Claw hand

1. CLAW HAND
Presenter : Dr Vinay
Moderator : Dr Satish sir
Chair person : Dr. Srinivas rao sir

2. Definition
 Flattening of transverse
metacarpal arch and
longitudinal arches, with
hyperextension of MCP
joints and flexion of PIP
and DIP joints

3. Normal anatomy
 Movementsof MP jointsand IP joints independent
Movements of 2 IP joints coordinated ; flexionof
DIP joint brings about flexion of PIPjoint
(1) Flexion of distal phalanx draws dorsal expansion
distally by loosening tension on central tendon
(2) Flexion of DIP joint tenses obliqueretinacular
ligament causing this ligament to slide volarward
and impart flexion force to PIP joint

6. Intrinsic Plus Hand
 Caused by musclesimbalance
between spastic
intrinsics (interosseoi and
lumbricals)weak extrinsics(FDS,
FDP, EDC)
 Characterized by MCP flexion PIP
& DIP extension

7. Intrinsic Minus Hand (Claw Hand)
 Caused by imbalance
between strongextrinsics
and deficient
intrinsics Characterized by
MCP hyperextension
 PIP & DIP flexion

8. Patho-anatomy of deformity
 Paralysis of interossei and lumbricals
Unopposed MCP joint extension & IP joint flexion
by digital extensors & flexors
Without stabilization of MCP joints in neutral/slight
flexed position, long extensor function “blocked” at
MP joint by diversion of thistension to sagittal
band, producing hyperextension and effectively
blockingthe extensor's abilitytoextendPIP joint.‡

9.  Middleand distal phalangescollapse into flexion
Normal cascadeof digital extension disrupted, in that
during any attempt toactivelyopen finger, MP joint
extends first and will extend more than the PIP joint,
Normal sequenceof digital closurealso reversed, in
that IP joint flexion precedes MP jointflexion
 Independence of MP and IP joint motionlost

10. MEDIAN NERVE
• Arises in the axilla by two roots -
lateral (C5, C6, and C7) and medial (C8 and T1)
from the lateral and medial cords of brachial plexus.
• Its root value is C5, C6, C7, C8, and T1 spinal
segments .

11. Median nerve enters the anterior compartment of arm at the
lower border of teres major.
In the arm, initially it lies lateral to the brachial artery, then crosses
in front of the artery to reach its medial side. (i.e., level of
insertion of coracobrachialis).
Enters the cubital fossa where it lies medial to the brachial artery.
It leaves the cubital fossa by passing between the two heads of the
pronator teres and gives off anterior interosseous nerve.
In the forearm , it passes behind (the tendinous arch) of flexor
digitorum superficialis and runs downwards deep to the muscle.
At the wrist,5 cm. proximal to flexor retinaculum it becomes
superficial exactly in the midline.
It then enters the palm through the carpal tunnel (deep to flexor
retinaculum) and divides into lateral and medial terminal
branches.

14. SENSORY FUNCTION
• The median nerve is responsible for the cutaneous
innervation of part of the hand. This is achieved via
two branches:
• Palmar cutaneous branch – Arises in the forearm
and travels into the hand. It innervates the lateral
aspect of the palm. This nerve does not pass
through the carpal tunnel, and is spared in
carpal tunnel syndrome.
• Palmar digital cutaneous branch – Arises in the
hand. Innervates the palmar surface and fingertips
of the lateral three and half digits.

17. ULNAR NERVE
• Ulnar nerve is on of the major terminal Branches
of Brachial Plexus. It is the continuation of medial
cord of brachial plexus which arises from the
anterior Division of the lower Trunk.
Root Value:
• The fibers of ulnar nerve arise from the eight
cervical and first thorasic nerve, so the root value
of ulnar nerve is C8 and T1. These (C8,T1)
coordinate to form the lower trunk of brachial
plexus.

