleeping in prone position with pillows bridging the bony prominences

Relieve pressure

Avoid wetting

Choice of bed

Stryker bed

Profiling bed with multiple layers of varying density foam

Dry

Wrinkle free

Skin Care

Examine and relieve pressure regularly

Keep clean

Avoid damage

Frequent posture change

Treat minor abrasions

Log Rolling

Needed for nursing care of paraplegic and quadriplegic patients.

Avoids further damage to spinal cord & detioriation of neurology.

Log rolling

Log rolling

BLADDER MANAGEMENNT

AIMS –

1.Preservation of renal function

2.Continence

3.Prevention of infection

4.Achieve fluid balance

Catheterization

TYPES

1.Indwelling catheterization.

2.Intermittent catheterization.

3.Condom catheterization.

4.Suprapubic catheterization.

Indwelling catheterization

Catheter is left in place

urethra / SPC

no touch technique under strict aseptic precaution.

Intermittent catheterization

Prereqisites:

1.Strict aseptic techniques.

2.Catheterize 6 hourly initially

3.Restrict fluids to 1500 ml/24 hrs

4.Culture regular urine samples and treat significant UTI

Disadvantages

Calculi

Weekly or biweekly bladder wash

Frequent blockages

Infection

periurethral abscess, urethral diverticulum, fistula formation and epididymoorchitis

Self Intermittent Catheterization

Optimum requirements

1.Absent or minimal detrusor activity

2.Large bladder capacity

3.Sufficient manual dextrity

4.Pain free cathterisation

5.Patient motivation

●

Condom Catheterisation

Used in spastic bladder which empties on its own leading to soiling of clothes.

Allergic reaction.

Negates disadvantage  of urethral catheterization.

Suprapubic Catheterization

Avoids urethral instrumentation and attendant problems.

Permits high fluid intake

No fluid restriction

Disadvantages :-

1.Catheter blockage.

2.Surgical site infection

3.Technical demanding

Long term prevention of UTI

High fluid intake

effective bladder training

urinary antiseptics

Biweekly catheter change

Regular bladder wash

Bowel Care

Stretching >>>signals to spinal cord>>

Reflexive emptying

OR

Stretching>>spinal cord>>brain>>

Voluntary emptying or holding

Why Bowel Care ?????

To prevent:-

Constipation

Hemorhoids

Malnutrition

Fluid imbalance

Bowel Care Program

1.Avoiding constipation.

2.Maintaining a good consistency in stool.

When feces becomes too dry and firm, more difficulty in emptying , allowing bacteria to remain in body for a longer period ,cause of infections and other problems.

Firm stool  irritates the colon and cause hemorrhoids

.

Bowels Management

Diet- a high rich fiber diet.

Avoid caffeine

laxatives, stool softeners

enemas

Manual removal of fecoliths

 Take Home Message

   Back, bladder and bowel care is a very important aspect in orthopedic patient care because these…

Have a profound impact on the overall recovery of the patient.

Hamper rehabilitation.

Lead to additional morbidity.

WRITER’S CRAMP

Synonyms – Mogigraphia , Scrivener’s palsy

Writer's cramp is a form of task-specific focal dystonia. Dystonia is an involuntary, sustained muscle contraction causing twisting movements and abnormal postures; focal dystonia means only one body part is affected.
Writer's cramp is the most common dystonia occurring in the setting of repetitive movement disorders. A focal dystonia can sometimes be the first manifestation of a generalized dystonia.


Incidence - One study estimated the prevalence to be 69 cases per 100,000 populations; this is thought to be an underestimation because a high percentage of patients never seek medical
assistance.


Pathophysiology
Normally, an antagonist muscle relaxes when an agonist muscle is contracted. Patients with dystonia have simultaneous contraction of both groups of muscles. Spinal reciprocal inhibition, a
process that inhibits the antagonist muscles when the agonist muscles are active, is reduced in patients with writer's cramp. This is most probably due to aberrant descending commands.
Abnormalities in the basal ganglia lead to abnormalities of sensory processing and motor output.
The normal increase in cerebral blood flow in the supplementary motor area is reduced in response to vibration and abnormal somatosensory evoked potentials. These provide evidence for the
abnormal sensory processing in patients with dystonia. Increased motor cortex excitability along with decreased cortical inhibition causes abnormal motor output.

Sex - Prevalence is slightly higher in men; the male-to-female ratio is 1.3:1.

Age - Typically, patients present in the third to fifth decades, and women usually present earlier
than men.

