WRIST AND HAND

COMPLEX

Zeel Vyas
Khilti Furia
Guided by : Dr Mansi Bhartiya
ANATOMY OF WRIST AND HAND
INJURIES AFFECTING THE
STRUCTURES OF WRIST AND HAND

SOFT
TENDON NERVE
TISSUES

VASCULA
BONE
R
 INJURIES

ATRAUMATI
TRAUMATIC
C
GENERAL CAUSES OF THE INJURIES
1. FALL ON AN OUTSTRETCHED HAND
2. SUDDEN JERKY MOVEMENTS
3. OSTEOPOROSIS
4. IN CHILDREN DUE TO UNDER DEVELOPED STRUCTURES.
5. OVERUSE
6. IMPINGMENT
7. DECREASE IN THE VASCULAR SUPPLY
ZONES OF THE HAND
Tendon healing
• Occurs through combination of 2 processes –extrinsic and intrinsic
• Extrinsic- formation of adhesions between the tendon and the
surrounding tissues.
• Intrinsic- healing relies on the synovial fluid for nutrition and occurs
only between tendon ends.
• Other factors- age, general health, scar formation, level of injury,
trauma extent, pulley integrity, surgical technique.
Treatment of flexor tendon
lacerations
• Less than 25%- beveling the cut edges
• Between 25-50%- repaired with 6.0 nylon suture
• More than 50%- epitenon suturing

• Tendo-fix repair
A stainless-steel tendon repair device.

FDP lacerations repair- tendon is reinserted into the distal phalanx with a pull
out wire.
Quadregia effect
Rehabilitation after flexor tendon
repair
• Factors- timing, location, compliance,
• Active mobilization
• Kleinert splintage
• Lag sign
Flexor digitorum profundus
avulsion(Jersey finger)
• Most common in the ring finger
• The condition occurs when the player grabs the opponent’s jersey
and feels sudden pain as the distal phalanx is forcibly extended as it is
concomitantly actively flexed.
• 4 types of avulsion
• Type 1- retraction of the FDP to the palm
• type 2-Retraction to PIP joint
• Type 3- bony fragment distal to A4 pulley
• Type 4- avulsion of FDP from the fractured fragment.
• Surgical procedures include DIP Arthrodesis, tenodesis and staged
tendon reconstruction.
• Rigid bony fixation that prevents dorsal subluxation of the distal
phalanx.
• FDP Tendon repair independent of bony fixation.
Extensor tendon injury
• Anatomy
Mallet finger ( zone 1)
• Avulsion of the extensor tendon from its distal insertion at the
dorsum of the DIP joint producing an extensor lag at DIP joint
• Avulsion may occur with or without detachment of bony fragment
from the distal phalanx.
• Mallet finger has either a bony origin or a tendinous origin.
• Clinically – flexed or dropped position of DIP joint and actively unable
to extend the joint.
Classification of mallet finger
• Type 1- extensor tendon avulsion from the distal phalanx
• Type 2- laceration of the distal phalanx
• Type 3- deep avulsion injuring the skin and tendon
• Type 4- fracture of the distal phalanx
A- transepiphyseal fracture in a child
B- Less than half of the articular surface involved with no
subluxation.
C- more than half of the articular surface involved and may
involve volar subluxation
• Stack splint
• Perforated thermoplastic splint
• Aluminium foam splint
• Surgical- transarticular pinning of DIP joint
• extensor tendon shortening
• Tenodermodesis
• Reconstruction of oblique reticular ligament, central slip tenotomy
Gamekeeper’s thumb
Triangular fibrocartilage complex
injury
De Quervain’s tenosynovitis
Intersection syndrome of the wrist
Dorsal and volar carpal ganglion
cysts
KIENBOCK’S DISEASE
 RA – Hand

• It is a systemic autoimmune disease

• Characterised by inflammatory arthritis & extra articular involvement
• Etiology :
• Genetic predisposition – HLA- DR B1
• environmental trigger – Epstein Barr Virus

• Deformities :
 Boutonniere Deformity
 Swan Neck Deformity
 Ulnar Drift
 Z thumb Deformity
 Opera- glass Hand
 Pathology

Activation + accumulation of CD4 T cells

Cascade of inflammatory responses – resulting in activation of macrophages & synovial cells

Causing proliferation of the synovial cells – leading to increased production of destructive enzymes
( elastase & collagenase )

This activates the B lymphocytes to produce various antibodies

In turn activates endothelial cells via increased production of M1

Causing increased adhesion & accumulation of inflammatory cells

Producing RANK’L – activating OSTEOCLASTS causing subchondral bone destruction

this cascade of inflammatory responses leads to PANNUS formation

Boutonniere Deformity
• Definition – it is the deformity of finger
With PIP in flexion , DIP in hyperextension
Extensor tendon injury over zone III

• MOI
1. Direct trauma – burns / laceration : external force on the central slip –
causing stretch leading to failure of extensor mechanism
2. RA- hand : synovial proliferation at the PIP, stretches the extensor
mechanism, compromising the central slip leading to inability to
extend fully  extensor lag
• Rupture of the central slip  all extensor forces are transmitted to the
DIP  producing hyperextension at DIP with lateral band intact  PIP
protrudes through extensor hood – causing PIP Flexion

• SIGNS & SYMPTOMS :

i. Loss of extension at PIP
ii. DIP into Hyperextension
iii. Middle IP cannot be straightened
iv. Weak grip, grasp
v. Swelling & pain

• Special test :
Elson test https://www.youtube.com/watch?v=0qVMBbOua24
Swan neck deformity
• Definition – PIP in hyperextension
DIP into flexion
Reciprocal MCP flexion can also be present