19. Ulnar Innervated Muscles
•Forearm:
•Flexor Carpi Ulnaris (C7, C8, T1)
•Flexor Digitorum Profundus III & IV (C7, C8)
•Thenar:
•Hypothenar Muscles (C8, T1)
•Adductor Pollicis (C8, T1)
•Flexor Pollicis Brevis (C8, T1)
•Fingers:
•Palmer Interosseous (C8, T1)
•Dorsal Interosseous (C8, T1)
•III & IV Lumbricles (C8, T1)
•Digiti Minimi:
•Abductor Digiti Minimi (Quinti) (C8, T1)
•Opponens Dgiti Minimi (C8-T1)
•Flexor Digiti Minimi. : ( C8-T1)

20. Claw thumb in Ulnar palsy
CMC joint affected by paralysisof adductorpollicis,
FPB, and first dorsalinterosseous
MP and IP jointsof thumbunder control of extrinsic
flexors and extensors, with proximal phalanx behaving
like intercalated bone.
MP joint will go into hyperextension and IP joint into
flexion becauseof thegreaterextensor momentat the
MP joint and the lesser extensor moment at the IP
joint, respectively.
 “Z”-thumbdeformity

21. Types of claw hand
 Partial : due to paralysis of ULNAR nerve ;
clawing is seen in little and ring fingers only
a) Low Ulnar nerve palsy
b) High Ulnar nerve palsy
 Total : due to paralysis of both ULNAR &
MEDIAN nerves; clawing seen in all 5 fingers
a) Low Mixed Ulnar & Median nerve palsy
b) High Mixed Ulnar & Median nerve palsy

22. Partial Claw hand
Flexion Extension Deformity
MCP Joint Lumbricals
paralyzed
Extensor
Digitorumactive
Hyper extensionof
MCP jOINT
PIP Joint FDS active Interossei
paralyzed ( low
Ulnar palsy)
Flexion of PIP
joint
DIP Joint FDP active Interossei
paralyzed
Flexion of DIP
FDP paralyzed
( high Ulnar
Palsy)
Interossei
paralyzed
Neutral position

24. Total Claw Hand
Flexion Extension Deformity
MCP Joint Lumbricals
paralyzed
Extensor
digitorum active
Hyper extensionat
MCP
PIP Joint FDS paralyzed Extensor
digitorum active
Extension of PIP
DIP Joint FDP paralyzed Extensor
digitorum active
Extension of DIP

28. ETIOLOGY
 Traumatic
 Compressive neuropathy
 Brachial plexus injury
 Infective ( Leprosy, Poliomyelitis)
 Peripheral neuropathies
 Systemic diseases ( DM, Porphyria, Malignancies)
 Drugs and Toxins (Lead, Arsenic, Dapsone, etc)
 Hereditary (CMTD, Syringomyelia, Lipid storage diseases)
 Ischemia
 Primary Nerve neoplasm

29. Pattern of Injury
Low mixed Ulnar and median nervepalsy
High mixed Ulnar and Median nervepalsy
Low Ulnar nervepalsy
High Ulnar nervepalsy

30. LOW ULNAR NERVE PALSY
• Weakness of PINCH – due to paralysis of
ADDuctor Pollicis & 1st Dorsal interossei
• Weakness of GRIP – due to paralysis of most
of finger intrinsics
• Sometimes Clawing of Ring & Little fingers –
due to paralysis of all intrinsics

31. High ulnar palsy
• Weakness of PINCH, GRIP & CLAWING
of Ring & Little fingers
• Functions of FDP of ring & little fingers
lost
• Function of FCU are lost

32. MEDIAN NERVE PALSY
LOW MEDIAN NERVE
• Loss of opposition of thumb
• Loss of sensibility over the
sensory distribution of
nerve
• Paralysis of two radial
Lumbricals
HIGH MEDIAN NERVE
LOSS OF :
• Pronation of forearm
• Flexion of wrist
• Flexion of index & middle
fingerds
• Flexion of thumb
• Opposition of thumb
• Sensation over median
distribution

33. COMBINED MEDIAN & ULNAR NERVE PALSY
LOW:
• Complete anaesthesia of
palm and loss of function of
all intrinsics of both finger
and thumb
HIGH:
• Entire hand is anaesthetic
except for its dorsal surface
and only muscles available
for transfer are those
innervated by radial
muscles- Brachioradialis,
ECRL, ECU, EIP.