Clinical

History –
Incoordination, cramping, and aching of the hand with task-specific movements are usually the
initial complaints.
The hand assumes a semiflexed position of the fingers with possible hyperextension of the fingers
and hyperflexion or extension of the wrist with supination or pronation.
The symptoms become exaggerated with attempts to perform a specific task, such as writing. In somecases, the hand may dart across the page with a sudden jerk.
A related condition is primary writing tremor. Affected individuals exhibit a prominent large amplitude tremor only with writing.

Physical
Neurologic examination findings are usually normal.
Subtle findings include mild dystonic postures developing either spontaneously or with movement and reduced arm swing.
One third of patients have a tremor in the affected arm or hand while writing or when the extremity is outstretched. Observation of the limb during writing is an important part of the examination; the
assumption of dystonic postures should be demonstrable. Patients affected with primary writing tremor, a variant of writer's cramp, may exhibit a large-amplitude tremor only during writing. In
contrast to essential tremor, action or sustentation tremors are not seen with other tasks such as holding a full cup of liquid or coordination testing. Dystonic posturing is usually not seen with this condition.

Causes
Writer's cramp frequently affects persons who write a great deal or perform other repetitive hand movements such as typing.
Approximately 5% of patients have a positive family history of a similar condition.
Five to ten percent report an accident or injury to the hand or arm immediately preceding the onset of symptoms.
Several possible, but rare, associations have been reported, including C6 ruptured disk, lithium use, basalganglia or cortical tumors, arteriovenous malformations (AVMs), and stroke. However, most cases are idiopathic.

Differential Diagnoses

Dopamine-Responsive Dystonia
Multiple Sclerosis
Parkinson Disease
Wilson Disease
Primary writing tremor
Postural tremor
Idiopathic torsion dystonia

Workup

Imaging Studies - MRI - If a structural lesion is suspected
Procedures - Electromyography/nerve conduction studies
To evaluate for nerve injury, if trauma is the suspected cause
Confirm diagnosis by showing simultaneous contraction of agonist and antagonist muscles

Treatment

Medical Care

Approximately 5% of patients have spontaneous remission, most probably in the first 5 years.
However, the majority of these patients have relapses.Treatment is generally disappointing.
Transcutaneous electrical nerve stimulation (TENS) delivered to the forearm flexor muscles for
a 2-week period has been found to improve symptoms for upto 3 weeks after treatment.
Behavioral changes may help.
Biofeedback, hypnotherapy, and relaxation therapy have been tried.


Activity

Altering the grip of the pen and/or increasing the diameter of the pen used is the first step in treatment. Patients can use a writing device or other means of transcription, such as typing or dictation.

Medication

Several classes of drugs have been used in patients with writer's cramp. Anticholinergics have had conflicting results. Beta-blockers have helped the tremor in a few patients. Botulinum toxin injections seem to have the best results.

Anticholinergic

Blocking cholinergic innervation of the basal ganglia is hypothesized to increase the dopaminergic effect,thereby reducing dystonia.
Trihexyphenidyl (Artane)
Substituted piperidine that inhibits parasympathetic system. Available as 2 mg tab or 2 mg/5 cc
elixir.

Adult

Start with 1 mg PO qd, then increase by 2 mg at intervals of 3-5 d up to 6-15 mg/d divided tid
Dosing Interactions Contraindications Precautions
Dosing Interactions Contraindications Precautions
Beta-adrenergic blockers
These agents help reduce the tremor.
Propranolol (Inderal, Betachron E-R)
Class II antiarrhythmic, nonselective, beta-adrenergic, receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. Available as 10 mg, 20 mg, 40 mg, and 80 mg tablets and 60 mg, 80 mg, 120 mg, and 160 mg long-acting tablets (Inderal LA)


Neurotoxins
Neurotoxin complex blocks neuromuscular conduction by binding to receptor sites on motor nerve  terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. When injected intramuscularly, it produces a localized chemical denervation muscle paralysis.

Botulinum toxin type A (BOTOX®)
Local intramuscular injections weaken overactive muscles, reducing dystonic symptoms.
Pediatric - Administer as in adults

Adult - 40 mg PO bid initially; increase as tolerated; not to exceed 240-320 mg/d divided bid/tid

Pediatric - 2-4 mg/kg PO divided bid; increase as tolerated; not to exceed 16 mg/kg/d

Adult - Injections usually given under EMG guidance and should be administered by physicians experienced in giving the injections
Pediatric - Not established

Follow-up

Prognosis - The prognosis is good.
Patient Education - Patients should reduce the task-specific activities that precipitate the
condition.

