CHAPTER 7

Wrist and Hand

 288 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

EXAMINATION POINTS FOR A HAND CASE

{The topic is difficult with respect to the examination as various
specifications are to be remembered and detailed. Precision and
tests are tough to learn.
Read: 4-6 times for MS and DNB candidates}

History taking
(In a broad division try to first ascertain what you are dealing
with – deformity/neurological condition/painful or
inflammatory condition, then it will be prudent to proceed):
• Pain: Onset (injury/spontaneous; acute/insidious), type,
location, duration, remote injury (RSD), aggravating and
relieving factors, activity restrictions, guarding of wrist and
hand.
• Swelling: Onset (as above), location, duration (also whether
temporary or permanent), relieving and aggravating factors,
flare-ups (severity, frequency, duration), previous treatment
if any, association with fever/stiffness, discolouration.
• Deformity: As above + abnormal contours, palm and finger
alignment.
• Loss of function: (A key factor as hand in itself is an organ,
45 per cent of hand function is utilized for grasp, 45 per cent
for pinch (key, tip, chuck pinch), 5 per cent for hook
function and in rest 5 per cent hand functions as a paper
weight (most primitive function))
• Loss of power: Any decreased strength or dexterity.
Apart from above it is very important to ask for history
of hospitalizations and treatment (type, dose, frequency,
response and side effects), details of trauma if present,
dominant hand, effect on occupational functioning and
ADL.

Examination
Inspection (keep the hand on a pillow with whole ipsilateral and
contralateral upper limb exposed):
 WRIST AND HAND 289

Alignment
• Whether viewed from dorsal or volar aspect with fingers
and thumb in adduction – the forearm, wrist and hand
(middle finger) should be in a straight line (axial alignment).
Ulnar deviation of MCP joint and radial deviation of wrist
are observed in rheumatoid arthritis (RA).
• Dislocation of PIP joint is visible as a step off (sagittal
malalignment). Rupture of extensor slip in RA produces
flexion deformity of fingers at MCP joint (Vaughan-Jackson
lesion). Dinner fork deformity is seen in Colle’s fracture.
• Rotational malalignment is judged in two ways:
– Ask patient to partially flex the fingers together at MCP
joint – nails of index finger and those of ring and little
finger face away from that of long finger in supinated
hand.
– Ask patient to flex fully each finger in turn – the fingers
should unfailingly point towards the scaphoid tuberosity.
Dorsal aspect:
• Nails: vasculitic changes (local infarction – RA), splinter
haemorrhage, periungal telengiactases (SLE, scleroderma),
pin-size pitting (psoriasis), hyperkeratosis, onycolysis,
discolouration, ridges, anaemia, dilated capillary loops over
nail fold, paronychia, subungal haematoma.
• Fingers (examine from DIP to MCP): Mallet finger (avulsion
of EDC, EPL for thumb), redness, sausage shaped digits,
nicotine stains, arthritis mutilans, tophi, swan neck/
boutonniere deformity, Z-deformity of thumb, Bouchard’s
nodes, Heberden nodes, Garrod pads, ulnar deviation,
benediction attitude, clawing of fingers, contractures, tele-
ngiectasia, mucous cyst, inclusion cyst, sebaceous cyst, skin
and appendages (normally there are no hair from MP and
distal).
• Hand: Dropped knuckle (# metacarpal), fore-shortening of
metacarpal, wasting in first web space, wasting of interossei,
skin and appendages, carpal bossing.
• Wrist: Head of ulna (prominent in pronation disappears in
supination), silver fork deformity, ulnar deviation, volar
290 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

subluxation, volar-ulnar subluxation, cystic swelling

(ganglion).
Radial aspect:
• Thumb and 1st MCP joint (basilar joint): (Skier’s thumb or
gamekeeper’s thumb), swelling (1st MCP arthritis).
• Wrist: Anatomical snuffbox (bound dorsally by EPL and
volarly by APL and EPB) for swelling.
Volar aspect:
• Fingers and palms: As above + pulp spaces for pits
(Raynaud’s phenomenon) and swelling (Felon), swelling
over volar aspect of finger (GCT tendon sheath or cystic
swelling), jersey finger (avulsion of FDP), flexion arcade of
fingers, palmar skin for pits and cords/ nodules
(Dupuytren’s contracture), signs of flexor tendon sheath
infection (Kanavel’s signs – fusiform swelling extending
along MP and PP into distal palm + tenderness along volar
aspect + finger held in flexed position + passive extension
causes pain), thenar and mid palmar spaces for infection,
thenar and hypothenar wasting.
• Wrist: As above + tendon of Palmaris longus (ask patient
to touch the tips of thumb and little finger and flex the wrist
– tightens the palmar fascia and makes tendon prominent),
FCR, FCU, compound palmar ganglion.
Ulnar aspect:
• Hypothenar wasting, head of ulna (capita ulna syndrome
– in RA the volar subluxation of carpals and dorsal
subluxation of ulnar head accentuates the deformity with
prominent head of ulna).

Palpation
Make a note of temperature.
Dorsal aspect
• Fingers: for mallet finger, collateral ligaments especially for
thumb, joint swelling and effusion, MCP joint for collateral
ligament tenderness.
 WRIST AND HAND 291

• Metacarpals for deformity, tenderness, first metacarpal base

for Bennett’s fracture.
• Wrist for radial styloid, De Quervain’s disease (tenovaginitis
of 1st dorsal compartment – APL, EPB), lister tubercle (2 cm
ulnar to radial styloid), anatomic snuff box (for dorsal
branch of radial artery, # scaphoid, 3-4 mm distal to it is
basilar joint), 2 nd dorsal compartment (ECRL, ECRB,
intersection syndrome, ganglion is most likely to occur
here), 4th dorsal compartment (EDC tendons in RA), TFCC
just distal to ulnar styloid.
Palmar aspect
• As in inspection confirm the findings of felon, flexor sheath
infection, mid-palmar space, thenar space
• Swelling of ganglion, GCT tendon sheath, trigger finger
(catching of tendon in pulley)
• Tubercle of scaphoid, hook of hamate, pisiform, pisiohamate
ligament and Guyon’s canal, FCR, median nerve (between
Pl and FCR), volar carpal ligament (proximal limit
corresponds with the distal radial crease).

Movements
Wrist motion (with elbow flexed in 90º) – dorsiflexion (60-70º),
palmar flexion (60-80º), radial (20º) and ulnar deviation (30-40º)
Finger movements: Flexion at DIP (70-90º), PIP (110º), MCP joint
(80-90º). Hyperextension at MCP joint is quite normal and is
maximum at Index finger (up to 70º). Other method is to
measure the finger tip to transverse palmar crease distance for
serial assessment and follow-up. Restricted flexion at IP joints
can be due to capsular contracture/ intrinsic contracture or
extrinsic tightness. Perform Bunnell-Littler test to differentiate
the two. Passively flex the IP joint with MCP in extension
followed by MCP in flexion. Restriction due to intrinsic muscle
tightness will increase the passive flexion at IP joint with MCP
flexion due to relaxation of intrinsic muscles. In extrinsic
tightness the flexion decreases due to tightening of structures
with MCP flexion hence restricting flexion further.
 292 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Abduction and adduction: Abduction and adduction is possible at

MCP joint due to “cam effect” – the metacarpal heads are
shaped like cam (larger volar articular component as compared
to linear distal) so that in extension the collateral ligaments are
lax allowing movement in coronal plane (this is also the reason
for ‘James position’ of immobilization). This is not possible at
IP joints – bicondylar joints without a ‘cam’. The presence of
abduction and power of adduction is more important than the
range of abduction! (just compare with other side).
Thumb movements: Flexion, extension, adduction, abduction,
opposition
Motor power and muscle/tendon function:
• Wrist flexors (FCR/ FCU), extensors (ECRL, ECRB, ECU),
radial deviators (FCR, ECRL, ECRB, APL), ulnar deviators
(ECU, FCU)
• Finger flexors (FDP – hold PIP individually and ask patient
to flex DP; FDS – ask patient to flex the PIP while holding
other three fingers in extension, this defunctionalises the
FDP as it is a single unit muscle). This test is less reliable
for index finger as the FDP to IF may be separate.
• Abduction (dorsal interossei) and adduction (palmar
interossei) of fingers, card test.
• Thumb flexion (FPL, FPB), radial abduction or extension
(APL), palmar abduction (APB), adduction (Adductor
pollicis), opposition (APB, OP), froment’s test (Adductor
pollicis)

Sensation Testing
Percussion: Tinel’s test
Vascularity
Neurological examination for various nerves (See Chapter 7 :
Case I)
Special tests:
• Carpal tunnel compression tests
1. Tinel’s sign
2. Phalen’s test: Wrist flexed by gravity for 60 sec
 WRIST AND HAND 293

3. Durkan’s median nerve compression test: Manual

pressure over median nerve at carpal tunnel for 30 sec
4. Reverse Phalen’s test: Wrist and fingers extended for
2 minutes
5. Tourniquet test: Arm tourniquet inflated above systolic
pressure for 60 secs
6. Hand elevation test: Hand elevated above for 60 sec
7. Wrist flexion and carpal compression test: In a supinated
forearm with flexed wrist compress the median nerve
with direct pressure
8. Closed fist test: Tight fist for 60 sec
• Stability testing:
1. MCP joint
2. IP joint
• Carpal instability:
1. Scaphoid shift test of Watson: Tests scapholunate
instability
2. Luno-triquetral ballottement test for lunotriquetral joint
3. Mid-carpal instability
• DRUJ instability:
1. Piano key test
2. DRUJ compression test
• TFCC test: TFCC compression test
• Grind test for basilar (trapezio-metacarpal joint) joint
arthritis
• Finkelstein test for de Quervain’s disease.
• Allen’s test for radial and ulnar arterial circulation.

CASE I:
PERIPHERAL NERVE INJURIES
{This is a very important and favourite topic that is bound to
come if case is present. The diagnosis is simple and
straightforward to those who have practiced the case otherwise
not only examination or diagnosis but the management will also
be formidable!
Read: 6-8 times (MS Orth and DNB candidates}
294 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Diagnosis
The patient is a 28-year-old male with post-traumatic, non-
recovering, complete right high radial nerve palsy for past
9 months (with or without non-union/ united fracture of
humerus).

1. What do you mean by high/low nerve (radial/median/

ulnar) palsy?
Ans. Radial nerve:
Complete palsy (very high): Triceps paralysed (injury in
axillary region)
High: Triceps and often anconeus preserved but rest all
paralysed (injury around radial groove till it pierces
septum).
Low: BR and ECRL preserved ( posterior interosseous
nerve (PIN) palsy; ECRB in 58 per cent cases is supplied
by PIN so it may also be spared in some cases).
For ulnar and median (See Chapter 7 : Case II; Q 21-23)

2. Why do you call it non-recovering?

Ans. The nearest muscle to the site of injury (Brachioradialis)
has not been reinnervated and the tinel’s is still localized
at the site of injury.

3. What function is lost in nerve (radial/median/ulnar)

palsy?
Ans.
Radial:
1. Inability to extend fingers (1,2,3,4,5) {low} and wrist
{low+high}
2. Inability to stabilize the wrist (wrist drop) and thumb
(radial abduction of thumb) {low+high}
3. Loss of grip strength (accessory forearm flexion) {High}
4. Accessory forearm supination {Very High}
5. Sensory loss (radial 2/3 dorsal sensation)
Ulnar (also See Chapter 7: Case II; Q21, 23, 29, 30):
1. Loss of grip strength (impairment of power grip > precise
grasp) {High}
 WRIST AND HAND 295

2. Flexion of distal phalanx 4,5 {High}

3. Digital balance 4,5 {High}
4. Loss of finger function (flexion (partial), adduction,
abduction) {High+Low}
5. Loss of thumb adduction and weakness of thumb flexion
{High+Low}
6. Sensory loss (medial 1½ digits – Low; Ulnar 1/3 volar –
High)
Median nerve:
1. Loss of thumb opposition, finger stabilization 1,2
{Low+High}
2. Weakness of wrist and partial loss of finger flexion 2,3;
complete for 1 {High}
3. Forearm pronation {High}
4. Sensory loss (Radial volar 2/3 hand)
Combined low median and ulnar nerve:
1. Thumb opposition+ adduction + flexion (partial)
2. Finger abduction and adduction
3. Finger stabilization
4. Sensory loss (volar hand + dorsal ulnar 1½)

4. What is the course of radial, ulnar and median nerves?

Ans. Radial nerve (C5-T1): Formed in front of subscapularis
from posterior cord  passes anterior to lattissimus dorsi
muscle  to pass through triangular space accompanied
with profunda brachii artery to posterior aspect of
humerus into radial groove (not spiral groove; radial
groove is few mm above spiral groove) where it is
separated from bone by medial head of triceps coursing
obliquely laterally  pierces the lateral intermuscular
septum around 122 mm above lateral epicondyle  passes
into anterior compartment emerging beneath
brachioradialis  deep branch (PIN) pierces supinator
muscle to emerge into extensor compartment of forearm
 forms cauda equina of spinner 8 cms distal to elbow
joint.
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Ulnar nerve (C8-T1, rarely C7 also): Formed from medial

cord of brachial plexus  runs inferomedial to axillary
artery to continue behind brachial artery over triceps
muscle  passes straight to posterior aspect of medial
epicondyle in “ulnar groove” between medial epicondyle
and olecranon process  passes between two heads of
FCU (the so-called “cubital tunnel” better called humero-
ulnar aponeurosis  remains deep to FCU overlying FDP
muscle accompanied with ulnar artery  passes
superficially; emerging beneath FCU to reach Guyon’s
canal at wrist.
Median nerve (C6-T1): Formed from medial and lateral
roots of median enters arm in close relation to brachial
artery. In the cubital fossa nerve lies lateral to brachialis
tendon and passes b/n two heads of pronator teres 
gives AIN  continues in forearm sandwiched b/n FDS
and FDP  emerges just proximal to wrist b/n FDS and
FCU  passes through carpal tunnel  lies anterior and
radial to FDS tendons  divides in hand into recurrent
motor and sensory branches.

