Injury 52 (2021) 2053–2067

Contents lists available at ScienceDirect

Injury
journal homepage: www.elsevier.com/locate/injury

Flexor tendon injuries: Repair & Rehabilitation

Oliver Pearce a, Matthew T Brown b, Katrina Fraser c, Luca Lancerotto d
a
Trauma Registrar, Trauma & Orthopaedic Department, Southmead Hospital, Southmead Road, Bristol BS10 5NB, UK
b
Fellow in Hand & Wrist Surgery, Lothian Hand Unit, St John’s Hospital, Livingston, West Lothian EH54 6PP, UK
c
Clinical Specialist Occupational Therapist (Hand Therapy), Lothian Hand Unit, St John’s Hospital, Livingston, West Lothian EH54 6PP, UK
d
Consultant Hand & Plastic Surgeon, Lothian Hand Unit, St John’s Hospital, Livingston, West Lothian EH54 6PP, UK

a r t i c l e i n f o a b s t r a c t

Keywords: Flexor tendon injuries are common and occur mostly by penetrating trauma. Suspected flexor tendon in-
Flexor tendon juries require a thorough clinical assessment and often are not isolated injuries. A detailed understanding
tendon injury
of flexor tendon anatomy and spatial relationships is essential, especially when repairing multi-tendon
tendon repair
injuries. Principles of flexor tendon repair include a strong suture construct, minimising gap formation
flexor rehabilitation
between tendon ends, preserving tendon blood supply and providing a smooth repair interface. Moreover,
adequate exposure of the zone of injury using full-thickness skin flaps and preservation of neurovascular
and pulley structures is essential. In this article an overview of contemporary management strategies is
presented. Today’s hand surgeons and therapists can choose from a variety of treatment options when
managing these important and potentially life-changing injuries.
Crown Copyright © 2021 Published by Elsevier Ltd. All rights reserved.

Introduction
Flexor tendon injuries are common and occur mostly by pen-
etrating trauma. The highest incidence is observed in males and
those aged 20-29 years, with work-related injuries accounting for
25% of acute presentations [1]. Tendon injury may be classified
as acute or chronic, and as either direct or indirect [2]. Acute in-
jury may result from blunt or penetrating trauma, or from a sud-
den activity-related insult causing distal avulsion. Tendons exhibit
high mechanical strength, flexibility and elasticity to facilitate their
unique role in locomotion [3,4]. Advances in our understanding
of tendon biology, healing, material properties and design, repair
techniques, and rehabilitation regimes have improved outcomes for
these important and potentially life-changing injuries. This review
aims to present an evidence-based, comprehensive and practical
overview of contemporary flexor tendon injury management.
Functional anatomy
A detailed understanding of flexor tendon anatomy and spatial
relationships is essential, especially when repairing multi-tendon
injuries. Furthermore, anatomical variations exist, with specific ex-
amination techniques helping to identify such differences [5].
The thumb has a single proper extrinsic flexor tendon, the
flexor pollicis longus (FPL). The index, middle (long), ring and little
fingers have two: the flexor digitorum superficialis (FDS) and the
flexor digitorum profundus (FDP).
The FPL is a deep flexor that originates from the mid-radius
and neighbouring interosseous membrane and is innervated by the
anterior interosseous branch of the median nerve. It traverses the
carpal tunnel radially en route to its insertion at the base of the
distal phalanx of the thumb. The thumb has an additional flexor
muscle, the flexor pollicis brevis (FPB), which is an intrinsic mus-
cle of the thenar eminence that contributes to flexion of the thumb
metacarpophalangeal joint (MCPJ).
The FDP muscle originates from the proximal three quarters
of the ulna and interosseous membrane and has dual innervation
from the anterior interosseous branch of the median nerve (in-
dex and middle fingers) and the ulnar nerve (ring and little fin-
gers). The middle, ring and little fingers share a common FDP mus-
cle belly. The FDP inserts into the base of the distal phalanx and
acts as a primary flexor of the distal interphalangeal joint (DIPJ)
and a secondary flexor of the proximal interphalangeal joint (PIPJ)
and MCPJ. The FDS muscle originates from two heads: medial epi-
condyle of the distal humerus (common flexor origin) and the
proximal radius. It is innervated by the median nerve, which lies
on its deep surface. The FDS is a primary PIPJ and a secondary
MCPJ flexor. In the carpal tunnel, the FDP tendons lay deep and
side-by-side, whereas the FDS tendons are arranged in two layers:
those to the middle and ring fingers are volar to the tendons to the
index and little fingers. In the palm, FDS tendons are superficial to
FDP tendons to the same digit, and the two tendons to each finger
run in tunnels formed by the vertical fascial fibres of Legueu and
Juvara (the common digital neurovascular pedicles and lumbrical
muscles are located between each pair). Each FDS tendon divides