• MOI
Damage to the Extensor tendon mechanism
A closed avulsion to DIP while digit is extended – damage to the
extensor tendon causing LAXITY at the volar plate & tightness at the
triangular ligament – laxity causing PIP to hyperextend
• SIGNS & SYMPTOMS :
i. History of inflammation
ii. Swelling, stiffness
iii. Gradual difficulty in PIP flex
iv. Snapping sensation during flexion
• Stages :
Nalebuff classification :–
Type 1 – PIP flexible all position of MCP
Type2 – PIP flexion limited in certain MCP position
Type 3 – PIP flexion limited irrespective to MCP position
Type 4 – PIP joint stiff poor radiographic appearance

• Special test : Bunnell Littler Test

https://www.youtube.com/watch?v=Ni78ZWBIpTM

• Assessment : A/PROM – MCP, PIP, DIP

Ulnar Drift
• Definition –
Ulnar Drift/ shift – is a deformity produced by ulnar translation of PIP
base with w.r.t MC head

• MOI-
Muscles pull the distal carpal bones proximally, collapse into zig-zag
deformity – laxity of the ulnar collateral ligament.
Increased intra-articular pressure causing muscle imbalance.
• Signs & symptoms –
i. enlarged MCP joint & ulnar deviation
ii. Impingement at the TFCC structure

• Assessment
ROM – UD, RD
Muscle strength
Z deformity of Thumb
• Definition –
Occurs due to synovitis of the joint capsule at the MC joint of the
thumb

• MOI –
Stretching of EPB & EPL tendon – results in subluxation.
Volar placement of the tendons, forces MCP joint flexion – secondarily
causing IP joint to hyperextend
• Signs & symptoms –
i. Pinching at the thumb
ii. Lost of opposition function
iii. Grip & grasp activity affected due to loss of opposition
Opera-Glass Hand
• Definition –
Occurs in extreme cases of RA, as there is resorption & shortening of
the articular bones leading to instability

• MOI –
Starts at the articular surface – bones become shorter due to the
comprehensive forces that pulls the extensor & flexor tendon  further
pulling the shortened bones into the hand  this collapse is similar to
appearance like an opera- glass
• Signs & symptoms –
i. Significant hand functional disability
ii. Collapse shortens the span of fingers – creating small arc of grasp but
unequal
iii. Profound instability
Physiotherapy Management
 TENDON GLIDING EXERCISES

https://www.youtube.com/watch?v=DRr4qzxCSqY - therapeutic exercises

TRIGGER AKA STENOSING FLEXOR

FINGER TENOSYNOVITIS
OR
DIGITAL TENOVAGINOSIS

MOST COMMON TENDON "PAINFUL SNAPPING

ENTRAPMENT OF PHENOMENON"
HAND/WRIST
• Possible Causes –
Idiopathic
Post menopausal woman
Diabetes
Trauma/ Occupational Factors
Other conditions : DQ, Tennis elbow, RA, Dupuytren contracture

• MOI -
A difference in size between the flexor sheath & flexor tendon  leads to
abnormalities of the gliding mechanism  causing abrasion between the two
surfaces  progressive inflammation between the tendons & the sheath
• CLINICAL FEATURES –
 Palpable nodule at thicken a1 pulley area/ palmar crease / MP flexion
increase of thumb felt
 Locking of finger - can’t extend
 Tendon movement through sheath  palpable - sometimes audible
crepitations +
 Pathology
A1 PULLEY GOT THICKENED / FIBROSED

HENCE, INABILITY OF 2 FLEXOR TENDONS ( FDS + FDP) TO SLIDE SMOOTHLY UNDER A1

SO SNAPPING OCCURS WHEN ACTIVELY FLEX/EXTENDS IP JOINT

SO GLIDING DOESNT OCCUR; RATHER IT CATCHES AND GIVES AWAY

MORE FORCE NEEDED, CREATES MORE TENSION, SO TENDON SLIDES

SUDDEN JERKY MOVEMENT AS TENDON NODULE PULLS THROUGH CONSTRICTED PULLEY

MOMENTARY LOCKING OF FELXOR TENDON (WHEN EXTENDING) FOLLOWED BY  FLEXION

 TREATMEN
T

EARLY STAGE LATE STAGE

 EARLY
STAGE
1. Rest

2. Local US

3. Heat- cold combo

4. NSAIDS

All extensions ↑ : CMC, IP

5.

6. SPLINTING: (IN EXTENSION), night splints

7. Stretching exercises https://www.braceability.com/blogs/articles/trigger-finger-exercises

 LATE
STAGE

LOCAL ANALGESICS/ SPLITTING OF

HYDROCORTISONE / TIGHT TENDON
CORTICOSTEROIDS/ SHEATH

1/3 RD PATIENTS 2/3 RD PATIENTS

 CONGENITAL HAND
DEFORMITIES
A. Problems in the formation of the
parts
Radial & Ulnar Club hand -
insufficient development of the
radius/ ulna with the absence of the
thumb
B. Failure of parts to separate
Simple Syndactyly – fused fingers
Complex Syndactyly
Duplication / Polydactyly – extra digits
C. Undergrowth of fingers
Small fingers, muscles are missing, bones under- developed or complete
absence of a finger

D. Overgrowth of fingers/Macrodactyly E. Cleft hand /Ectrodactyly

Aka Split hand
REFERENCES
• Brotzman
• Ebnezer – 5th edition
• Maheshwari – Orthopaedics
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1395797/
• Kisner