5 What will you do for this patient?

Ans. I will do a thorough examination of motor, sensory loss.
Look for reinnervation (e.g., brachioradialis for motor
recovery – radial, FCU for ulnar, etc. and advancing tinel’s
for nerve regeneration). I will also document the findings
with EDS. I will get X-rays of the arm in AP and lateral
projection to look for status of fracture.

6. What are the requirements of a patient with radial nerve

palsy?
Ans.
1. Wrist extension
2. Finger (MCP) extension
3. Combination of thumb extension and abduction
(What is available? - motors innervated by ulnar and median
nerve)
 WRIST AND HAND 297

7. What about sensory deficit?

Ans. The sensory deficit is notable but really not a disability
and is partially covered up by lateral cutaneous nerve of
forearm. So it can be neglected unless there is painful
neuroma.

8. How does status of fracture affect the treatment?

Ans. Osseous union should be promptly addressed to stabilize
the limb and prevent additional injury to soft tissues
especially nerve. In this case I will have to prepare for
bony surgery also, according to the findings. Had the
duration been less (say 3 months) then I would have fixed
the bone along with exploration of a non-recovering
nerve. Fracture in acceptable position with recovering
nerve would have been managed with POP immobili-
zation otherwise surgery to fix fracture was indicated even
in recovering nerve.

9. What is the role of non-operative treatment?

Ans. Goals:
1. Maintaining full ROM.
2. Preventing contractures particularly of 1st web space.
It is undertaken while waiting for spontaneous nerve
recovery and obviously in the interim period to surgery.
Usually a dynamic cock-up splint (external splint) is used
for this purpose. However, internal splintage can also be
done.

10. How will you treat this patient?

Ans. I will do tendon transfer.

11. What are the prerequisites for tendon transfer?

Ans. In order of importance:
1. Correction of contractures (all joints must be supple)
2. Adequate strength of the transferred tendon
a. 85 per cent of power is a must (Steindler) – graded as
good power
298 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

b. “Omer” stated that a muscle loses at least one grade

of strength after transfer so for useful post-operative
movements 4/5 power is a must.
3. Straight line of pull: No pulley is ideal or minimum
number of pulleys should be made.
4. One tendon – One function, i.e., flex or extend
5. Synergism: Synergistic transfer should be preferred as
much as possible, however, there are a lot of violations
of this rule.
6. Expendable donor: There should be no functional
morbidity following use of a tendon
7. Tissue should be in equilibrium (tissue equilibrium –
termed by Steindler)
a. Soft tissue induration should subside
b. No reaction in wounds
c. Joints are supple
d. Scars should be as soft as possible
8. Pass tendon below fascial planes/sheaths and not below
incision line/scar (best b/n subcutaneous fat and fascial
sheath).
9. Amplitude of transferred tendon should be as near to the
original tendon for which the transfer is being done.
10. Try preserving the nerve and vascular supply to muscle
and vascular supply to tendon.
11. Insertion of the tendon should be as close to the insertion
of paralyzed tendon; at same angle; if split transfer then
keep both slips in same tension.
12. Try to restore sensibility of distal organ before treat-
ment.
13. Arthrodesis/joint procedure should be done before
tendon transfer.
14. The disorder should be a non-progressive one.
15. Keep dissection to a minimum around the muscle to be
transferred and achieve meticulous hemostasis to prevent
adhesion formation.
 WRIST AND HAND 299

12. What if the amplitude of transferred tendon is less

than the tendon for which transfer has been contemp-
lated?
Ans. Amplitude can be increased by two ways:
1. Converting a monoarticular muscle into bi/multiarticular,
e.g., (FCU/FCR  EDC). The effective amplitude of
motion is enhanced due to tenodesis effect by active volar
flexion of wrist.
2. Muscle release from surrounding, e.g., brachioradialis
transfer (violates pt. 15 Q 11).

13. When will you do a tendon transfer?

Ans. In general, till the time a functional recovery is expected
to occur; one can wait else do a tendon transfer.
Early transfer can be done if there is gap > 4 cms or
there is excessive scarring/skin loss over the nerve, some
may also include injection palsy and gunshot injuries in
this category. Otherwise, transfer is usually done after
waiting for around 1 year following injury (whether an
interim repair has been attempted or not). (Remember
the exact time for transfers as such vary according to the
nerves involved and surgeon’s preference).

14. Why do you wait for a year?

Ans. I will give adequate time for the nerve to regrow and
possibly re-innervate the muscle. Neuro-muscular
junctions in the muscle degenerate if not re-innervated
in about a year’s time, so it is prudent to do tendon
transfer after year as the likelihood of regaining function
is meager. Moderate to severe atrophy of muscles is seen
by 3 months, mod-severe fibrosis seen by 11 months,
beyond 3 years there is fragmentation and disintegration
of muscle fibers; hence ideal reinnervation can be
expected after 1-3 months, functional reinnervation up to
1 years, no reinner-vation >3 yrs.
300 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

15. What are the various tendon transfers for radial nerve
injury?
Ans. I. JONES transfer (violates point no. 6 Q 11):
Classical (1916):
1. PT  ECRL and ECRB;
2. FCU  EDC III-IV;
3. FCR  EPL; EDC II, EIP
Classical (1921):
1. PT  ECRL and ECRB
2. FCU  EDC III-IV
3. FCR  EDC II, EIP, EPL, EPB, APL
Modified JONES: PT  ECRB and rest as above
II. FCR transfer (of Starr; Brand; Tsuge)
1. PT  ECRB
2. FCR  EDC II-V
3. PL  rerouted APL
III. Boyes Transfer (Superficialis transfer)
1. PT  ECRB
2. FCR  APL and EPB
3. FDS III  EDC II-V via interosseous membrane
4. FDS IV  EIP; EPL via interosseous membrane
IV. FCU Transfer (Standard Transfer, this is not
modified Jones transfer)
1. PT  ECRB
2. FCU  EDC
3. PL  rerouted EPL

16. Which one will you do?

Ans. {Look for PL and ECRB power in examination}. I will
do FCU transfer. (If PL is absent then say Boyes transfer.
If the innervation to ECRB is not lost then PT transfer is
unnecessary )

17. What options are available if PL is absent?

Ans. Options in the order of preference:
1. Do Boyes transfer.
2. Substitute FDS III and IV for PL (Tsuge and Goldner)
 WRIST AND HAND 301

3. Use brachioradialis (possible only in PIN palsy)

4. Use FCU transfer to both thumb and finger extension
(violates pt no. 4).

18. What is meant by rerouted EPL?

Ans. It means that EPL is taken out of dorsal retinaculum (in
the region of snuff box and junction is made between PL
and EPL). This gives a combination of abduction and
extension force on thumb.

19. What are the problems with standard transfer (FCU

transfer)?
Ans. The main problem is of excessive radial deviation
which is due to:
1. Removal of the only preserved ulnar deviator (FCU) in
radial nerve palsy.
2. PT  ECRB transfer. ECRB is a radial deviator (albeit less
than ECRL)
3. In PIN palsy ECRL may be spared that leads to excessive
radial deviation.

20. How will you avoid them?

Ans. Mainly by two methods:
1. Planning itself: If you are too concerned by radial
deviation then do FCR/Boyes transfer
2. Alter the insertion of tendon by centralizing the ECRL
(attach to IV metacarpal) or alternately one may attach
the proximal resected end of ECU to (PT  ECRB)
transfer which is not preferred as it limits total excursion.

21. What is internal splint and what is its rationale?

Ans. Principles:
1. Should not  function in remaining hand
2. Should not create deformity
3. Should be phasic or capable of phasic conversion
E.g., PT  ECRB transfer described by Burkhalter for
radial nerve palsy.
302 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Indications:
1. Substitute function during nerve regrowth eliminating the
need of splintage.
2. Helper following reinnervation  aiding power of
normally innervated muscle
3. Substitute in cases where results of repair are poor or
nerve irreparable.

22. Which type of nerve is radial nerve?

Ans. Radial nerve is a primary motor nerve with a small sensory
component. Ulnar and median nerves are mixed nerves.

23. Does the type of nerve have any impact on outcome of

repair?
Ans. Yes, primary functioning nerves whether sensory or
motor have a better outcome as the chances of cross union
and resultant fiber atrophy are minimum and also single
modality (sensory/motor) dominant nerves have similar
fibers which reform better.

24. What is Holstein Lewis fracture and what is its

importance?
Ans. Spiral fracture of M/3rd and L/3rd junction of humerus
with proximal spike over lateral aspect just at the site
where radial nerve touches humerus. Commonly radial
nerve palsy was thought to be associated with fracture.

25. What will you do for a patient who comes with fracture
of humerus with radial nerve palsy?
Ans. I will wait for return of nerve function as according to
Steindler’s formula for nerve regeneration [(1mm = 1Day)
+ 30 days for motor recovery to manifest (N-M junction)
and nerve ends to sprout]. Usually for, e.g., nerve injury
is 90-120 mm above lateral condyle. Now for brachio-
radialis to get reinnervated that arises 20 mm above
lateral condyle it will take 70-100 days + 30 days =
4-5 months. This is the time duration one can wait
(calculate as for other fractures). This is based on the
 WRIST AND HAND 303

premises that often the nerve injury is apraxia or

axonotomesis with nerve in continuity and fair recovery
is seen in over 90 per cent cases.

26. Will you always follow this regime ‘or’ will you always
prefer to wait?
Ans. No, I will do early exploration of radial nerve for palsy
associated with:
1. Radial nerve injury secondary to manipulation of fracture
(absolute indication)
2. Open fractures
3. Fractures in which satisfactory alignment is not possible
by closed methods
4. Fractures with associated vascular injury
5. Patients with multiple trauma.

27. If you find a gap on exploration what will you do?

Ans. I will see whether nerve ends can be coapted without
tension. If not then I will mobilize the nerve and still if
not possible then I will do nerve grafting.

28. How will you assess the tension at suture site?

Ans. Wilgis  take a single suture bite with 8-0 suture and if
a knot cannot be tied without tension (or if it breaks) then
there will be unacceptable tension at suture site (or a gap
>4 cms).
Millesi  gap of  2.5 cms after keeping the limb in
functional position indicates possibility of tension.
Elbow flexion >90º or wrist flexion >40º required for nerve
approximation indicates tension.
Brooks: If gap cannot be closed after mobilizing the nerve
then there is bound to be tension.

29. How will you overcome nerve gap?

Ans. Following in isolation or combination are often required:
1. Mobilization
2. Transposition
3. Limb positioning
304 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

4. Resection osteotomy
5. Nerve stretching and bulb suture (neuroma to glioma
suture)
6. Neuromatous neurotisation (e.g., intercostal nerve for
brachial plexus)
7. Nerve grafting
8. Nerve crossing (ulnar  median)
9. Addition of non-neural tubes (e.g., vein segment).

30. How much mobilization can be done for a nerve?

Ans. Depends on the type of nerve but in general mobilization
>6-8 cms  perfusion. ( 8 per cent tension  venular flow,
10-15 per cent - tension: blood flow arrest).

31. What are various types of nerve grafting?

Ans. The various options are:
1. Trunk grafting using full-thickness segment of major
nerve trunk (disadvantage – central necrosis/total graft
dissolution)
2. Cable graft using multiple strands of cut nerve sewn at
both ends (drawback – wastes axons and ignores
anatomic localization of function)
3. Pedicle grafting often preferred for high combined ulnar
and median nerve palsy where ulnar nerve is used as a
pedicle graft to repair median nerve.
4. Interfascicular nerve graft (group fascicular nerve
grafting)
5. Individual fascicular nerve grafting – often done for
paucifascicular nerve, e.g., ulnar nerve at elbow or for
thin/terminal nerves, e.g., motor thenar branch of distal
digital N.
6. Free vascularised nerve graft.

32. From where one can harvest nerve for graft?

Ans.
1. Autogenous:
a. Lateral cutaneous nerve of thigh
b. Medial brachial and antebrachial cutaneous nerve
 WRIST AND HAND 305

c. Radial sensory nerve

d. Sural nerve (up to 40 cms of graft)
e. Lateral cutaneous nerve of forearm (up to 20 cms)
f. Terminal branch of PIN (for digital nerves)
2. Autologous vessels and muscle
3. Allograft nerve
4. Artificial conduits (veins/collagen conduits).

33. What if you find a sharp cut on exploration?

Ans. I will do nerve repair.

34. What are various types of nerve repair you know of?
Ans. Again a tricky question, begin by speaking one of the following
– if unacceptable switch to other!
Depending on duration from injury:
1. Primary repair – within hours
2. Delayed primary – within 5-7 days
3. Secondary – any repair > 7 days
Depending on the technique used:
1. Epineural
2. Group fascicular
3. Individual fascicular (funicular).

35. What do you mean by conditioning effect?

Ans. In clean sharp injuries a delay of 2-3 weeks was often
advocated on the premises that a ‘primed’ neuron will
regenerate faster at its peak metabolic activity due to
“conditioning effect”. Conditioning effect presupposes
that axons regenerate quickly if they have been damaged
previously.

36. What is the structure of a peripheral nerve?

Ans. Epineurium has two parts-internal and external, former
permeates the nerve ensheathing individual fascicles and
the latter is a condensation of collagen encasing the
fascicles as a group. Epineural fibrosis and scar formation
after nerve injury is a function of epineurium.
306 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Perineurium is an extension of blood-brain-barrier made

up of up to 10 concentric lamellae of flattened cells that
are ‘dove-tailed’. Removal of perineurium causes nerve
function to fail. Up to 15 per cent stretch, there is no injury
to perineurium but it fails for stretch >20 per cent.
Endoneurium acts as a packing material of collagen tissue.
There is no elastin. Participates in the formation of
Schwann cell tube.

37. What is fascicle?

Ans. Termed funiculus by Sunderland it is the smallest unit of
nerve that can be manipulated surgically.

38. What do you understand by Wallarian degeneration?

Ans. It is the reactive change of a nerve to injury whereby
distal stump is cleared of axoplasm and myelin along with
regenerative changes in proximal stump. It is initiated by
macrophage ingrowth stimulating Schwann cells. Schwann
cell proliferation peaks around 3rd day and continues up
to 2 weeks. The distal stump once cleared by Schwann
cells and macrophages is left in the form of a tube that
shrinks in size. Proliferating Schwann cells form ‘bungers
bands’. The proximal stump degenerates till nearest node
of ranvier from where new sprouts grow (2-5 sprouts
within 6 hrs). Those sprouts that establish end organ
contact persist rest all (those entangled at scar site ‘scar
delay’ and those missing their ‘receptive tubes’) are
pruned away.