34. CLINICAL FEATURES OF ULNAR NERVE PALSY
1. Wasting of interossei :1st dorsal interossei is the
1st to become noticably effected. There is
hallowing of the skin on the dorsal aspect of 1st
web space
2. Hypothenar wasting
3. In High UNP, wasting of ulnar half of the forearm
4. Brittle nails
5. Trophic ulcers of hand in ulnar distribution area

35. TESTS OF ULNAR NERVE
1. FCU : wrist joint is flexed against resistance,
hand tends to deviate towards radial side

36. 2. Dorsal Interossei :

37. 3. CARD test for Palmar Interossei:

38. 4. ADductor Pollicis & 1st Palmar Interossei

39. 5. Abductor Digiti Minimi : ask to Abduct little
finger against resistance.
6. Flexor Digitorum Profundus: middle phalanx of
ring & little finger is supported and DISTAL IP
joint flexed against resistance
7. SENSATION : loss over ulnar
distribution(medial 1/3rd of palm & dorsum of
hand and ulnar 1 & 1/2 fingers)

40. CLINICAL FEATURES OF MEDIAN NERVE PALSY
• Thenar wasting
• Simian/Ape thumb deformity
• Atrophy of pulp of index finger
• Cracking of nails
• Tropic changes
• Wasting of lateral aspect of forearm

41. TESTS FOR MEDIAN NERVE
• FPL
• FDS & FDP
• Opponens Pollicis
• ABductor Pollicis Brevis

42. CLINICAL DIAGNOSIS OF NERVE INJURIES
• Immediately after a severe injury to an extremity,
recognition of a peripheral nerve injury is not
always easy. Pain is often so severe that patient
cooperation is limited at best
In the upper extremity
• loss of pain perception in the tip of the little
finger - ulnar
• loss of pain perception in the tip of the index
finger-median and
• inability to extend the thumb - hitchhiker’s sign -
radial nerve injury

43. SPECIFIC SIGNS AND TESTS FOR
MOTOR DYSFUNCTION

44. Bouvier’s maneuver :
 Dorsal pressure over
proximal phalanx to
passively flex MP joint
results in straightening of
distal joints and temporary
correction of claw deformity
 Extensor digitorum tendon
can extend middle and
distal phalangeswhen
proximal phalanx stabilized

45. Duchenne's sign :
Hyperextension at MCP
joints & flexion at IP
joints
Andre-Thomas sign :
On palmar -flexon of
wrist exaggeration of
deformity

46. Pitres-Testut sign : Inability toactively move long
fingers in radial and ulnardeviationwith palm placed
flat
Cross your fingers test : Inability to crossmiddle
fingerdorsallyover index finger, or index over
middle finger
Masse's sign: Flattened metacarpal arch and lossof
hypothenar elevation

47.  Jeanne’s sign :
Hyperextension of MP
jointof thumbduring key
pinch orgross grip
 Bunnell’s O sign :
Combined hyperextension
at MP jointand
hyperflexion of IP joint
(noticed when patient
makesa pulp to pulp pinch
with thumb and index
finger)

48. EPL
 Froment’s sign : Thumb IP
joint flexion while
attempting to perform lateral
pinch
FPL

50. Pollock's sign : Inability to flex distal phalangesof
ring and littlefingers
Partial lossof wrist flexion mayoccur becauseof
paralysis of FCU
Weakness of ulnar sidegrip

52. CLASSIFICATION OF PARALYTIC CLAW HANDS
 Type I: Supple claw hands withno hypermobile joints
and no contractures at IPjoints
 Type II: Hypermobile joints; PIP joints hyperextension >
20 degrees
 Type III: Mobile joints in association with adaptive
shortening of long flexors, usually superficialis tendons,
with no IP jointcontracture
 Type IV: Contracted claw hands ; PIP joint flexion
contracture of 15 degrees or more,due to volarskin, joint
capsule, or volarplatecontracture ± adaptive shortening
of long flexors
 Type V: Claw hands withattrition of dorsal extensor
apparatus at PIP joint with “hooding deformity,” fibrous or
bonyankylosisof PIP joint, and MP joint extension
contracture

53. DIAGNOSTIC TESTS
1. IMAGING:
• High-resolution ultrasound and MRI can
accurately assess the physical integrity of
• the nerve immediately after injury and provide
valuable
• information for surgical decision making.
Intraneural and
• perineural injuries also can be identified with
both of these
• techniques.

54. 2.ELECTRODIAGNOSTIC STUDIES-
NCV & EMG
• Best and most accessible correlative electrophysiologic
confirmations of a peripheral neural injury
• The presence, location, severity, and possibly the prognosis of
the neural insult can be determined, and
• Information regarding the recovery pattern can be obtained
when the study is done sequentially over time.
• Alternative electrophysiologic uses include
Dynami electromyographic assessment when considering
-optimal muscle transfer strategies, before tenotomy, or
botulinum toxin injections in central and peripheral neuropathic
conditions.
• Electrical stimulation can be used for optimal nerve
localization when considering blocks or ablation procedures.