https://doi.org/10.1016/j.injury.2021.07.036
0020-1383/Crown Copyright © 2021 Published by Elsevier Ltd. All rights reserved.
O. Pearce, M.T. Brown, K. Fraser et al.
Fig. 1. Flexor pulley system of the finger and thumb. The pulley system is formed
from the condensations of the osseofibrous synovial sheath resulting in five annular
pulleys (A1-A5) and three cruciate pulleys (C1-C3). The thumb is formed of three
main pulleys, two annular pulleys (A1, and A2), and one oblique pulley (OP) formed
from the insertion of adductor pollicis.
at the MCPJ into radial and ulnar slips, which permit FDP passage
up through FDS. After rotating 180°, the FDS slips reunite beneath
the FDP tendon at the ‘Camper’s chiasm’ before they redivide and
insert onto the middle three fifths of the middle phalanx.
The tendon pairs to each finger lie encased within a tendon
sheath distal to the MCPJs, which isolates them from the surround-
ing tissues. The tendon sheath is comprised of two mirror mem-
branes, an outer parietal (fibrous) layer and an inner visceral (syn-
ovial) layer coating the tendon, which are in continuity with each
other at the proximal and distal ends. The virtual space between
the two membranes is filled with synovial fluid, which has a lu-
bricating function that facilitates tendon gliding and contributes
to tendon nutrition. Condensations, or thickenings, in the fibrous
sheath result in five annular pulleys (A1-A5) and three cruciate
pulleys (C1-C3) (Fig. 1). The A1, A3 and A5 pulleys originate from
the volar plates of the MCPJ, PIPJ and DIPJ, respectively. The thumb
has a unique pulley configuration including two annular pulleys
(A1, A2) and an extension of the adductor pollicis aponeurosis
forming a single oblique pulley (O1) overlying the proximal pha-
lanx, which is considered the most important. The digital pulley
system provides a series of fulcrums ensuring tendons remain ad-
jacent to the axis of the phalanges. This facilitates the conversion
of linear translation to rotational torque at the IPJs. Historically,
the A2 and A4 pulleys are considered critical in the prevention
of ‘bow-stringing’ and subsequent loss of functional excursion. The
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Injury 52 (2021) 2053–2067
Fig. 2. Flexor synovial sheaths, bursae and the Space of Parona. The thumb and
little finger synovial sheaths are continuous with the radial (blue asterisk) and ulnar
bursae (red asterisk), respectively. The bursae may communicate directly or through
rupture via the Space of Parona in the distal forearm.
synovial sheaths of the index, middle and ring fingers run from the
distal palmar crease to the DIPJ. In contrast, the synovial sheaths of
the thumb and little finger are continuous with the radial and ul-
nar bursae at the wrist, respectively. There is potential for commu-
nication between the synovial sheaths of the thumb and little fin-
gers, through either direct communication or rupture via the Space
of Parona in the distal forearm. The Space of Parona is a virtual
space between the pronator quadratus and the FDP tendons.
Pyogenic flexor tenosynovitis is an infection of the flexor ten-
don sheaths, which may complicate open injuries. Infection within
the thumb or little finger sheaths may rapidly progress to its con-
nected sheath counterpart (Fig. 2). Inoculation during open tendon
injury necessitates a thorough intra-operative assessment and all
wounds will require irrigation ahead of tendon repairs. Overt infec-
tion is a contraindication to tendon repair and staged debridement
and washouts will be required.
Verdan described five distinct zones along the entire flexor
tendon course, with zone 1 distal and zone 5 most proximal
(Fig. 3), with different implications for tendon healing and repair
[6]. Zone 1 lies distal to FDS insertion and includes only FDP within
the synovial sheath. Zone 2 extends from the insertion of FDS to
the proximal border of the A1 pulley, with the intimate arrange-
ment of FDS and FDP within the tendon sheath in this zone con-
O. Pearce, M.T. Brown, K. Fraser et al.
Fig. 3. Verdan’s flexor tendon zonal classification. Five zones of the digital flexors
(red lines) and three zones of the thumb (green lines) form the zonal classification
of flexor tendon injuries. Zone 1 is distal to FDS insertion on the middle phalanx.
Zone 2 is proximal to this up to the proximal border of the A1 pulley. Zone 3 is
between this and the distal margin of the carpal tunnel. Zone 4 represents the area
within the carpal tunnel. Zone 5 forms the area of flexor tendons proximal to this.
The thumb has three distinct flexor zones (green lines): zone Th1 is distal to the
interphalangeal joint (IPJ), zone Th2 is between the IPJ and MCPJ, and zone Th3 lies
between the MCPJ and carpometacarpal joint.
tributing to challenges for primary repair [7]. Zone 3 extends from
the proximal border of the A1 pulley to the distal margin of the
transverse carpal ligament and includes the origins of the lumbri-
cal muscles from each FDP tendon. Zone 4 represents the contents
of the carpal tunnel. Zone 5 covers the forearm proximal to the
carpal tunnel. The thumb has three distinct flexor zones: zone Th1