39. What is topographic sensitivity?

Ans. Reinnervation of correct muscle within motor system or
correct patch of skin in sensory system.

40. How do you classify nerve injuries?

Ans. Seddon’s classification:
Neurapraxia ( ‘Sunderland’s type I); only physiological
disruption of nerve function – recovers of its own.
 WRIST AND HAND 307

Axonotomesis ( ‘Sunderland’s type II-IV); physio-

logical disruption with partial anatomical (increasing)
disruption of nerve – recovery possible (70%) but later
may need surgical intervention in higher grades.
Neurotemesis ( ‘Sunderland’s type V); complete
anatomical and physiological disruption of nerve – always
needs surgical intervention.

41. What is type VI nerve injury?

Ans. Combination of types I-V (added by Mackinnon)

42. What is intrinsic minus hand?

Ans. Fingers: Hyperextension at MCP joint + flexion at IP joints
± adduction of fingers
Thumb: adduction and hyperextension at MCP joint +
Flexion at IP joint.

43. What are synergistic muscles?

Ans. Synergism is the endless repeated coordination of
anatomically different groups of muscles to perform a
given action e.g., wrist extensors + finger flexors + finger
adductors “or” wrist flexors + finger extensors + finger
abductors.

44. What is the earliest sign of nerve recovery?

Ans. Advancing tinel’s sign

45. What is Tinel’s sign and what is its utility?

Ans. Paresthesia (fornication) experienced along the nerve
distribution (not at the percussion site) on gentle percussion
from distal to proximal over the nerve (1917, Jules Tinel)
Cause: Bare young hyper-excitable unmyelinated sprouts
from injured proximal end.
Seen in: Sunderland’s grades II-V.
Importance:
1. Advancing Tinel’s can be used to calculate and gauge pro-
gression of recovery (spontaneous or following repair)
308 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

2. Non-progressing Tinel’s indicates interruption of nerve

regeneration
3. Static Tinel’s at injury site and one present distally also
indicates poor prognosis.
4. Advancing Tinel’s seen only in grades II and III. (IV and
V grades show it only after repair)
Fallacies:
1. Few sensory sprouts and partial regeneration may give
a false positive Tinel’s sign.
2. No estimate of motor recovery should be made from
Tinel’s sign as it indicates sensory recovery from sensory
sprouts.
3. Single time estimation is also useless and needs to be
regularly followed.

46. What do you mean by autonomous zone, intermediate

zone and maximal zone?
Ans. Autonomous zone is the area exclusively (no other nerve
has interference in this zone) supplied by nerve in
question. While clinically testing for sensory loss a
somewhat larger area is outlined that contains overlap
from other nerve and this is intermediate zone. In actual
there is a still larger area that can only be tested by
blocking the other nerves, however, it is clinically
irrelevant as it has predominant brain representation by
other nerve, this is maximal area.

47. What are the autonomous zones of radial, ulnar and

median nerves?
Ans. Radial nerve: Coin shaped region over the dorsum of
stretched 1st web space.
Median nerve: Volar distal aspect of index finger.
Ulnar nerve: Volar ulnar aspect of distal little finger.

48. What is EDS?

Ans. EDS (electro diagnostic studies) comprises of EMG
(electromyography), NCS (nerve conduction studies) and
 WRIST AND HAND 309

Strength-duration curve. Normal muscle is electrically

silent on EMG (embryonic muscle show fibrillation till 
6 weeks of foetal life). Denervated muscle starts showing
fibrillation potential by 18-21 days (three weeks). If
renervation occurs fibrillation potential decreases and
motor unit action potential (MUAP) of low magnitude
appear. Giant MUAP are seen in a partially denervated
muscle which is additionally reinnervated by nearby
nerve.
Normal conduction velocity  50 m/sec (slightly more
in sensory nerves), demyelization reduces speed; unmyeli-
nated fibers have  10 m/sec of conduction velocity.
Sunderland type I injury may show delay at the site of
injury but otherwise NCS and EMG is normal.

49. What is strength-duration curve?

Ans. A graph plotting the intensity of electrical stimulus to the
length of time it must flow to produce response.

50. What is chronaxie and rheobase?

Ans. Rheobase (Rheos = current or flow; base = foundation)
is the minimal amount of stimulus strength that will
produce a response when applied indefinitely (practically
a few milli-seconds).
Chronaxie (chronos = Time; axie=axis) is the stimulation
duration that yields a response when stimulus strength
is set to exactly 2 × rheobase.

51. What is F-wave and H-reflex?

Ans. They are part of NCS (others are motor and sensory CS):
F-wave – stimulation of motor nerve and recording
action potential from muscle supplied by it. The stimulus
travels up the nerve to spinal cord then back to limb. It
measures the conduction b/n nerve and spinal cord
(others measure conduction within limb).
H-reflex – in this case afferent impulse travels up the
sensory nerve and travels down motor nerve to produce
discharge.
310 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

52. What is the importance of upward kink in SD

curve?
Ans. It indicates partial denervation.

53. What do you mean by opposition of thumb?

Ans. (1) Thumb abduction  (2) MCP flexion  (3) Internal
rotation and pronation  (4) Radial deviation of proximal
phalanx  (5) Motion of thumb towards fingers.

54. What tendon transfer will you do for low ulnar nerve
palsy?
Ans. Reconstruction system:
Requirements:
i. Thumb adduction
ii. MCP flexion
Available:
i. Wrist extensors
ii. FDS
iii. Index proprii (EIP)
Transfers:
1. Thumb adduction: ECRB  abductor tubercle (Smith/
Boyes).
2. MCP flexion with integrated IP flexion: ECRL (Brown’s
4 tailed; EF4) or FCR (if flexion contracture at wrist);
tendon grafts passed volar to transverse carpal
ligament attached to A2 pulley or radial band of dorsal
apparatus (see Chapter 7: Case II).
3. Palmar arch and adduction of little finger: EDM tendon
split and ulnar half transferred to radial collateral
ligament of PP or radial band of dorsal apparatus.
4. Thumb-Index finger ‘tip pinch’: Accessory slip of APL
to 1st dorsal interosseous and MP joint arthrodesis. If
MP joint already arthrodesed EPB may be trans-
ferred.
5. Volar sensations: Proximal medial digital nerve
translocated to distal ulnar digital nerve.
 WRIST AND HAND 311

55. What are methods for high ulnar nerve palsy?

Ans. 1, 2, 3, 4, 5 as above +:
1. Wrist flexion (ulnar side) {not frequently done}: FCR  FCU
or PL  FCU
2. DIP flexion for RF and LF: FDP (IF and MF)  tenodesed
to FDP (RF and LF).

56. Which transfer is done to obtain opposition with

adduction of thumb?
Ans. FDS (RF) transfer through pulley of volar carpal ligament
(Royle Thompson); remember that FDS transfer can be done
for low ulnar nerve palsy in place of one described above but
for high ulnar nerve palsy FDP is paralyzed so this is
contraindicated. It’s always more comfortable not only to
practice and master one technique but for exams also to
remember only one method and not get confused! Other very
commonly asked transfer is littler’s (“muscle”) transfer
of Abductor digiti minimi.

57. What reconstructive method will you use for combined

low median and ulnar nerve palsy?
Ans. This is a severe injury with complete volar anesthesia and
intrinsic palsy. Make the hand supple first and do transfers
as below:
1. Finger intrinsic function: Brand’s EF4 using ECRB or
Brown’s EF4 using ECRL.
2. Opposition for thumb: Do Riordan’s transfer (FDS
through FCU pulley) or Burkhalter transfer (EIP). But it
is better to remember thumb adduction as suggested in
low ulnar palsy as it also works for high median and ulnar
and high median and low ulnar combined palsies: Of
course this does not give opposition! (remember – we do
not have perverted memories – make it simple).
3. Sensory as above.

58. What is combined high median and ulnar nerve?

Ans. What patient loses?
1. Sensation of hand
312 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

2. Thumb abduction/opposition
3. MP joint flexion
4. Finger flexion
5. Wrist flexion
What must be replaced?
1. Sensation of hand
2. Thumb abduction/opposition
3. MP joint flexion
4. Finger flexion
5. Wrist flexion
Transfers:
Thumb adduction: ECRB  adductor tubercle
Thumb opposition  Burkhalter (EIP)
Finger flexion: ECRL  FDP and tenodesis of all fingers
Wrist flexion: ECU  FCU
But this may make extension of wrist quite weak, so one
may do wrist arthrodesis that spares all wrist extensors
for transfer quite safely.

59. What is Camitz transfer?

Ans. PL  APB, but done only in partial low median palsy to
provide opposition (in reality a pseudo-opposition) e.g.,
carpal tunnel syndrome.

60. What is the cause of nerve ‘palsy’ in postinjection nerve

palsy?
Ans. As such injection into or through nerves should not cause
palsy, however, some drugs act as fibrosing agent (e.g.,
tetracyclines, preservatives with injectable diclofenac) that
lead to ‘progressive’ fibrosis. This constricts the nerve and
cause palsy.

61. What is the treatment?

Ans. Do not wait, and if the patient presents early > 3 weeks
do neurolysis (endoneurolysis). Late cases (> 3 months)
showing no recovery should be treated with tendon
transfer. For immediate presentation one can wait for up
 WRIST AND HAND 313

to no longer than 3 weeks to give benefit for recovering

from possible neurapraxia due to local nerve injury or
oedema.

62. How do you classify fibrosis?

Ans. Millesi Types (added to Sunderland classification):
A. Epifascicular epineurium involved.
B. Interfascicular epineurium involved.
C. Endoneurium involved.
Type I/II and A/B need neurolysis.

63. What are the types of neurolysis?

Ans. Epineural, perineural (interfascicular), endoneural,
hemicircumferential neurolysis.

64. What are the various tests for ulnar nerve palsy?
Ans. Following are the tests in the order of importance:
1. Froment’s sign/Bunnel ‘O’ sign/newspaper sign: Paralysis
of 1st dorsal and 2nd palmar inter-osseous muscle with
Adductor pollicis paralysis. Patient flexes thumb as a
trick/compensatory maneuver.
2. Card test: To test palmar interossei (PAD= palmar-adduct;
DAB=Dorsal-abduct)
3. Wartenberg sign: EDM unopposed by 3rd palmar
interossei.
4. Jeanne’s sign: Loss of key pinch (Adductor pollicis)
5. Bouvier’s maneuver: Passive block of MCP hyper-
extension facilitates IP extension.
6. Duchenne’s sign: loss of MCP flexion
7. Pitres-stut sign: Inability to cross fingers e.g. IF on MF
tests P1D2.
8. Pitres-stut sign 2: Inability to make cone with extended
fingers
9. Pitres-stut test: Inability to radial and ulnar deviate MF.
10. Masse’s sign: Wasting and loss of metacarpal arch.
11. Pollock sign: Inability to flex DIP of RF and LF (paralysis
of ulnar half of FDP)
12. Look for wasting in 1st web space (Ist dorsal interosseous)
314 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

13. Impairment of precision grip.

14. Andre-Thomas sign.

65. What are anomalous innervations for ulnar nerve?

Ans.
1. Martin-Gruber anastomosis: In proximal forearm b/n
Median/AIN and ulnar nerve – additional intrinsic
innervations.
2. Riche-Cannieu: Motor ulnar branch with recurrent branch
of median – complete/partial intrinsic innervations
3. Ulnar nerve always contains fibers from C8 and T1;
additional C7 in 5-10 per cent  FCU
4. FDP innervation – all ulnar to all median
5. Dorso-ulnar surface of hand may be innervated by radial
nerve.

66. What are the boundaries of Guyon’s canal?

Ans. Wall formed proximally by pisiform and distally by hook
of hamate
Floor by transverse carpal ligament, hamate and
triquetrum bones
Roof by pisio-hamate ligament.

67. Can you outline the formation of brachial plexus and

its branches?
Ans. (Learn this by heart as it may be asked anywhere and at any
instance)
Formation:
From C5-C8 nerve roots just lateral to scalene muscles,
if a component of C4 received then it is termed pre-fixed;
if from T1 – post-fixed. Roots  Trunks (Upper C5,6;
middle C7; lower C8,T1)  Divisions (anterior and
posterior; behind clavicle)  Cords – named after their
relation to axillary artery (lateral – anterior division of
upper and middle trunk; medial – anterior lower;
posterior – posterior divisions of all three trunks)
 WRIST AND HAND 315

Branches from the roots

1. Dorsal scapular nerve (C5) supplies rhomboids and
levator scapulae and runs down deep to levator scapulae.
2. Nerve to subclavius (C5,6) supplies subclavius.
3. Long thoracic nerve (C5,6,7) supplies serratus anterior
Branches of the upper trunk (lower and middle have no
branches)
Suprascapular nerve (C5, 6) supplies supra-spinatus and
infraspinatus
Branches of the Lateral cord (L2M) (anterior divisions of
upper and middle trunk)
1. Lateral pectoral nerve (C6) supplies upper half of
pectoralis major
2. Lateral head of median nerve (C6,7)
3. Musculocutaneous nerve (C5, 6, 7) supplies coraco-
brachialis, biceps and brachialis and then becomes lateral
cutaneous nerve of the forearm.
Branches of the medial cord (M4U) (anterior division of
lower trunk)
1. Medial pectoral nerve (C7,8) supplies the sternocostal
fibers of pectoralis major
2. Medial cutaneous nerve of the arm (T1)
3. Medial cutaneous nerve of the forearm (C8, T1)
4. Medial head of median nerve (C8 and T1) joins the lateral
head and supplies most of the flexor muscles of the
forearm, the three thenar muscles and two lumbricals.
5. Ulnar nerve (C7,8 and T1) supplies the ulnar forearm
flexors and most of the intrinsic muscles of the hand.
Branches of the posterior cord (ULNAR)
1. Upper subscapular nerve (C6,7) supplies subscapularis
2. Lower subscapular nerve (C6,7) supplies subscapularis
(lower part) and teres major
3. Nerve to latissimus dorsi (Thoraco dorsal nerve (C6,7,8))
4. Axillary nerve (C5) passes backwards through the
quadrilateral space in contact with the neck of the humerus
and supplies deltoid and teres minor.
 316 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

5. Radial nerve (C5,6,7,8 and T1) supplies muscles of the

extensor compartment of the arm and forearm leaves the
axilla through the triangular space below teres major.