55. 3. TINEL SIGN:
• Elicited by gentle percussion by a finger or percussion hammer
along the course of an injured nerve.
• A transient tingling sensation should be felt by the patient in the
distribution of the injured nerve rather than at the area percussed,
and the sensation should persist for several seconds after
stimulation.
• It should be tested for in a distal-to-proximal direction.
• Positive Tinel sign is presumptive evidence that regenerating axonal
sprouts that have not obtained complete myelinization are
progressing along the endoneurial tube.
• With progressive regeneration, the positive response fades
proximally, presumably because of progressive myelinization along
the more proximal part of the regenerated segment.
• Distal progression of the response along the course of the nerve in
question can be measured, and some have used the rate of this
progression to establish prognosis or suggest the need for
exploration

56. 4. SWEAT TEST:
• Sympathetic fibers within a peripheral nerve are resistant to
mechanical trauma.
• The presence of sweating within the autonomous zone of
an injured peripheral nerve reassures the examiner to a
degree, suggesting that complete interruption of the nerve
has not occurred.
• iodine starch test & ninhydrin print test
5. SKIN RESISTANCE TEST:
• autonomous zone with absence of sweating shows an
increased resistance to the passage of electrical current.
• The adjacent innervated areas have a normal resistance,
and further decreased resistance in these areas can be
elicited by high external temperatures that do not affect the
denervated area.
6. ELECTRICAL STIMULATION

57. MANAGEMENT OF DEFORMED
HAND

58. EXERCISES:
• Done to overcome the contracture and to
prevent further deformity
SPLINTING:
• To immobilize all or part of hand in a position
that will promote healing & prevent deformity
• To correct an existing deformity & promote
function in that part
• To supply power to compensate for weakness

59. SURGICAL CORRECTION:
Active/Dynamic Procedure -
• include muscle substitute procedure by transfer of muscle-
tendon unit.
• They bring extra forces which are under voluntary control
similar to and in place of those lost because of muscle
paralysis.
• Eg: TENDON TRANSFERS
Passive/Static Procedure-
• attempt to restore equilibrium without introducing new
active muscle forces
• Eg: volar capsuloplasty & flexor pulley advancement,
Dermadodesis & flexor pulley advancements,
Capsulodesis:Zancolli technique

60. TENDON TRANSFER
• Procedure in which the tendon of a functioning muscle is detached
or divided at or near its insertion, mpbilized and reinserted into a
bony part or another tendon to supplement or substitute for the
lost function.
• Most imp points in considering muscle for transfer are:
EXPANDABILITY & STRENGTH
Strength graded 0-5:
• 0, zero—no contraction
• 1, trace—palpable contraction only
• 2, poor—moves joint but not against gravity
• 3, fair—moves joint against gravity
• 4, good—moves joint against gravity and resistance
• 5, normal—normal strength

61. PRINCIPLES OF TENDON TRANSFER
• Muscle to be transferred should be healthy(appear dark pink
or red)
• The strength of muscle to be transferred should be grade 4-5
muscle, usually losses strength by grade 1 when transferred
• There must be free ROM in the joint to be activated by
transplanted muscle
• Any bony deformity should be corrected by osteotomy
• It is desirable to use a synergistic muscle as it is easier to
rehabilitate the muscle after surgery
• Joint proximal to parts to be moved should be stabilised,
either by tendon action or by arthrodesis
- To restore thumb pinch – stabilize CMC joint in extension &
MCP joint in flexion
- To restore finger extension – MCP joint maintained in slight
flexion

62. PRINCIPLES OF TENDON
TRANSFER(contd…)
• Tendon should be attached under moderate tension
• When tendon is split to provide insertion to various
points, tension should be equal to all points
• Origin & the newly transferred insertion should be in a
straight line
• Transferred tendon should pass through a tendon
sheath/s.c fat(gliding bed)
• Should not pass through the raw bone
• Should not be done untill any scarred tissue has been
satisfactorily replaced
• Amplitude of motion should be sufficient

63. INDICATI0NS FOR TENDON TRANSFER
• Irreparable nerve damage
• Loss of function of a musculotendinous unit
due to trauma or disease
• In some non progressive or slowly progressive
neurological disorders