is distal to the IPJ, zone Th2 is between the IPJ and MCPJ, and zone
Th3 lies between the MCPJ and carpometacarpal joint. The specific
anatomical and management considerations for each zone will be
addressed later in this review.
Tendon structure & function
Macroscopically, healthy tendons are brilliant white and main-
tain a fibroelastic texture. Microscopically, tenoblasts and tenocytes
comprise 90-95% of the cellular volume, lying within an extra-
cellular matrix. The remaining cellular volume includes chondro-
cytes, and synovial and vascular cells. The extracellular matrix is
made of type 1 collagen and other extracellular components, pri-
marily synthetised by tenocytes, including glycoproteins and pro-
teoglycans (1-5%), elastin (2%), glycosaminoglycans and other acel-
lular elements. Collagen fascicles (comprised of multiple collagen
fibres) are enveloped in a thin connective tissue layer known as
the endotenon (type III collagen) (Fig. 4). This is formed from the
deep connecting extensions of the outer epitenon (type III colla-
gen) which is a loose connective tissue sheath within which vas-
cular, lymphatic and neural networks are present. Superficially, the
tendon is surrounded by a silky smooth ‘false sheath’ known as the
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Injury 52 (2021) 2053–2067
paratenon [8–11]. The epitenon and paratenon are together known
as the peritenon. The extrasynovial flexor tendons (zones III-V) are
surrounded by a filmy vascularized collagenous ‘microvacuolar’ or
loose areolar-like system, which aids tendon gliding and supports a
complex microvascular network [12]. Frictionless tendon gliding is
facilitated by proteoglycans, which bind directly onto collagen fib-
rils via glycosaminoglycan side chains. Tenocyte synthetic function
is both aerobic and anaerobic, a process that requires significantly
less oxygen when compared to skeletal muscle [13,14]. This low
oxygen requirement permits tendons to maintain load and tension
for prolonged periods in the absence of ischaemic damage. How-
ever, this results in slower tendon healing, especially when com-
pared to bone [15].
Tendons exhibit viscoelastic properties, including stress-
relaxation and creep, which is dependent on the relative content
of collagen, protein, water and proteoglycans [16,17]. Tendons
are highly deformable at low strain rates, which permits energy
absorption during prolonged mechanical loading. High strain rates
promote increased tendon stiffness facilitating the transmission
of explosive tensile forces from muscle to bone. Collagen fibrils
interdigitate with the deep myocyte recesses at the myotendinous
junction, which is the weakest zone of the muscle-tendon unit
[18–20].
Vascular Supply
Flexor tendon nutrition is provided by three different sources.
The vascular network of the tendon derives from vessels penetrat-
ing into the tendon at its extremities, the myotendinous junction
and bone-tendon interface (enthesis), and along its digital course
via the intrasynovial vincula system, or mesotenon (Fig. 5). This
vascular network corresponds to an “intrinsic” vascularity as de-
fined for other tendons. The intrinsic component most specific to
the long digital flexor tendons is the vincula system. The volar
branches of the digital arteries give rise to a vascular plexus that
reaches FDS and FDP tendons via a short (brevis) and long (longus)
vinculum to each. The vincula longa also have a practical implica-
tion for the repair of tendon divisions: the retraction of proximal
tendon stumps divided distal to the vincula will be limited within
the sheath, while tendons divided more proximally may retract fur-
ther proximal (the lumbricals also help prevent retraction). A sec-
ond, “extrinsic”, vascular contribution derives from blood vessels
penetrating into the peritenon from the surrounding areolar tissue
[12]. The extrinsic system is limited to the tendon segments out-
side the tendon sheath.
The long segments in which the tendon is physically separated
from surrounding tissues by the tendon sheath are relatively avas-
cular. These segments rely largely on a third source of exchange of
metabolites: diffusion from the synovial fluid [21]. The formal vas-
cular network within the sheath is predominantly dorsal. Without
an extrinsic contribution, this results in areas of relative hypoper-
fusion, which is further compromised at junctional zones, at areas
of torsion, friction or compression, and with advancing age [22,23].
The extensor tendons, by comparison, are without a synovial
sheath and receive extrinsic vascularity from paratenon vessels,
which penetrate the epitenon to run within the endotenon septa
for their entire length.
Tendon healing
Tendon healing occurs via sequential phases of inflammation
(first week), cellular proliferation (5 days – 4 weeks), and re-
modelling (months) (Table 1) [21]. Historically, tendon healing has
been attributed to intrinsic and extrinsic processes, with the rela-
tive contribution of each dependent on the presence of a synovial
sheath (i.e. zones 1 and 2), which supports extrinsic healing. This
O. Pearce, M.T. Brown, K. Fraser et al. Injury 52 (2021) 2053–2067