68. List the muscles innervated by radial, median and ulnar

nerves?
Ans. Radial: Arm – triceps, anconeus, radial half of brachialis,
brachioradialis, ECRL, ECRB
Forearm: Supinator, EDC, ECU, EDM, APL, EPB, EPL, EIP
Median: Forearm: PT, FDP (IF, MF), FDS (I-IV), FPL, PL,
PQ
Hand: APB, FPB (partial), OP, Lumbricals (I, II)
Ulnar: Forearm: FDP (RF, LF), FCU
Hand: Palmaris brevis, flexor digiti minimi, ADM,
Opponens digiti minimi, adductor pollicis, flexor pollicis
brevis (partial), all interossei, lumbricals (III, IV).

69. What are the various tests for median nerve?

Ans. Signs: Pointing index, ape thumb deformity (adducted
thumb) – Simian ‘hand’, thenar wasting, sensory deficit.
Tests:
1. Clasp test: Ask patient to clasp both hands – IF remains
extended
2. Pen test
3. Loss of opposition
4. Kiloh-Nevin sign: Ask patient to form ‘O’ with IF and
thumb using tips – patient will extend DIP of IF and IP
of thumb making peacock’s eye instead.

70. What is Hilton’s law?

Ans. It states that a nerve passing near a joint supplied that
joint.
{It is difficult at all times to understand learn and remember
tendon transfers, as a rule difficult aspects will not be asked
and if you pass in concepts then you may be forgiven for not
knowing all the details. What you are expected to know:
Type of palsy (high/low, complete/incomplete, recovering/non-
recovering)
 WRIST AND HAND 317

Basic principles of decision making

Examination of motor and sensory innervation and deficits
You should know how to examine:
FDS and FDP separately, wrist flexors and extensors,
demonstrate PL, movements of thumb and muscles especially
intrinsic muscles and their nerve supply.
Additionally you should know thoroughly the origin, course and
muscle innervation of three major nerves of UL
Extensor compartments, carpal tunnel and structures, guyon’s
canal may also be asked}

CASE II:
LEPROSY HAND
{Important but difficult case as regards the treatment part which
is quite similar to peripheral nerve injuries and needs constant
revision otherwise ‘all is volatile’. Identification may be easy and
barring few specific examination and characteristic points there
is nothing “special” in leprosy. Approach the case as for
peripheral nerve injury that helps learning then grab the specific
points for leprosy. Personally I will advise you to follow the practice
in your institute for a given set of nerve involvement and not get
confused in exams – remember not only does the eyes see what mind
knows but also the mind knows what eyes see!
Read: 6-8 times (MS Orth and DNB candidates)}

Diagnosis
The patient is a 28-year-old male with claw hand deformity of
left hand due to high ulnar nerve palsy as a residual of leprosy.
Findings: See Q1.

1. Why do you call it Hansen’s disease?

Ans. History: Long duration  Paresthesia (ants crawling),
patch (area) of numbness, glove and stocking anesthesia,
paralysis, trophic ulcer, epistaxis, pedal edema. Take
h/o residence in endemic area, family h/o, occupational
h/o, any other disease etiology leading to thickened
nerves.
 318 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Skin lesions: Macular, papular, nodules, infiltration ulcers,

burns, scar.
Palpate: Decreased sweating, roughness, scaling,
Nerves: (Cutaneous, superficial, peripheral)
Test for anesthesia
Motor weakness
Cardinal signs of Hansen’s: (three)
1. Anesthetic lesion
2. Nerve enlargement
3. Demonstration of Mycobacterium leprae in lesions
Other examination:
a. Ear lobe infiltration: Thickening and nodularity of ear
lobes
b. Superciliary madarosis (loss of lateral third eyebrows) late
feature of LL
c. Gynaecomastia (testicular atrophy) late cases of LL
d. Pedal edema
e. Trophic changes and ulcer formation (metatarsal heads
and lateral border of foot)
f. V and VII cranial nerves (only cranial nerves to be
involved in leprosy)
g. Lymph nodes (lepromatous spectrum)
h. Hepatosplenomegaly (occasional in lepromatous)

2. What nerves are commonly involved and how do you

examine them?
Ans. In the order of involvement: Ulnar (mixed, high, low),
median at wrist (then high), common peroneal at fibular
neck, facial, radial (superficial at wrist and distal forearm,
deep at arm), posterior tibial (clawing of toes and loss of
arch), greater auricular, supraorbital.
i. Supraorbital and supratrochlear: Examine from front 
run thumb/index finger from midline to lateral margin
of forehead); 2 cm from midline
ii. Greater auricular: Turn head to side  make sternocleido-
mastoid prominent  look for thickened nerve crossing
the muscle  run thumb/IF above below to feel as it slips
under.
 WRIST AND HAND 319

iii. Supraclavicular: 2 cm lateral to medial end of clavicle.

iv. Radial nerve in radial groove (arm) and over radius
(lateral aspect of forearm)
v. Ulnar nerve in cubital tunnel: Right side with left hand
and vice versa!
vi. Ulnar and radial cutaneous nerves over medial and lateral
aspects of wrist
vii. Median nerve: Flex elbow and deep palpation of nerve
at wrist between flexor tendons
viii. Common peroneal nerve: Patient sitting  flex knee and
feel for nerve 2 cms below fibular head
ix. Posterior tibial nerve: 2 cms below and behind medial
malleolus.
x. Sural cutaneous nerve: Between heel and lateral malleolus.

3. What is the old name of leprosy?

Ans. “Elephantiasis graecorum”. In India it has been known
as “Maharog” since ages.

4. What is meant by “lepra” and “kushtha”?

Ans. Lepra = bark/scaling; Kushtha = eating away.

5. Who discovered M. leprae and what was his hypothesis?

Ans. Gerhard Hendric Armauer Hansen (1873): first identified
it as an infectious disease rather than ‘older’ hereditary
concept.

6. Why are nerves involved and that too in a peculiar

distribution?
Ans. M. leprae enters through naked axons in epidermis 
perineural cells  endoneurium  localizes to Schwann
cells  it enters nerves through endoneural blood vessels.
Schwann cells are present only in peripheral nerves and
the nerves are at relatively cooler regions of body hence
particularly affected. (V and VII are the only cranial nerves
to be involved in leprosy).
320 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

7. How does nerve damage occur?

Ans. Immune reaction to bacterial antigens is the primary cause
of nerve damage. Also peripheral nerves (located in cooler
areas) are common sites for trauma  localize infection;
and also they pass through unyielding fibro-osseous
tunnel hence getting further traumatized following
thickening. In tuberculoid spectrum there is primary
damage by caseating necrosis and in lepromatous
spectrum there is slow ongoing fibrosis due to unchecked
bacterial proliferation in Schwann cells with secondary
ischemic damage to nerve (Vasculitis).

8. What is “Jogerson Lewandoz” law?

Ans. An infection when controlled by immunological
mechanisms result in granuloma formation.

9. How will you test the integrity of dermal nerves?

Ans. Pilocarpine test

10. What is methylene blue test?

Ans. One of the tests to prove that hypopigmented patches
are due to leprosy. Inject (36.5 ml) methylene blue  after
around 6 days the patches become blue and retain stain
due to lipid content of lepra cells.

11. What is the D/D of thickened nerves?

Ans. Hereditary sensory neuropathy, primary neuritic
amyloidosis, Dejerine-Sotta’s disease, Refsum’s disease.

12. What is morphological index?

Ans. Percentage of viable bacilli after counting 200 bacilli.

13. What is bacteriological index?

Ans. Number of bacteria in an average microscopic field.
Cochrane and Ridley scales commonly used to grade it
from 1+ to 6+.
 WRIST AND HAND 321

14. How do you classify leprosy?

Ans. WHO- Single lesion paucibacillary (SLPB), paucibacillary
(PB), multibacillary (MB).
Ridley-Jopling (1962): True tuberculoid (TT), borderline
tuberculoid (BT), borderline borderline (BB), borderline
lepromatous (BL), lepromatous leprosy (LL); modified in
1971 to include subpolar tuberculoid (TTs) and subpolar
lepromatous (LLs) types.
IAL (Indian Association of Leprologists) {1951  1953 
1981}: Tuberculoid, borderline, lepromatous, indetermi-
nate, pure neuritic. Previous maculoanesthetic type now
clubbed with tuberculoid.
NLEP (clinical) classification: Non-lepromatous (N) 
tuberculoid, maculoanesthetic, pure neuritic; lepromatous
(L); (N/L)  borderline and indeterminate.
Madrid (more useful):
Types – lepromatous (macular, diffuse, infiltrative, major
tuberculoid and pure neuritic), tuberculoid (macular,
minor tuberculoid, major tuberculoid, pure neuritic)
Groups – dimorphous, indeterminate (divided into
macular and neuritic)

15. What are lepra reactions?

Ans. Allergic inflammatory process which is not a part of
infective process either in its spread or resolution although
it may be associated one or more of these processes. The
disease itself is chronic and active for a long time with
bouts of exacerbating and sudden attacks of disease. They
describe only an episode in major disease. These reactions
are more common in lepromatous than borderline or
tuberculoid spectrum.

16. What are the types of lepra reaction?

Ans. Type I: Observed around neural elements and skin lesions
of borderline and tuberuloid types. They are likely due
to bacterial antigens which are killed by therapy and get
exposed to Cell-Mediated immunity. The reaction is
322 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

typically akin to lepromin reaction with presence of

epithelioid cells as the hallmark. It may be upgrading
(reversal) or downgrading types. Upgrading (reversal)
reaction is a BT to TT shift and downgrading one is a shift
to lepromatous spectrum with new lesions having their
characteristics.
Type II: (Aka – erythema nodosum leprosum, Roseolar
leprosy, Lepra fever) seen in lepromatous spectrum
with/without treatment. This reaction resembles “arthus
phenomenon” – Ag-Ab complex formed at specific sites.
Reaction is particularly located around medium sized
vessels.

Type 1 Type 2
Spectrum BT, BB, BL BL,LL
Lesion Existing lesion develop New modules arise
erythema and edema in crops
Nerve damage Frequent and severe Not so
Systemic signs Not common Fever, malaise, arthralgia,
lymphadenitis
Other organs Iritis, orchitis, Common
glomerulonephritis
do not develop.
Course Relapse infrequent Common
AFB Not seen Broken bacteria
Investigations Normal routine Urine – albuminuria
Pathogenesis Type-4 Ag-Ab reaction Type 3 Ag-Ab reaction
Histopathology Disorganized granuloma Vasculitis

Type 3 (Lucio phenomenon, Erythema necroticans): seen in

Mexican origin only, vascular lesion with diffuse
infiltration, does not respond to Thalidomide. Large
number of organisms seen.
17. What are the types of ENL?
Ans. Two types: Intermittent (divided into mild and severe
forms) and continuous (no reaction free period).
 WRIST AND HAND 323

18. What are the bony changes in leprosy?

Ans. Specific: Osteitis, periosteitis, bone cysts, bone resorption
(longitudinal/concentric/combined).
Non-specific: Erosions, osteomyelitis, osteopenia, septic
arthritis.
Minor changes: Honey combing, pseudocyst, enlarged
nutrient foramina, stippling.

19. What is reaction hand?

Ans. Subcutaneous nodules develop over dorsum of hand in
type 2 reaction. Infiltrating edema with pain and
functional incapacity is often present. If these features are
associated with arthritis of IP joint  reaction hand.

20. What is frozen hand?

Ans. Subcutaneous nodules heal by leaving scar (involves
palmer skin and aponeurosis)  Contracture produced
by fibrosis pulls up finger at MCP joint  pull in various
directions produces multi-forme deformities in fixed
position known as frozen hand.

21. How do you define low ulnar nerve palsy?

Ans. Anatomically – distal to olecranon fossa. Clinically –
involvement of intrinsic hand muscles.

22. What is high ulnar nerve palsy?

Ans. Anatomically – proximal to ulnar fossa. Clinically; involve-
ment of ulnar half of FDP and Flexor Carpi Ulnaris.

23. What do you understand by low and high median nerve

palsy?
Ans. Low median nerve palsy typically is defined by
involvement around wrist (carpal tunnel). Motor loss to
OP, APB, FPB, 1st and 2nd lumbrical with variable loss of
palmar cutaneous sensation. High median nerve palsy in
addition has motor loss to FDS, radial half of FDP, and
thumblong flexor (FPL), weakness of pronation (pronator
quadratus).
 324 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

24. What is deformity, disability, impairment?

Ans. Deformity: Alteration in form/shape/appearance of body
part which is visible.
Disability: Deterioration in one’s ability (capacity) which
is felt by the patient. Also defined as inability (or difficulty)
to carry out certain tasks.
Impairment: Anatomic, physiological and/or psychological
abnormality or loss resulting from disease/disorder that
may be temporary or permanent.

25. What are the types of deformity in leprosy?

Ans. Specific (LL/BL): Intrinsic plus finger, twisted finger, banana
finger, reaction hand, frozen hand.
Paralytic (BB/Neuritic): Claw hand, wrist drop, claw toes,
foot drop.
Feet: Trophic ulcer, scars and contractures, short digits.

26. What is the chemotherapy for leprosy?

Ans. MDT (Multi Drug Therapy)
Multi-bacillary (MB): Regimen for adults: Rifampicin 600
mg (per month), Dapsone 100 mg daily, Clofazimine 300
mg per month and 50 mg daily. {Children (10-14yr) – half
dose}.
Paucibacillary (PB): Rifampicin 600 mg monthly, Dapsone
100 mg daily. Single lesion (SLPB): Rifampicin 600 mg,
Ofloxacin 400 mg, Minocycline 100 mg (ROM regime).