64. RESTORATION OF PINCH-
RESTORATION OF THUMB OPPOSITION:
TRANSFER OF THE SUBLIMIS TENDON
RIORDAN BRAND

65. Other techniques for thumb opposition:
• Transfer Of The Extensor Indicis Proprius ---
BURKHALTER
• Transfer Of The Flexor Carpi Ulnaris Combined With
The Sublimis Tendon - GROVES AND GOLDNER
• Transfer Of The Palmaris Longus Tendon To Enhance
Opposition Of The Thumb –Camitz
• Muscle Transfer (Abductor Digiti Quinti) To Restore
Opposition- Littler And Cooley

66. RESTORATION OF ADDUCTION OF
THE THUMB
BOYES - Brachioradialis SMITH
• Transfer Of The Extensor
Carpi Radialis Brevis Tendon
To Restore Thumb
Adduction

67. RESTORATION OF ABDUCTION OF THE
INDEX FINGER
• Transfer Of The Extensor
Indicis Proprius Tendon
• Transfer Of A Slip Of The
Abductor Pollicis
Longustendon

68. RESTORATION OF INTRINSIC FUNCTION OF THE
FINGERS
• Principle (that the long finger extensors can extend
interphalangeal joints, provided that hyperextension of
the metacarpophalangeal joints is prevented) is the
basis for many of the operations for intrinsic paralysis.
The MCP joints can be stabilized by:
• capsuloplasty (Zancolli),
• tenodesis (Riordan),
• bone block (Mikhail),
• arthrodesis, or
• tendon transfers that actively extend the IP joints and
flex the MCP joints.

69. • Transfer Of The Flexor Digitorum Sublimis Of
The Ring Finger - BUNNELL, MODIFIED

70. TRANSFER OF THE EXTENSOR CARPI RADIALIS LONGUS
OR BREVIS
TENDON (BRAND)

71. TRANSFER OF THE EXTENSOR INDICIS PROPRIUS AND
EXTENSOR DIGITI QUINTI PROPRIUS
(FOWLER)

72. • RIORDAN modification of Fowler operation DOES NOT USE
the extensor digiti quinti proprius.

73. CAPSULODESIS
ZANCOLLI

74. Integration of Finger Flexion
Fowler tenodesis
 Wrist TenodesisTechnique
Fowler
 Incorporates active wristmotion
to tension static tendongrafts
 Free tendon grafts sutured to
extensor retinaculum of wrist
and passed in a dorsal to palmar
direction through the
intermetacarpal spaces, volar to
the DTML, through thelumbrical
canals, and onto the lateralbands
of dorsal extensor expansion of 4
fingers

75. LOW ULNAR NERVE PALSY
• Riordan transfer
• Bunnell
• Brand
• Zancolli capsulodesis

76. HIGH ULNAR NERVE PALSY
• Transfers described for low ulnar nerve palsy
can be used EXCEPT that the SUBLIMIS of the
RING FINGER MUST NOT BE TRANSFERRED
because the profundus of this finger is
paralyzed.

77. LOW MEDIAN NERVE PALSY
• Important functional deficits caused by low
median nerve palsy are
1.loss of opposition of the thumb and
2. loss of sensibility over the sensory distribution
of the nerve;
• Paralysis of the two radial lumbrical muscles is
of little consequence when the ulnar nerve is
intact

78. HIGH MEDIAN NERVE PALSY
Important functional
deficits caused are
• loss of pronation of the
forearm,
• flexion of the wrist,
• flexion of the index and
long fingers,
• flexion of the thumb,
• opposition of the
thumb, and
• median nerve
sensation.

79. COMBINED LOW MEDIAN AND ULNAR
NERVE PALSY (AT THE WRIST)
• Brand transfer, in which the ECRB is extended
by tendon graft.
• Opposition of the thumb can be restored by
the Riordan transfer

80. COMBINED HIGH MEDIAN AND ULNAR
NERVE PALSY (ABOVE THE ELBOW)
Only muscles available for transfer are muscles innervated by
the radial nerve—
• the brachioradialis,
• the extensor carpi radialis brevis,
• the extensor carpi radialis longus,
• the extensor carpi ulnaris, and
• the extensor indicis proprius.
Recommended treatment include –
• arthrodesis of the thumb metacarpophalangeal joint;
• Zancolli capsulodesis of the metacarpophalangeal joints of
all fingers and
• release of the flexor tendon sheaths at the same time

81. THANK YOU…