Medicolegal Pitfalls - Do not consider patients with writer's cramp and other action dystonias as having a psychiatric disorder.This could deprive the patient of evaluation by a movement
disorder specialist and hence the benefit of adequate treatment. Patients with writer's cramp do not have a higher incidence of psychiatric disorder than the general population.

Brachial Plexus Palsy( During Birth )

Brachial plexus palsy may be seen after injury to the brachial plexus during birth.
Incidences range from 0.1% to 0.4% of live births.

Risk factors –

 Large birth weight,
 Breech presentation,
 Shoulder dystocia,
 Prolonged labor,
 Forceps delivery.

The severity of the palsy depends on which roots of the brachial plexus have been
injured and the extent of injury. Although the incidence of birth palsy has remained
the same, the severity of birth palsies has diminished.
Brachial plexus palsy is classified according to the location of the injury of the brachial plexus.


Seddon classified the injuries into three types -  

The most common types are upper plexus palsy (Erb-Duchenne), in which the supraspinatus and infraspinatus muscles are the most frequently paralyzed;
Whole plexus palsy ("mixed"), in which there is complete sensory and motor paralysis of the entire extremity because of severe injury in all roots of the brachial
plexus;

Lower plexus palsy (Klumpke), in which the muscles of the forearm and hand together with parts served by the cervical sympathetic chain are paralyzed after injury of the eighth cervical and first thoracic nerve roots.

The injury to the brachial plexus can range from neurapraxia or axonotmesis to rupture of roots and avulsion from the spinal cord.
Upper root level injuries (C5-C6) occur most frequently (approximately 90% of patients) and have the best prognosis; lower plexus and whole plexus injuries have the worst prognosis but are much less common.
Geutjens found a higher incidence of avulsion of the upper roots in babies with brachial plexus palsy who were born breech. The babies with avulsions of the upper rootshad a worse prognosis for recovery after exploration and microsurgical-grafting.

Narakas proposed a more detailed classification based on the clinical course of children with brachial plexus palsies during the first 8 weeks after birth; his classification includes a prognosis for each type of injury .

Clinical Features

The diagnosis usually is evident at birth.

In upper root involvement-

The arm is held in internal rotation and active abduction is limited.

The elbow may be slightly flexed or in complete extension.

The thumb is flexed, and occasionally the fingers will not extend.

In complete paralysis, the entire arm and hand is flail.

Pinching produces no reaction.
Vasomotor impairment may be indicated by the relative paleness of the involved extremity.
Roentgenograms of the shoulder may reveal fracture of the proximal humeral epiphysis or fracture of the clavicle.
A clavicular fracture occurs in association with plexus palsy in 10% to 15% of patients.
Pseudoparalysis from a clavicular or proximal humeral fracture should resolve within 10 to 21 days. If limited motion persists after 1 month of age most likely a concomitant brachial plexus palsy is present.
A septic shoulder in an infant also can cause a pseudoparalysis, which can be differentiated from a brachial plexus palsy by evidence of systemic illness and resolution of the pseudoparalysis after the infection is treated.
Characteristic deformities usually develop promptly. The shoulder becomes flexed, internally rotated, and slightly abducted; active abduction of the joint decreases; and external rotation disappears . The shoulder may become posteriorly subluxated and eventually dislocated, or the humeral head becomes flattened against the glenoid.
Advanced glenoid changes were seen by the time the child was 2 years old.
Elbow flexion and forearm supination deformities can occur with a Klumpke palsy (C8-T1) or a mixed brachial plexus lesion. Progressive deformities occur because of weak or absent triceps, pronator teres, and pronator quadratus muscles with an intact biceps muscle. This creates progressive elbow flexion and supination deformity from the unopposed biceps muscle. Radial head dislocation may occur, and the wrist and hand usually are held in extreme dorsiflexion because of the unopposed wrist dorsiflexors.

Evaluation of the brachial plexus injury may include
 Clinical evaluation,
 Electrical diagnostic studies,
 Myelography,
 CT, and MRI.
 Combined myelography, CT, and MRI are more reliable than myelography
alone.
 Large diverticulae and meningoceles are indicative of root avulsions.

Treatment-

Minimal injuries respond well to conservative treatment and, although recovery may
require as long as 18 months, usually residual disability or deformity is slight.
Gilbert and Tassin, and Millesi have suggested that if no evidence of deltoid or biceps recovery is seen by the age of 3 months, surgical exploration should be considered.

The Toronto scale has been used to predict poor outcomes if microsurgical repair or
grafting is not done.