27. How long will you continue treatment?

Ans. MB: Life long monotherapy (dapsone); MDT till skin
smears negative; FDT (fixed dose treatment) 24 pulses (in
36 months); FDT 12 pulses in 18 months (1995).
PB: 6 pulses of PB – MDT.
SLPB: ROM therapy.
Treatment of reactions: Steroids (types I and II);
thalidomide (I); colchicines (II), chloroquine (I and II),
cyclosporine till subsidence of lesions and new lesion do
not appear.
 WRIST AND HAND 325

28. How do you diagnose and treat neuritis?

Ans. Suspect neuritis in: tenderness over nerve trunk with
thickening
Swelling/redness/increased temperature
Some functional loss in distribution.
Conservative (medical decompression): Anti-inflammatory
drugs; prednisolone (60 mg/kg reduced by 10 mg every
week till three weeks  good response treat with 30 mg/
kg till 6 months); heat; splint  if no improvement in
3 weeks then operate.
Operative: Indications:
1. Recent onset incomplete paralysis not responding to
conservative treatment
2. Sudden onset complete paralysis attributed to neuritis
3. Continued pain even in presence of paralysis
4. Deterioration/progression of disease on conservative
treatment
5. Symptomatic nerve abscess
Procedures:
1. External decompression by removing constricting
ligaments and /or arching tendon fibers, medial
epicondylectomy for ulnar nerve
2. Reduction of angulation stress: E.g. anterior transposition
of nerve
3. Decompression:
a. Epineurectomy
b. Hemicircumferential neurolysis (epineurium dissected
only from hemicircumference of nerve to preserve
blood supply)
c. Interfascicular neurolysis
Splinting and exercises (muscle strengthening – physio-
therapy; functional re-education – occupational therapy).

29. What is claw hand?

Ans. Claw hand is deformity of hand due to functional
malposition with clawing of fingers (in position of
extension or hyperextension at MCP joint and flexion at
326 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

IP joints) and loss of cascade (normal disposition of fingers

in relaxed hand). It can be due to low/high ulnar nerve
paralysis (partial claw hand) or due to combined ulnar
and median nerve paralysis (total or complete claw hand).
Other causes are soft tissue contractures, hand
compartment syndrome and sequel, forearm compart-
ment syndrome and VIC.

30. What is reversal of grasp or how does clawing

functionally affect patient?
Ans. Major hand functions include: Grasp, pinch, hook, and
grip. To achieve all or any of these functions hand must
first achieve lumbrical position (MCP flexion and IP
extension) followed by gradual MCP  PIP  DIP 
flexion occurring in coordination. In intrinsic paralysis
(intrinsic minus hand) extension at MCP occurs due
dominance and DIP and PIP sequences occur before MCP
flexion pushing the object away before grasping.

31. How will you assess this claw hand for treatment?
Ans. Claw deformity  forearm vertical on table with wrist
neutral  ask patient to actively extend fingers  assess
severity of deformity.
Assisted angle: Assesses extensor lag in IP joint. Patient
actively extends finger with examiner stabilizing MCP
joint (examiner basically replenishes lumbrical function)
 if assisted angle is present then flex MCP joint until
maximum active extension of IP joint is possible. If assisted
angle >30o then passive (static) procedures are contra-
indicated.
Contracture angle: Measures residual fixed flexion at IP
joint. (Examiner passively extends the finger to fullest and
measures the residual angle). Joint stiffness/skin/capsule
contracture causing contracture angle <30° is correctable
by physiotherapy.
FDS power: If FDS is involved then routine procedures
are contraindicated.
 WRIST AND HAND 327

FDP power: if FDP to RF or LF is < grade 4 MRC then

use of FDS of these fingers is contraindicated.
Volkmann’s sign: If positive then stretching by physio-
therapy is required before surgery.
Hypermobility of joints if present then use weaker muscles
for transfer to prevent later development of swan neck
deformity.

32. What are the prerequisites for surgery in leprosy hand?

Ans. Determined by various factors:
• Good clinical response to anti-leprosy treatment
• No attacks of reaction or neuritis during previous
6 months.
• No tenderness over nerve
• Deformity for at least 1 year (no possibility of spon-
taneous recovery)
• No joint contracture/joint damage
• < 10º hyperextension at PIP joint and <15º ulnar deviation
of fingers {ideally should be absent}
• Isolated contraction of muscle to be transferred must be
practiced
• Compensatory abnormal movement pattern must be
unlearnt and eliminated
• Supple hand
Most importantly explain to the patient that only motor
function will be restored and not sensory function.

33. How will you treat claw hand?

Ans. Primary requirement in claw hand is to provide flexion
at MCP joint.
Secondary is to achieve flexion at IP joint and coordination
and power.
I will get an X-ray done to look for condition of bones
and joints.
Passive (Static) treatment methods to provide flexion at
MCP joint (Achieve only first goal and also do not
address adduction of fingers)
• Zancolli’s anterior capsulorrhaphy of MCP joint.
328 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

• Extensor diversion graft (Srinivasan)

• Palande’s technique (capsulorrhaphy and flexor pulley
advancement)
• ECRL tenodesis
Tendon transfer (dynamic):
Even if RF and LF are involved, transfer of tendon to all
four tendons must be done to provide coordinated and
powerful movements:
1. Sublimis transfer (Modified Stiles-Bunnel FF4T phasic transfer)
– FDS of RF  4 tail/slips  IF (ulnar side) and rest of
fingers (radial side). Attach to dorsal lateral extensor
expansion. Specific attachment provides in addition
adduction of fingers. Tendon should pass anterior to MCP
joint (Bunnel originally used all 4 FDS slips that led to
intrinsic plus deformity).
2. Zancolli Lasso: Transfer of FDS of RF/MF to all fingers.
Here a lasso is created around A2 pulley system (modified
Lasso) to provide dynamic MCP flexion (remember
unassisted angle should be <30º).
3. Extensor to flexor 4 tailed (EF4T non-phasic, Brand): ECRL
tendon with fascia lata or palmaris or plantaris extension
attached as mentioned. Brand originally described it with
ECRB tendon and later modified with ECRB/ECRL.
4. Palmaris longus many tailed graft – if fingers are
hypermobile. (This weaker muscle will not cause swan
neck deformity).
5. Extensor indices transfer.

34. How do you ascertain adequate tension?

Ans. Karat’s method: Maintaining range of excursion between
4-6 cms.
Other method is to clinically pull one tendon slip that
should just start excursion in nearby slip.

35. How will you address thumb function?

Ans. Adduction of thumb lost in ulnar nerve (Adductor pollicis,
FPB - partial) and major thenar muscle functions (APB,
FPB, OP) lost in median nerve palsy (Claw thumb) – so
 WRIST AND HAND 329

treatment required mostly in total claw hand. Aim is to

provide pronation (Total claw hand) and adduction
(ulnar). Most commonly FDS to ring finger rerouted
around pisiform bone (Riordan’s opponensplasty) 
divided into two slips  one attached to dorsum of MC
(adduction) and other to dorsum of terminal IP joint
(pronation). Other transfers include lateralization of EPL
tendon at wrist, APL rerouting, ECU rerouting, FPL
transfer, intermetacarpal bone block.

36. What ancillary surgeries may be required?

Ans. Web space contractures  Z-Plasty (with or without skin
graft or Groin)
Arthrodesis of MCP and IP joint (bone destruction and
non-salvageable joints)
Surgery for Boutonniere’s, Swan neck and mallet
finger deformities may be required.

37. What are the prerequisites for tendon transfers in foot?

Ans.The following must be looked for:
• No planter ulcer or septic focus.
• No fixed equinovarus deformity or tarsal disorganization
• Condition of muscles: Powerful tibialis posterior (Grade
V or at least IV+)
• No contracture of tendo Achilles
• At least 20o ankle dorsiflexion
• Conditioning of tibialis posterior muscle for voluntary
contraction (training).

38. How will you manage Hansen’s foot drop?

Ans. Main aim is stability to have reasonable gait and stance.
I will get X-ray done to see status of bones.
• Early foot drop: I will do passive mobilization, splinting,
physiotherapy to strengthen muscles till one year as
spontaneous recovery is possible till that time.
• Established foot drop: Tibialis posterior transfer (non-
phasic)  split into two  attach each into EDL/EHL.
Two routes:
1. Circumtibial route is easier but pull is oblique.
 330 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

2. Trans-interosseous membrane: Direct pull but more

chances of adhesion.
Other method is to insert it into ligaments of foot or
middle cuneiform (not preferred)
Incomplete lesions with active peronei  do a transfer
of both peronei and tibialis posterior otherwise tendency
to eversion is increased.

39. How will you manage Claw-Toes?

Ans. Claw-toes arise due to posterior tibial nerve palsy (Three
stages – 1. Hyperextension of MTP joint: Toe tip touches
ground: Toe-tip ulcer; 2. Increased hyperextension: Toe
tip off ground: Increased IP joint flexion: Toe dorsum
ulcer; 3. Increased MTP hyperextension: Dorsal dislocation
of toe; Toe Ball ulcer.)
1. If toes are supple: Flexor to extensor transfer: FDL
transferred to dorsum of toe and extensor tendon.
2. Stiff toes with contracture: Shortening of toes (excision of
middle phalanx) and inactivation of long flexor tendons
with arthrodesis.

40. How will you manage foot ulcers?

Ans. Three types:
1. Lepromatous: MDT for leprosy and nitrofurazone
ointment.
2. Stasis ulcer (dorsum of foot and medial and lower third
of leg): Local hygiene, antisceptic cream, dressing, elastic
compression bandage and elevation, POP cast and skin
grafting.
3. Trophic ulcer (plantar ulcer caused by prominent
metatarsal heads, sensory deficit, weight bearing, increased
plantar fascia tension, loss of protective function of
sesamoids in FHB):
a. Acute (swollen hot foot with abscess): Drain-age, wash
and irrigate, regular dressing, elevate limb, antibiotics.
b. Chronic: Regular dressing with antisceptics (or MSGP
(Magnesium sulfate, glycerine, pro-flavine) solution),
POP cast, rest and immo-bilization (contraindicated for
 WRIST AND HAND 331

secondary complications – infection), Remove slough,

clean and dress to enhance granulation, split thickness
skin grafting, amputation.

41. What is “Hot foot syndrome” and how will you manage
it?
Ans. Acute neuropathic disintegration of foot  results from
neurological deficit. Foot is hot and swollen with collapsed
suspension system.

42. What other deformities can be found in foot?

Ans. Cocked up toe due to unopposed extensor action (treat
by extensor tenotomy); Rosette toes (bunching of toes)
treated by corrective bandaging, neuropathic foot can be
managed by triple arthrodesis but chances of failure are
high.

43. What vaccines are available for Hansen’s dis-ease?

Ans. Live M. leprae, killed M. Leprae.
Killed M. Leprae with adjuvant
Chemically modified M. leprae
BCG + M. Vaccae
Delipified M. leprae
M. Omega ( vaccine) {ICMR Delhi}
ICRC bacillus.

44. How do you make smears?

Ans. Slit smears: Incise 5×3 mm and scrape material from
posterior auricular patch.
Snip smears: Small piece of skin removed and crushed
under slide.

45. What is histoid leprosy and lazarine leprosy?

Ans. Histoid leprosy is seen in LL patients with or without
relapse. It has variable nodules, does not undergo ENL,
absence of globi and clears on treatment.
Lazarine leprosy (Lepra Manchada) are ulcerating lesions
arising over trunk and extremity seen in BT leprosy (also
seen in Lucio leprosy).
 332 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

46. What is SFG index?

Ans. Solid, fragmented and granular index:
2-0-0 (all solid) {SFG index = 10}
0-0-2 (all fragmented) {SFG index = 0}

47. What are the characteristics of M. leprae?

Ans. It is an atypical (slow growing, oxidizes DOPA) partial
(weakly) acid-fast bacillus that looks like a bundle of cigars
“globi” under microscope.

48. What are the stains for M. leprae?

Ans. Ziehl-Neelsen and Fite-Faracco stains with the later one
being better as the bacilli are acid-fast for only a particular
duration of their lifetime and Fite-Faracco sort creates acid
fastness in bacilli. (Hansen originally used osmic acid).

CASE III:
DUPUYTREN’S DISEASE
Diagnosis
The patient is a 52-year-old male with dupuytren’s contracture
of both hands involving the ring and little fingers.

Findings
• Painless nodules/cords over palmar aspect
• Garrod nodes/knuckle pads over PIP joint dorsally
• Painless flexion contracture of fingers
• Thinning of subcutaneous fat
• Adhesion of skin to contracture
• Pitting/dimpling of skin
• Lesion’s of plantar fascia (Ledderhose disease)
• Plastic induration of penis (Peyronie disease)

1. What is dupuytren’s contracture?

Ans. It is a proliferative fibroplasia of palmar tissue
predominantly involving the palmar fascia and palmo-
digital extension. The proliferation is seen in the form of
 WRIST AND HAND 333

nodules and cords that may soon after develop in

secondary flexion deformity of fingers.

2. What are various risk factors for the development of this

disease?
Ans. Male sex (M:F=10:1, occurs earlier in males), Scandinavian
and celtic origin, diabetes mellitus, epilepsy, alcoholism,
pulmonary TB, vascular insufficiency (?Free radicals,
?Platelet derived growth factor) and cigarette smoking
and heredity (autosomal dominant with variable
penetrance).

3. How do you classify dupuytren’s disease?

Ans. There are three phases:
1. Early: Skin changes + loss of normal architecture + skin
pits
2. Intermediate: Nodules and cords
3. Late phase: Above + contractures. This has four stages:
i. Ring finger MCP joint contracture
ii. Ring finger MCP + PIP joint contracture + Little finger
MCP
iii. Above + Little finger PIP joint and MCP joint of middle
finger
iv. Above + DIP joint hyperextension of ring or little fingers
or both.

4. Which finger is most commonly involved?

Ans. Ring finger (followed in order of involvement by little,
middle, index and lastly thumb).

5. What are dupuytren’s nodules?

Ans. It is a firm soft-tissue mass originating in the superficial
components of palmar and digital fascia which is fixed to
both skin and deep fascia. They are usually well-defined
and localized. In the palm they are located adjacent to
distal palmar crease while in fingers the nodules are
commonly found at PIP joint or at the base of fingers.
They are often painless but may become symptomatic
 334 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

when associated with stenosing tenosynovitis due to

direct pressure on A1 pulley. Over time they get regressed
to be replaced by cord.
The dorsal side equivalents are Garrod nodes (rare)
or knuckle pads which are prevalent in bilateral disease
and particularly the presence of former should suggest
one to search other sites for similar affection (Ledderhose
and Peyronie).

6. How does the nodule form?

Ans. The earliest change is the thickening of Grapow fibers
(these connect the fascia to dermis). There is hence the
development of thickening of skin associated with rippling
and dimpling. The local proliferation continues to form
a nodule or if skin retraction occurs then a pit. (Skin pit
caused by full thickness skin retraction is a reliable sign of early
dupuytren’s disease and is latter replaced by nodule or cord).

7. What is the pathogenesis of cord?

Ans. Cords are often the future of nodules, however, they may
arise de novo. Remember the cords or nodules are by
themselves not de novo structures but often the
fibroblastic proliferation in normal anatomical structures
that become thickened by myofibroblastic activity and
deposition of type III collagen. The cords involve the
palmar, palmodigital and digital regions and the exact
distribution is complicated necessitating sound anatomical
knowledge of hand, however the important features are
presented here.
For development of flexion deformity at MCP joint
the pretendinous cord is most important.
The spiral cord is the one that extends through palm
to digits and has four origins; the pre-tendinous band, the
spiral band, the lateral digital sheet, and the Grayson
ligament.
PIP joint contracture results from involvement of
central cord, lateral cord, spiral cord, retrovascular cord.
DIP joint contracture emerges from contracture of
retrovascular and lateral cord.
 WRIST AND HAND 335

8. What is the differential diagnosis?

Ans.
1. Non-dupuytren’s disease: Occurs in diverse ethnic groups
(Dupuytren’s disease occurs in whites), unilateral, usually
single digit, often associated with trauma, can
spontaneously improve (rarely needing surgery)
2. Epithelioid sarcoma
3. Occupational thickening of skin and hyperkeratosis
4. Localized PVNS, palmar ganglion, inclusion cyst are
differentials for large dupuytren’s nodule
5. Post-traumatic contracture.

9. How do you treat the patient?

Ans. General guidelines are as follows:
Observation is limited to a patient with static disease and
minimal contracture or functional compromise.
Surgery is the keystone to treatment for majority.
Typical indications are flexion deformity of >30º at MCP
joint and flexion contracture of 15º at PIP joint in the
presence of a well-developed cord. The following
procedures are done with their individual merits and
demerits:
1. Percutaneous fasciotomy: Preferred for palmar cords in
older patients. Higher recurrence rate; limited dissection
required but greater danger to nearby tendons.
2. Fasciectomy: Partial, regional, limited remains the most
widely done procedure. Lower recurrence rates.
3. Segmental aponeurectomy: Through multiple small C-
shaped incisions in palm or digits segments of diseased
fascia are removed.
4. Total fasciectomy and digital Z-plasties: Higher compli-
cations
5. Dermofasciectomy: Simultaneous excision of skin and
diseased tissue. Low recurrence rates but limited to
recurrent disease or treatment failures or very severe
disease due to extensive dissection needed.
6. Salvage procedures: Amputation (PIP flexion deformity
>70º, recurrent disease with exuberant scar tissue), dorsal
 336 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

wedge osteotomy of proximal phalanx, arthrodesis of PIP

joint with partial resection of proximal phalanx,
arthroplasty of PIP joint.
Surgical release of PIP joint contracture is needed for
residual deformity >40º.

10. What are the complications of surgery?

Ans. Various complications are known, viz., neuro-vascular
injury, hematoma, infection, stiffness, reflex sympathetic
dystrophy, recurrence (true recurrence – disease at the
operative site or disease extension – recurrence outside
the primary surgical site), and inclusion cyst formation.

11. What can you offer to a patient unwilling for surgery?

Ans. Local agents have been tried with variable efficiency:
• Calcium channel blockers for early disease
• Collegenase for advanced disease
• Trypsin and hyaluronidase (enzymatic fascio-tomy)
• Steroid injection and local -interferon injections.

12. What are the poor prognostic factors?

Ans. Male sex, family history, ulnar side lesions, alcoholism and
epileptic patients, bilateral disease, etc are associated with
poor prognostic factors.

CASE IV:
FLEXOR TENDON INJURY
Diagnosis
Forty two-year-old male with 15 days old complete cut injury
to FDS and FDP of ring and middle fingers of right hand in
zone II.

Findings
• Scar mark over palmar aspect of hand healed with primary/
secondary intention
• Loss of finger flexion cascade
 WRIST AND HAND 337

• Palpable gap at the injury site

• Palpable nodule (of retracted tendon) proximal to injury site
(commonly at A2 pulley or at FDS chiasm or in palm)
• Inability to actively flex the finger at PIP and DIP (examine
both for all injured fingers) of RF and MF
• Loss of sensation distal to the injury site (cut injury to digital
nerve(s). Loss of sweat and two point discrimination

1. Why do you say it is a cut of both FDS and FDP?

Ans: (Also see section 7a. examination of hand, motor power and
muscle/tendon function). There is complete absence of finger
flexion at both PIP and DIP joints on testing active finger
flexion.

2.
How do you interpret the finger flexion cascade to
localize tendon injury?
Ans: (Observing flexion cascade is better than probing the wounds
in many circumstances). Allowing the wrist to drop free
into extension there is a passive tenodesis effect of long
flexors that bring all four fingers into a smooth flexion
cascade (‘arcade’) with incremental flexion from IF to LF.
Also there is flexion at IP joint of thumb. Any break in this
smooth transition indicates pathology (the interpretation
is true for Zone 1-3 injuries and some zone 4 injuries).
A finger held with slight flexion at both IP joints but
with a break in cascade  FDS injury
A finger is straighter than others but there is slight
flexion at PIP joint  FDP injury (if there is no history of
cut injury then suspect FDP avulsion; “Jersey finger” –
especially for RF).
A completely straight finger  injury to both FDP and
FDS.

3.
What else would you like to know from patient’s history
of injury that has a bearing on management?
Ans: I would specifically enquire if the finger was in flexion or
extension at the time of injury.
338 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

4. What is the implication?

Ans: Injury inflicted at finger flexion suggests that the level of
wound; cut FDS and cut FDP will be different and is a
favorable situation as ‘bunching’ at repair is less likely
with minimal chances of cross union and adhesions or
mechanical block later during rehabilitation training.
An injury in extension would although make it easier
to find the cut structure through smaller incision, however
there are higher risk of healing process and tendons
becoming one scar unit.

5. What in examination would prompt you to look for

possible other injuries?
Ans: Cut injury of both tendons in zone 2 will raise alarm for
associated digital neurovascular injury. Cut injury at zone
3 often implicates injury to digital nerves and superficial
arch injury. Cut flexor tendons except Palmaris longus at
Zone 4 should be explored for median nerve injury.
Similarly cut injury to FCU often indicates ulnar
neurovascular injury.

6. What are the zones of hand?

Ans: Verdan described 5 zones for flexor region of hand as
shown in table below:
Zone Limits (with suggested modification)
1 Insertion of FDP tendon at DP to insertion of FDS at MP
2 (No Man’s land) Insertion of FDS at MP to A1 pulley –
corresponds to distal palmar crease
3 A1 pulley to distal limit of transverse carpal ligament
(only the central limited part of tendons supplied by
mesotenon and attached to lumbricals are proposed to
be included in this zone)
4 (Enemy territory) Underneath the transverse carpal ligament
– between proximal and distal limits (synovial coverage
of flexor tendons extends up to 4 cm proximal to proximal
limit and some authors include this also in zone 4)
Contd...
 WRIST AND HAND 339

Contd...
Zone Limits (with suggested modification)
5 Muscles tendons and other structures proximal to
proximal limit of carpal ligament. Extensive laceration of
muscles in this region is termed “Spaghetti wrist/full
house injuries”
(Remember only the classical ones unless you aspire to become a hand
surgeon or encounter a hand surgeon in exams!)

7. Why is zone 2 called ‘no man’s land’?

Ans: Bunnell (1918) introduced the term “no man’s land” for
zone 2 following dismal results of primary repair and
admonished surgeons to primarily remove the tendon
and graft later. Problems primarily arise due to limited
space fibro-osseous tunnel containing two tendons and
multiple pulleys and minimal areolar tissue to allow
gliding despite best of repairs. Since then with advances
in suture material and techniques along with better
understanding the term should be upgraded to “some-
man’s land”.

8. What will you do for this patient?

Ans: (Considering the wound is favorable – healed without
infection/necrosis). I will ensure suppleness of joints and
absence of reflex sympathetic dystrophy. I will explain the
need of exploration and tendon repair with arrangements
for tendon grafting and repair of digital nerve to the
patient. Prognosis and need of all these procedures will
be explained to the patient.
(Any injury more than three weeks old is a strong candidate
for tendon grafting as the suture retaining strength of tendon
decreases and myostatic contractures develop precluding
apposition of tendons without excessive IP flexion)

9. What care will you take during repair?

Ans: Proper exposure using mid-lateral incisions or Bruner
incisions or both. Minimal tissue handling, avoid
340 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

devascularization of tendons, avoid bunching (stuffing),

strong enough repair for early mobilization, maintaining
or reconstructing pulley system.
I will expose the injury site through the transverse
wound and a mid-lateral incision (as nerve is also
involved). I will milk the tendons through the sheath using
gentle pressure on palm and flexing the MP joint; else I
will expose the retracted tendons in palm and pass a
catheter through the digital sheath with tendons tied to
the same and deliver through wound.

10. What are Bruner incisions?

Ans: Extensile zigzag incisions suitable for pure tendon injuries
that keep away the scar site from repair as much as
possible and do not produce function limiting wound
contracture.

11. What should be the characteristics of suture material for

repairing tendon?
Ans: The suture should have high tensile strength; have easy
knotability; having minimal tissue response; not be
extensible, for preventing gaping; be absorbable late after
healing of tendon and have ease of use.

12. What suture technique will you use for repair?

Ans: I will use locked cruciate core suture technique (or
otherwise modified Kessler) using 4-0 ethibond along with
Lin-locking epitendinous suture (or simple locked
epitendinous suture) using 6-0 prolene to ‘tidy up’ the
repair.

13. What tendons will you repair?

Ans: I will repair the FDP and one slip of FDS using four-strand
technique. However if FDS is cut proximal to Camper’s
Chiasm then I will repair both using the core suture and
epitenon repair technique. If the cut in both tendons are
at the same level then only repair the FDP.
 WRIST AND HAND 341

14. Why will you use the four strand technique?

Ans: It is agreed upon that more the number of suture
filaments cross the repair site the more is strength of
initial repair (time-zero). However, the strength of repair
is weakest at fifth-day and may drop anywhere from half
to one fifth of time-zero strength. Now it is believed that
some 14.7N strength is required to flex finger against
moderate resistance so that 3-5 times this measure (around
45N) is required for the time-zero suture techniques. Most
of the 4-strand suture techniques easily surpass this 45N
limit (especially the Becker and locked cruciate techniques
– 60N) also some strength is provided by epitendinous
technique (10-50%). Two strand techniques are hence
weak and 6 and 8 strand techniques are too bulky
possibly.

15. What other suture techniques you know of?

Ans: The following are various suture techniques:
• Two strand techniques: Bunnell (condemned), Mason-
Allen, modified Kessler
• Four strand techniques: Strickland, Lee, Robertson,
Becker, modified Becker and Locked cruciate
(McLarney)
• Six-strand techniques: Savage, Sandow, Lim
• Eight-strand technique: Silva
“Strands” mean the number of suture filaments actually
crossing the repair site.

16. How will you protect tendon surfaces and repair?

Ans: The following should be practiced: Using a strong
nonabsorbable suture, employ at-least two independent
sutures, using atraumatic technique, minimize exposed
knots and sutures, minimize exposed raw surfaces of
tendon, no strangulation of blood supply to tendon ends.

17. What if repair is not possible?

Ans: There is a high chance that the repair is not possible
(difficult after two weeks) and then I will arrange for
 342 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

tendon graft using Palmaris longus tendon in single stage

if the peritendinous tissue is healthy (not scarred and
provide gliding) else I will use a two-stage grafting
technique (less likely).

18. What is two-stage tendon grafting and rationale?

Ans: (Ensure supple skin, sensate digit, adequate vascularity and
full passive ROM of IP joints). If the tendon bed and
peritendinous tissue are badly disrupted so that the gliding
sheath for tendon is not available and /or pulley system
is damaged, I will place a silicone sheath in place (as spacer)
so that pseudo-sheath develops around it which will act
as tendon sheath for the future graft preserving or
reconstructing A2 and A4 pulley. Stage II performed at
least 3 months after; requires extrasynovial grafts from
palmaris longus or plantaris or toe extensor passed
through the formed tunnel using rail road technique.

19. How will you manage injury to pulley?

Ans: Out of eight pulleys (5-annular and 3-cruciate) A2 and A4
are the most important (oblique pulley for thumb) to
prevent bowstringing of flexor tendon (A2 pulley) and
reducing the angle of attack (A4 pulley) for flexor tendon
to provide smooth flexion. Primary repair is possible only
if care has been taken to deliver the tendons through L-
shaped incision across the pulley. Else a damaged pulley
will be reconstructed using extensor retinaculum sheath
(distal half to third) or Palmaris longus tendon graft.
(It is easier to remember the important pulley locations A2 is
located in proximal half of proximal phalanx and A4 is located
in middle third of middle phalanx)

20. How will you manage tendon injury in zone 1?

Ans: Avulsion injury of FDP – ‘Jersey finger’ is classified into
three types (Leddy and Packer):
• Type I – Avulsion injury with proximal tendon stump
retracted into palm. Urgent repair required as tendon
degeneration (both nutrient vinculae ruptured) and
 WRIST AND HAND 343

myostatic contractures are highly likely. Delayed

presentations (>21 days) require DIP fusion, FDP
reconstruction around FDS (not through chiasm), no
treatment or excision of FDP.
• Type II – Tendon retracts to FDS decussation at PIP
joint (commonest). Short vinculum only is ruptured.
Repair to bone.
• Type III – Larger piece of bone gets caught at the level
of A4 pulley. ORIF using pull-out suture or suture
anchors.
Cut injury of FDP is treated depending on the length of
distal stump left. If more than 0.75 cm of distal stump
remains – repair the tendon under A4 pulley (modified
Kessler). For small stump either advance the tendon and
attach to volar plate (the volar plate moves with distal
phalanx) or bone. If Quadriga effect is expected then one
may consider conversion to ‘superficialis finger’ or suture
the proximal tendon to distal stump and bring out the
suture through fingertip as pull out sutures.