This scale consists of grading elbow flexion, elbow extension, wrist extension, finger extension, and thumb extension. These muscle groups are scored as 0 (no motion), 1 (motion present but limited), or 2 (normal motion) for a maximal score of 12. A score of less than 3.5 predicted a poor long-term outcome without microsurgery.
The aim of treatment in the initial stages is prevention of contractures of muscles and joints.

Gentle passive exercises are begun to maintain full range of passive motion of all joints of the upper extremity, especially full extension of the fingers, hand, and wrist,full pronation, and supination of the forearm, full extension of the elbow, and full
abduction, extension, and external rotation of the shoulder.
Microsurgical nerve repair or grafting has been reported to give satisfactory results in carefully selected patients.

CT scanning and myelography, followed by electromyographic and nerve conduction velocity studies. If these studies show root avulsion from the spinal cord, they recommended no surgery.
If the CT scan and myelogram are normal, they recommended exploration of the brachial plexus and repair of any injuries. Most authors recommend electromyography and CT myelography or MRI evaluation before surgical intervention. The timing of microsurgical intervention still is controversial and rangesfrom 1 to 6 months.

The indications for microsurgical intervention
 Absence of biceps recovery (usually by 3 months of age),
 Toronto score of less than 3.5,
 Total plexopathy with Horner syndrome.

Surgery in unresolved brachial plexus palsy usually is directed toward improving shoulder function and joint contractures. Sever recommended anterior subscapularis
release to correct mild to moderate internal rotation contracture.
Hoffer recommended in addition an anterior release transfer of the latissimus dorsi and teres major to the rotator cuff to improve function.

Wickstrom recommended external rotation osteotomy of the humerus for severe fixed rotation contracture.
Waters recommended that patients with grade I (normal), II (mild increase in glenoid retroversion), or mild grade III (slight
posterior subluxation) glenohumeral deformities have an anterior musculotendinous lengthening of the pectoralis major and posterior latissimus dorsi and teres major transfer to the rotator cuff.
Patients with advanced grade III, grade IV, or grade V glenohumeral deformities should have a humeral derotation osteotomy.
In Klumke palsy , where elbow flexion and forearm supination deformity occur, the biceps tendon can be Z-lengthened and rerouted around the radius to convert it from a supinator to a pronator ; this improves elbow extension and forearm pronation.

MADELUNG DEFORMITY

MADELUNG DEFORMITY

Madelung deformity is an abnormality of the palmar ulnar part of the distal radial physis in which progressive ulnar and volar tilt develops at the distal radial articular surface, with dorsal subluxation of the distal ulna.

First described by Malgaigne in 1855 and later by Madelung in 1878.
It is believed to be a congenital disorder, although it seldom is obvious until late childhood or adolescence.
It is a rare anomaly, accounting for only 1.7% of hand anomalies in Flatt's series.
The cause of Madelung deformity is uncertain;
it has been shown to be transmitted in an autosomal dominant pattern.
Other Madelung-like deformities have occurred after trauma, as reported by Vender and Watson in a gymnast, and after infection or neoplasm.
There is no definitive method of distinguishing these from idiopathic Madelung deformity.

Vender and Watson classified Madelung and Madelung-like deformities into four groups:
1. posttraumatic,
2. dysplastic (dyschondrosteosis or diaphyseal aclasis),
3. genetic (e.g., Turner syndrome), and
4. idiopathic.


They believe that acquired deformities usually can be distinguished by a lack of appropriate physical findings, unilaterality, less severe carpal deformities, and the appropriate history of repetitive injury or stress.

A deformity of the wrist similar to Madelung deformity frequently is associated with dyschondrosteosis, the most common form of mesomelic dwarfism.
This disorder consists of mild shortness of stature, shortness of the middle segment of the upper and lower extremities, and Madelung deformity.

Other associated conditions include mucopolysaccharidosis, Turner syndrome, achondroplasia, multiple exostoses, multiple epiphyseal dysplasia, and dyschondroplasia (Ollier disease).
Madelung deformity typically consists of volar subluxation of the hand, with prominence of the distal ulna and volar and ulnar angulation of the distal radius. It is more commonly bilateral and affects girls more frequently than boys. A family history of the deformity often is present. The deformity usually manifests in late childhood or early adolescence, with decreased motion and minimal pain. As growth occurs, the deformity worsens in appearance. 

X-ray abnormalities are seen in the radius, ulna, and carpal bones. The radius is curved, with its convexity dorsal and radial, and there is a similar angulation of the distal radial articular surface.

The forearm is relatively short. The distal radial epiphysis is triangular because of the failure of growth in the ulnar and volar aspects of the physis; early closure of these aspects of the physis also is frequent. Osteophyte formation may be visible at the volar ulnar border of the radius.