21. What is ‘superficialis finger’?

Ans: For small distal stump in cut FDP tendon in zone 1 the
proximal stump is sutured to middle phalanx and the
proximal end of distal stump is sutured to the neck of
middle phalanx to prevent hyperextension deformity at
DIP. The method is also used for non-reconstructible
pulley in zone 2 with bowstringing of FDP.

22. What will you do for zone 4 injury?

Ans: As the space is limited so repairs are limited to terminal
digital flexors. I will repair FPL and Index profundus
independently while profundi to middle, ring and little
fingers are combined anatomically into single unit.
Superficialis tendons to repair should be so chosen that
they will not be in contact with any other tendon repair.
I will keep the carpal ligament open.
344 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

23. How will you manage the patient in postoperative

period?
Ans: I will manage the patient with Strickland active motion
protocol (See table below) designed for four-strand repair
with epitendinous suture (Indiana protocol). This
incorporates the early active motion exercises with
tenodesis motion in a Kleinert-type hinged splint.

0-3 days 0-4 weeks 4 weeks 5 weeks 6 weeks 8 weeks

Dorsal blocking Passive DIP Dorsal Active IP Blocking Progressive

splint (DBS) extension with blocking flexion with exercise resistive
with wrist in PIP and MCP splint MCP if active exercises
200 and MCP flexion (DBS) (15 removed extension tip to begin
in 500 flexion repetitions/2hrs) during followed by distal Unrestricted
Tenodesis Passive PIP exercise full digital palmar use of hand
splint (TS) extension with Tenodesis extension crease at 14 weeks
allowing 300 DIP and MCP exercise > 3 cm
wrist extension flexion (DBS) (15 continue
and full wrist repetitions/2hrs) (TS)
flexion, Tenodesis
maintaining exercises within
MCP in 500 hinged splint (TS)
flexion (15 repetitions/
2hrs)

24. What is the rationale of this program?

Ans: From the original description of Kleinert using the elastic
flexion pull against active extension various observations
have modified the postoperative regime.
• Passive DIP extension with PIP and MCP flexion glides
FDP away from FDS suture site
• Passive PIP extension with DIP and MCP flexion glides
both tendons away from wound
• Combined MCP flexion and wrist extension produces
the least tension on repaired site
• Tendon loses its tensile strength in first 2 weeks and
gliding function by 10 days.
• Work of flexion (resistance to tendon gliding) at 1 week
is least for repairs protected for first 3 days compared
to those mobilized immediately (during edema) or at
7 days
 WRIST AND HAND 345

• IP joint flexion is critical to preventing adhesion (it is

difficult to determine in Kleinert regime if flexion is
really occurring at IP joints or MP joint only)
• Wrist joint with greatest moment arm for flexor
tendons produces greatest tendon excursion so
tenodesis exercises have been added to active exercises.

25. What is Kleinert regime for postoperative rehabilitation

of tendon repair?
Ans: The protocols for tendon repair have moved a full circle
from early active mobilization in 1920s to immobilization
to passive mobilization (Kleinert and Duran) to active
mobilization (last two decades). Kleinert passive
mobilization protocol involved the use of a protective
splint with wrist and MP joints in flexion and IP joints in
extension; whereby active extension was encouraged
while flexion was passive using elastic rubber-band. This
slowly progressed to progressive resistive exercises.

26. What is Quadriga effect?

Ans: Quadriga (Roman 4-horsed chariot – single driver holding
reins to 4 horses) syndrome was first described by Verdan
in 1960. The common muscle belly of FDP to four fingers
(and analogous EDS – extensor quadriga) limits
independent function of flexor tendons to individual
finger. Also the muscle belly can contract effectively only
if excursion of all the tendons is normal. Thus, if one of
the tendon is fixed or its amplitude altered then
proportional effect will be evident in all the other slips
(reduced flexion) and often produces forearm pain.
Pseudoquadriga is produced by fixed contractures of IP
joints.

27. How much advancement is considered critical to

produce Quadriga effect?
Ans: More than 1 cm advancement has been found to clinically
produce quadriga effect.
 346 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

28. What is lumbrical plus finger?

Ans: The term refers to extension (paradoxical) at IP joints (the
action of lumbricals) on attempted flexion. This condition
is seen in cases where the tendon graft is either too long
or sutured in lax tension or has ruptured in attempted
reconstruction for zone 2 or sometimes 3 injuries using
tendon graft. The force in these cases is transmitted
through the lumbrical muscle tendon unit instead of flexor
tendon and hence paradoxical movement is produced. It
is important to demonstrate full ‘passive’ flexion before
making diagnosis of lumbrical plus finger.
(Remember and do not confuse: The superficialis finger is a
treatment method while lumbrical plus finger is a complication
of reconstruction)

29. Why is maintaining IP joint extension and MP flexion

for immobilization so stressed upon?
Ans: During immobilization; MP joints should be maintained
in more than 50° flexion as the collateral and accessory
collateral ligaments are lengthiest in 50-70° flexion at MP
joint. In case stiffness develops the ligaments will hence
not contract and limit the flexion during rehabilitation,
however immobilization in extension will produce
contracted ligaments and capsule that are difficult to stretch
later by physiotherapy. This differential length (19 mm
in flexion and 14-17 mm in extension) is due to differential
radii of metacarpal head and eccentric volar placement
(Cam effect) which places PP farthest from metacarpal
epicondyle (the origin of collateral ligaments) during
flexion. The effect is not seen in IP joints and prevention
of flexion contracture here is priority (hence extension).
Such a cast with MP joint in flexion and IP in extension
is called “Clam Digger cast”.

30. How do you manage partial lacerations?

Ans: Tendon lacerations of up to 90% of their thickness are
stronger than completely cut repaired tendons so a partial
laceration must never be made complete. In general
 WRIST AND HAND 347

lacerations up to 25% may be simply trimmed. Epitenon

repair is done for lacerations involving 25 to 50% of
tendon width. Larger lacerations are repaired as for a
complete tear without disturbing the remaining intact
tendon.

CASE V:
CARPAL TUNNEL SYNDROME
(TARDY MEDIAN PALSY)
(Simple case to diagnose and present and is good to score marks.
Simple and straight questions and answers.
Read times 4-5 MS and DNB candidates)

Diagnosis
The patient is a 40-year-old female with non-traumatic
incomplete right low median nerve palsy most likely due to
carpal tunnel syndrome.

1. Why do you call this carpal tunnel syndrome?

Ans:
A: Short history-
1. Tingling and numbness sensation in the typical median
nerve distribution in the radial three and a half digits
(thumb, index, long, and radial side of ring) prominent
in night (“nocturnal acroparesthesia”). Variable amount
of deep throbbing pain present diffusely over hand
climbing to forearm or arm may be described.
2. In late cases symptoms may progress to gritty or numb
feeling in fingers, weakness of grip or pinch and
diminished finger dexterity.
3. Tinel’s and Phalen’s test (Wrist hyperflexd for 60 secs;
acceptable if Tinel’s positive; sensitivity 0.59, specificity
0.93) are positive.
4. On inspection of the right hand there is thenar muscle
wasting. The thumb cannot be opposed to the fingertips.
Testing for APB revealed MRC power grade 3 compared
348 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

to the opposite normal side with reduced muscle bulk and

tone present. {In advanced cases one may find thumb to
be lying in the plane of the palm – a simian thumb (ape-
thumb deformity). There may be atrophy of the pulp of
the index and main fingers; dystrophic nail changes. There
may be signs of ulceration or burns seen in the hand or
fingers. However, testing for FPL revealed normal power.
(Distinguishes with high median nerve palsy)}

2. What other differentials have you ruled out?

Ans: Also called CTS mimics:
• Median nerve contusion
• Cervical radiculopathy (double-crush syndrome)
• Thoracic outlet syndrome
• Pronator syndrome
• Idiopathic brachioplexitis (Parsonage-Turner syndrome/
neuralgic amyotrophy)
• Intracranial neoplasm
• Multiple sclerosis
• Cervical syringomyelia
• Pancoast tumor
• Peripheral nerve tumor (schwannoma, hamartoma, etc.)
• Lower trunk brachial plexopathy
• Ulnar neuropathy
• Radial neuropathy
• Generalized neuropathy (diabetes/mononeuritis multiplex)
• Churg-Strauss syndrome.

3. What else would you like to examine?

Ans: Examination of neck to exclude any proximal abnormality
(like double crush syndrome). Examine for causes of
proximal median nerve compression.
1. Supracondylar process of humerus (also known as
ligament of Struthers).
2. Bicipital aponeurosis: Resist elbow flexion with
forearm supinated.
3. Between heads of pronator teres : Resist forearm
pronation with elbow extended/negative Phalens test
at wrist.
 WRIST AND HAND 349

4. Proximal arch of FDS (Isolate long finger PIP joint

flexion).
Simple test is to look for FPL weakness that identifies high
median nerve palsy.

4. How do you perform Tinel’s test and what is the

significance?
Ans: The Tinel’s sign is elicited by percussing in the midline
from 2.5 cm proximal to 4 cm distal to the wrist crease.
Presence of paresthesia along with a positive Phalen’s test
has sensitivity of 0.41 and specificity of 0.9.

5. Are there any other tests you can do to identify critical

median nerve compression?
Ans: Durkan’s test: Manual pressure over carpal tunnel for 30
secs – positive if paresthesia (electric test or tingling)
elicited in the median nerve distribution. More sensitive
than Phalen’s test (acceptable if Tinel’s positive).
Wrist extension test (Reverse Phalen’s test; pray position):
Active extension of wrist for 2 minutes (acceptable if
Tinel’s positive).
Tourniquet test (Gilliat and Wilson): Arm tourniquet inflated
above systolic pressure for 60 secs – not significant.
Closed fist sign: Making tight fist for 60 secs – significant
only if one more sign positive.
Hand elevation test: Hand elevated above head for 60 secs
– not significant.
Ames test: To detect malingering. Make a fist and ask to
press the fists together – identifies malingering if positive.

6. What are the other names for carpal tunnel syndrome?

Ans: Acroparesthesia, thenar neuritis, median neuropathy at wrist.

7. What are other clinical tests that can be performed in

this case?
Ans: Hand diagram (Patient marks site of pain or altered
sensation on outlined hand diagram), Hand volume stress
 350 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

test (Hand volume measured by displacement, repeat after

seven minutes stress test and ten minutes rest), static two
point discrimination, moving two point discrimination,
vibrometry, Semmes-Weinstein monofilaments.

8. Do you know of any invasive test?

Ans: Direct measurement of the carpal tunnel pressure by Wick
method. Normal pressure inside carpal tunnel is
2.5 mm Hg. Complete intraneural flow stasis is seen at
pressure above 80 mm Hg. ‘Critical pressure’ for
microvessels to cause Obliteration and consequent
ischemia is 40-50 mm. In patients with CTS the pressure
has been found to be elevated to a range of 12-43 mm Hg.

9. How will you investigate this case?

Ans: I will get Electrodiagnostic studies (nerve conduction
velocities and electromyography):
• A distal motor latency of more than 4.2 ms and a
sensory latency of more than 3.5 ms are considered
abnormal.
• There is increased median-to-ulnar latency difference
of the fourth finger SAP (>0.5 ms).
• Electromyography may show signs of nerve damage,
including increased insertional activity, positive sharp
waves, and fibrillations at rest, decreased motor
recruitment, and complex repetitive discharges in
Adductor pollicis muscle.

10. What do you achieve with EDS?

Ans: Confirm the clinical suspicion of CTS. EDS-
1. Localizes the lesion.
2. Depicts involvement of motor, sensory fibers; defines
physiologic basis (axon loss demyelination)
3. Severity of lesion.
4. Time course of lesion (evidence of reinnervation or
ongoing axonal loss).
In preoperative work-up EDS allows quantification of
severity and type of lesion. Should the outcome of surgery
is less than satisfactory it can be of some value in litigation.
 WRIST AND HAND 351

It should not be used as a substitute for clinical examination

as EDS is more sensitive and may come positive even in
‘clinically silent’ patients.

11. Is there any role of CT/Ultrasonography/MRI in carpal

tunnel syndrome?
Ans: Ultrasound dynamic stress testing in neuromuscular
ultrasound may demonstrate compression of median
nerve between contracting thenar muscles ventrally and
taut tendons dorsally. Mean diameter may decrease by
40% while in normal population there is a tendency of
no change or median nerve enlargement by 17%. Cross-
sectional area of <9.9 sqmm is taken as a cutoff for median
nerve compression at pisiform level.
CT shows the bony structures clearly, but does not define
the soft tissues accurately.
MRI shows high soft-tissue contrast may demonstrate
space occupying lesion as a cause. Most importantly MRI
is useful in postoperative failed cases (investigation of
choice) to look for real canal widening, incomplete
ligament resection, scarring or algodystrophy.

12. What is carpal tunnel and what are its boundaries?

Ans: A cylindrical, inelastic osseo-ligamentous space (open on
both sides) bound dorsally by concave carpal arch (floor)
and volarly by unyielding carpal ligament. The depth
varies from 10-13 mm.
Carpal ligament (roof) attaches to the hook of the
hamate, triquetrum, and pisiform medially; and the
scaphoid, trapezium ridge, and fibroosseous flexor carpi
radialis sheath laterally.

13. What are its contents?

Ans: The most ventral (palmar) structure in the carpal tunnel
is the median nerve. Lying dorsal (deep) to the median
nerve in the carpal tunnel are the nine flexor tendons
(4FDS, 4FDP, 1FPL) to the fingers and thumb. Total of 10
structures in tunnel.
 352 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

14. What is the commonest site for median nerve

compression in the tunnel?
Ans: The compression has been localized to the thickest part
of TCL which is somewhere 1 cm distal to the proximal
border of ligament. This level has been identified to be
in line with hook of hamate.