The ulna is subluxated dorsally, the ulnar head is enlarged, and the overall length of the ulna is decreased. The carpus appears to have subluxated ulnarward and palmarward into the distal radioulnar joint, which usually is spread apart. The carpus appears wedge shaped, with its apex proximal within the lunate.

Treatment Because children with Madelung deformity usually have minimal pain and excellent function, a conservative approach is warranted initially.

Surgery should be considered for severe deformity or persistent pain, usually from ulnocarpal impingement of the carpus.
Vickers and Nielson reported some success with resection of the abnormal portion of the radial physis and insertion of fat as a form of surgical prophylaxis. In their series all 17 patients had pain relief and no progression of the deformity after surgery. Distal radial osteotomy with ulnar shortening (Milch recession) is a preferred treatment in skeletally immature patients. The radial osteotomy may be a closing or opening wedge as needed for alignment.

Osteotomy combined with a judicious Darrach excision of the distal ulnar head may be used in skeletally mature patients.
Watson, Pitts, and Herber performed balanced radial osteotomies combined with a matched ulnar resection in 10 patients. They reported that radial length was preserved better using this technique; experience with this technique is relatively less.
Resection of Dyschondrosteosis Lesion TECHNIQUE (Vickers and Nielsen)

Under tourniquet control, make a volar transverse incision 1.5 cm proximal to the most proximal wrist crease, passing either on the ulnar side to the flexor carpi radialis and palmaris longus or on the radial side.

Protect the median nerve and radial artery. Continue the approach radial to the mass of the digital flexor tendons to the distal edge of the pronator quadratus muscle, some of which can be mobilized at the radial end.
Using an osteotome, make the initial longitudinal osteotomy in the radius, parallel to the long axis of the forearm, about 5 mm from the radioulnar joint.
In patients with extreme volar subluxation of the carpus, take care not to mistake the lunate for the underlying radius. Reflect the small fragment of the distal radius ulnarward with the osteotome to preserve what exists of the flimsy connections between it and the ulna and to leave some support for the lunate. A sagittal section of the distal radius should now be visible. Magnification is recommended. If the initial osteotomy is too shallow, a white sheet of fibrous tissue and cartilage is seen. Make successive osteotomy cuts 1 mm thick until the physis is clearly identified. When first seen the physis is thin and wavy and significantly narrowed. When the physeal cartilage is clearly defined, carefully remove bone from the metaphyseal side with a gouge or burr so that the profile of the cartilage is above the bone and is intact from the dorsal periosteum to the volar periosteum to prevent a new bar of bone from forming. Identify and excise the abnormal volar ligament tethering the lunate to the radius. Deflate the tourniquet and obtain hemostasis, using bone wax if necessary. Reinflate the tourniquet and flush with normal saline to remove all bone chips and blood. Obtain a generous quantity of fat from the proximal forearm medially and insert to fill the surgical cavity completely. This fat must make intimate contact with the entire length of the physeal cartilage, isolating the bony epiphysis from the bony metaphysis. Soft tissues fall together to hold the fat in place. Suture the skin and apply a short arm volar slab or a crepe bandage. 


AFTERTREATMENT. The bandage should be worn for 2 weeks depending on the degree of the deformity.

 Closing Wedge Osteotomy Combined with Darrach Excision of Distal Ulnar Head TECHNIQUE (Ranawat, DeFiore, and Straub)

Make a dorsal longitudinal incision over the distal forearm, detach the extensor retinaculum from the radius over the extensor digitorum communis tendons, and reflect the retinaculum and the tendon of the extensor digiti minimi ulnarward. If the patient is skeletally mature, expose the distal radioulnar joint and excise about 1 cm of the distal ulna. If the patient is skeletally immature, expose the ulnar shaft and perform an appropriate cuff recession as described by Milch. Next perform an osteotomy parallel with the distal articular surface of the radius. Resect an appropriate wedge of bone based radially and dorsally from the distal end of the proximal fragment of the radius and appose the raw surfaces. Stabilize the osteotomy with Kirschner wires so that the distal articular surface of the radius is facing volarward 0 to 15 degrees to the long axis of the radius and ulnarward 60 to 70 degrees. Close the incision in routine fashion and apply a long arm cast.

AFTERTREATMENT.
The cast and pins are removed 4 weeks after surgery, and active exercises of the wrist are begun. The osteotomy incision is protected with a cast or splint until there are sufficient radiographic and clinical signs of bone healing. Normal activities are progressively resumed.
After the final cast is removed, protective splinting may be necessary for 8 to 10 weeks after surgery.