15. What are the risk factors for carpal tunnel syndrome?
Ans: Certain risks factors have been identified but are not
proven causative factors:
• Increased age (30-60 yrs)
• Female gender (F:M=3)
• Obesity
• Cigarette smoking
• Vibrations associated with job tasks (rock drilling) –
exertional CTS
• Repetitive movements of wrist and finger flexion
• Keyboarding (computer associated disease).

16. What are the causes of CTS?

Ans: Causes can be:
1. Idiopathic
2. Anatomic:
a. Acute form (fracture, crushing hand injury,
hemorrhage, burn, median artery thrombosis,
infection, pregnancy)
b. Distal radius malunion
c. Carpal canal stenosis (deformity congenital or acquired)
d. Anomalous structures (palmaris profundus, proximal
origin of a Lumbrical, reversed palmaris longus,
anomalous branch of radial artery)
e. Space occupying lesions (ganglion, lipoma, fibroma,
synovial sarcoma, neuroma, neurofibroma,
hemangioma)
3. Occupational (exertional CTS)
4. Systemic
a. Pregnancy
b. Endocrinopathy (diabetes mellitus, thyroid disease,
growth hormone)
 WRIST AND HAND 353

c. Congestive heart failure

d. Collagen and autoimmune diseases (tenovaginitis,
rheumatoid arthritis, scleroderma, gout,
chondrocalcinosis, etc.)
e. Amyloidosis
f. Polyneuropathy
g. Alcoholism
h. Myeloma
i. Consequential forms (oral contraceptives, anticoagulants,
lack of vitamin B6)
j. Children’s forms
k. Congenital diseases (mucopolysaccharidosis,
mucolipidosis).
17. Carpal tunnel has tendons and nerves as contents but can
you think of any muscular cause of carpal tunnel
syndrome?
Ans: Yes, aberrant muscles (lumbrical, reversed palmaris
longus, palmaris profundus) can decrease the volume of
carpal tunnel.
18. Are there any vascular causes of CTS?
Ans: Yes, anomalous branch of radial artery, hypertrophied or
aberrant median artery and vein, hemangioma, A-V
malformation in the tunnel.
19. How will you manage this case?
Ans: The following is based on general consensus. Mild to
moderate cases that are not rapidly advancing and are
not due to acute cause (see above) should be given a fair
conservative trial. I will operate advanced and late cases
only on an urgent basis and counsel for elective surgery
to patients showing evident denervation in median nerve
distribution and pronounced sensory loss particularly
supported by electrodiagnostic studies.
20. What is non-surgical treatment for carpal tunnel syndrome?
Ans: Splinting, activity modification supplemented with oral
medications are mainstay of conservative management
of CTS.
354 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

Splinting: Especially at night and intermittently during day

provide good relief in majority of cases, particularly those
having positive Phalen’s test.
Oral medications: Anti-inflammatory medication ±
neurotropic vitamins (B6, methylcobalamin) ± steroids ±
diuretics to reduce carpal tunnel pressure.
Local adjunctive measures like ultrasonics, laser therapy and
iontophoresis have variable non-documented effects.

21. What is the role of corticosteroid injections?

Ans: Steroid injections provide rapid relief but there is no
documented benefit after 3 months over oral steroids and
over long term when compared to splinting and NSAIDs.
There is no concrete information as to type, dose or
location of injection. They may be of help in patients with
symptoms less than 1-year, normal two-point
discrimination, no thenar atrophy, less than 1-2 msec
prolongation of sensory motor latencies and no
denervation potentials (mild or moderate cases). Failure
to improve with steroid injections is a poor prognostic
factor and even surgical release may not be helpful in
these cases.

22. What are the poor prognostic factors where conservative

treatment often fails?
Ans: Age older than 50 years, duration of symptoms longer
than 10 months, constant paresthesia, stenosing flexor
tenosynovitis, and a positive Phalen test result in less than
30 seconds.

23. What are surgical approach to carpal tunnel syndrome?

Ans:
1. Open carpal tunnel release
a. Wrist-palm incision (Milford, Taleisnik, Phalen, etc.)
b. Double incision technique by Wilson
c. Palm only incision (Lee et al)
d. Minimal open release (Bromley et al)
2. Endoscopic technique (single portal technique of Agee and
double incision technique of Chow)
 WRIST AND HAND 355

24. What are the complications of open release?

Ans: Iatrogenic nerve injury (palmar or motor cutaneous
branch), injury to thenar branch (commonly aberrant),
scar tenderness, pillar pain (most common complication
following release due to laceration of palmar cutaneous
branch), weakened grip strength, injury to superficial
palmar arch and recurrence.

25. What are the contraindications for endoscopic release?

Ans: Wrist stiffness, proliferative synovitis and space occupying
lesions.

26. What is the role of internal neurolysis during open

release?
Ans: Once popular this has been absolutely abandoned and is
counterproductive.

27. What are common causes of failed release and persistent

symptoms or recurrent CTS?
Ans: Incomplete ligament release, fibrosis/painful scar, tendon
adhesions to nerve, missed double-crush syndrome,
recurrent tenosynovitis. Others are reformation of the
flexor retinaculum, scarring in the carpal tunnel, median
or palmar cutaneous neuroma, palmar cutaneous nerve
entrapment.

28. How will you manage failed CTS?

Ans: A very difficult problem even for experts. Reevaluate with
EDS studies, MRI is a must. At revision surgery neurolysis
of median nerve with fat or muscle transfer and vein
wrapping are some of the methods described to improve
results.

CASE VI:
MALUNITED DISTAL RADIUS FRACTURE
{This is a very common case to see in our subcontinent. Not
a frequent exam case but in regions or places where large
number of DNB students appear for exams, the case may be
356 PRACTICAL ORTHOPEDIC EXAMINATION MADE EASY

kept. It is a fact that not many surgeons expertise in treatment

of malunited distal radius fractures so the questions will be more
directed to treatment of distal radius fractures rather.
Read times 6-8 times to grab the different concepts}
Diagnosis: This is a 56-year-old female with a malunited distal
radius fracture. There is 1 cm of radial shortening and reduced
grip strength.
Findings of a typical malunited Colles fracture.
1. Inspection
a. Dinner fork deformity
b. Shortening of forearm
c. Mannus rectus or valgus
d. Swelling at wrist
e. Prominent ulnar head.
2. Palpation (above +)
a. Distal radial swelling
b. Irregular distal radius
c. Tenderness at carpal region or dorsal wrist joint line (late
cases due to degenerative changes) or wrist instability.
d. Wrist widening.
3. Movements
a. Reduced palmar flexion, ulnar deviation and
combination of other movement loss depending on
stiffness and wrist instability
b. Reduced forearm movements (supination and pronation).
4. Reduced grip strength.
5. Shortening of radius.
6. Wrist widening (measurements).

1. What type of malunion is this, would you like to be more

specific?
Ans: This appears to be extraarticular malunion but I would
need radiographs to confirm absence (or presence) of
intraarticular extension of original fracture. Dorsal
malunions are further classified as type I (correctable DISI)
or type II (fixed DISI).
 WRIST AND HAND 357

2. What other malunions you know of?

Ans: Apart from intraarticular and extraarticular malunions, can
also be subgrouped as volar (Smith’s) or dorsally (Colles)
displaced malunions with shortening.

3. What would you like to do for this patient?

Ans: Firstly I would like to get radiographs to primarily
evaluate the fracture. I will order standard AP, lateral and
one clenched fist X-ray of wrist (to look for carpal
instability).

4. What else can you expect to see on X-rays?

Ans: Reflex sympathetic dystrophy (algodystrophy) changes,
associated ulnar styloid fracture.

5. What are the consequences of malunion that concern

patient?
Ans: Intraarticular malunions produce irregular cartilage surface
(late degenerative changes). Extraarticular malunions alter
intracarpal, radiocarpal and DRUJ (distal radioulnar joint)
mechanics. Grip strength is reduced. TFCC (Triangular
fibro-cartilage complex) strain may produce constant
ulnar pain on activity. Altered loading patterns and
premature osteoarthritis is quite possible.

6. How do you define malunion of distal radius on

radiographs?
Ans: There is no constant definition. Agreed values are as
follows: radiocarpal (RC) malunion – RC joint stepoff of
> 1 mm. Dorsal malunion– 10 degrees of extension and
more (greater than 20 degrees from normal). There is still
more disagreement on malunion in coronal plane (< 10
degrees of radial inclination is considered significant),
acceptable distal radius shortening (loss of 5 mm or more
of radial height is considered significant), acceptable
displacement of DRUJ surface and malunion of ulna. (It’s
all dependent on onlooker, in view of an experienced surgeon
a displacement is a displacement and malunion if united! – really
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a bookish definition, but I am sorry). Any malunion associated

with radiocarpal subluxation is a significant malunion and
needs corrective action.

7. What is the incidence of malunion?

Ans: Most common complication following distal radius fracture.
Around 23-25% radiological malunion is seen. Clinically
symptomatic malunion is very low somewhere around
5-7% following various treatment methods.

8. What are the values for various parameters of distal

radius?
Ans: Radial inclination = 17 – 25 degrees (22 degrees av.)
Palmar/volar tilt/inclination = 2–20 degrees (11 degrees av.)
Radial length/height (from distal radius lunate fossa to
radial styloid) = 9.9 – 17.3 mm (mean of 11 mm), <9 mm
is significant.
Ulnar variance (from distal radius lunate fossa to ulnar
articular surface) = –2.3 to ± 4.6 mm (average 0.9 mm),
on a zero rotation view.

9. What is the most concerning aspect of distal radius

malunion?
Ans: Dorsal tilt disables most of the mechanics around distal
radius that concerns all patients, additionally for a manual
labourer radial length is of additional concern as it
weakens the grip strength. For intraarticular malunion
development of wrist arthritis is a big concern (some 91%
patients develop arthritis having step-off >2 mm while
only 11% develop arthritis if the step-off is <2 mm), and
should be managed with priority.

10. How will you manage dorsal tilt?

Ans: I will do an osteotomy (at the or as close to) from dorsal
approach and do tricortical iliac bone grafting under
fluoroscopy control to reproduce the distal radius
anatomy (as compared to the normal side). Similarly for
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other malunions wedge-shaped grafts in different lengths

and stabilised using volar or dorsal locked plates (as the
case may be) are used – nothing very special.

11. How will you manage intraarticular malunion?

Ans: I will get a CT scan of the distal radius malunion and plan
surgery accordingly. In general the simple intraarticular
malunions and malunions with dorsal subluxations are
better dealt with dorsal approach while volar radiocarpal
subluxation with malunion are better treated with volar
approach. There is a trend to avoid incising the volar
stouter capsule for good functional outcome and also
familiarity of intraarticular reduction through dorsal
approach (die-punch reduction) makes this approach
preferable. DRUJ and TFCC needs specific management
on a case to case basis.

12. What various named fractures do you know?

Ans: Colles (pronounced as ‘collis’ – English literature) fracture
(Pouteau fracture – French): Dorsal displacement and tilt,
volar displacement and tilt, impaction and supination.
Fracture of ulnar styloid may or may not be a component.
Smith’s fracture (Smith-Goyrand fracture): Reverse of Colles.
Barton’s fracture: Intraarticular shear fracture of dorsal rim
of radius with radiocarpal subluxation.
Reverse Barton’s fracture (volar Barton fracture; Smith-
Goyrand II): Fracture of volar rim of radius with radiocarpal
subluxation (many people consider volar Barton as
Barton’s fracture – this is incorrect it is reverse Barton’s
fracture. Also Smith fracture 1 is extraarticular fracture
with volar displacement and Smith fracture 2 is
intraarticular fracture with volar subluxation as described).
Chauffeur’s fracture: Radial styloid fracture.
Hutchinson’s fracture: Radial styloid fracture ± scapholunate
disruption.
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Moore’s fracture: Distal radius fracture with ulnar

dislocation and entrapment of ulnar styloid fracture under
annular ligament.
Die-punch fracture: Fracture through lunate fossa
(depressed fracture).

13. What is Colles fracture?

Ans: As typically described by Colles – extraarticular fracture
occurring at the corticocancellous junction of distal radius
some one and a half inch above (around 4 cm) the carpal
surface, more so a transverse fracture throwing the
carpus dorsally with dorsal displacement and angulation
at the fracture site.

14. How do you classify distal radius fractures?

Ans: There are a lot of classifications but the preferred are
Melone’s, universal and AO (remember any one),
Fernandez and Frykman’s are of historical significance
only.
Melone’s classification: Based on distal radius ‘4 parts’
divided into (a) radial styloid, (b and c) dorsal medial and
dorsal lateral parts (of lunate fossa) and (d) radial shaft.
• Type I: Stable, undisplaced and minimally comminuted
(Colles equivalent)
• Type II: Comminuted, stable displacement of medial complex.
– Posterior displacement – die – punch #: moderate to
severe displacement;
– Displaced # involving radioscaphoid joint – involves
more than simple radial styloid
• Type IIb (irreducible) – ‘double die-punch’ # (irreducible
injury)
– Dorsal medial component fragmentation – persistent
radiocarpal incongruity > 2 mm
– Requires open reduction ± bone grafting for restoration
of articular congruity
• Type III: Die-punch or lunate load fracture (depressed
fracture)
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– Involves additional # from shaft of radius that projects

into flexor compartment (volar spike)
• Type IV: transverse split of articular surfaces, wide
separation with rotational displacement
– ORIF with plating ± bone grafting.

15. What is Kapandji method of fixation of distal radius?

Ans: Intrafocal ‘double basket like’ pinning typically described
for extraarticular fractures. The k-wires pass through the
fracture site (interfocal) and act to buttress the distal
fragment in position resisting the displacing forces.

16. What is the role of external fixator for fixation of distal

radius?
Ans: Typically indicated for open fractures for wound
management. It has been used for distraction
(ligamentotaxis) reduction of severely comminuted
fractures to maintain alignment. The role of spanning
external fixators has reduced now with the introduction
of locked plates (internal fixator) and anatomic reduction.
Non-spanning dynamic fixators have come into vogue for
ease of application, minimally invasive surgery and no
implant remaining in the body after removal at fracture
union.