Fig. 4. Microscopic hierarchical structure of tendons. The tendon proper and fascicles are covered by a defined connective tissue sheath called the epitenon and endotenon,
respectively.

Fig. 5. Extrinsic blood supply to the flexor tendons. Radial and ulnar digital arteries supply a vascular plexus that travels within the short and long vincula. Flexor tendon
vascularity is predominantly dorsal.

Table 1
Tendon healing stages.

Stage Time Description

Inflammatory First week Inflammation is characterised by the immediate development of a fibrin clot while recruitment of neutrophils,
macrophages, platelets and erythrocytes facilitate neovascularisation and primary stabilisation of the tendon ends
within the zone of injury [32].
Proliferative 5 days – 4 weeks From approximately 1-4 weeks, fibroblasts mediate the synthesis of proteoglycans, type III collagen and other
extracellular matrix components [33]. Collagen organisation is disordered, and cellularity and water content increases.
From 21 days (week 4) longitudinal organisation begins, with fibroblast proliferation from the endotenon (intrinsic)
taking over collagen synthesis and resorption.
Remodelling Months to years From 6-8 weeks, decreased cellularity and matrix synthesis (including type III collagen) is accompanied by increased
type I collagen synthesis. Organised collagen forms longitudinal bundles along the tendon axis to increase tendon
strength [34].

dual theory oversimplifies the complex interplay of cells, matrix,
gene expression and growth factors; however, it provides a reason-
able baseline description [24,25].
The extrinsic response initially far outweighs the intrinsic re-
sponse in zones 1 and 2. In the hours and days following injury,
inflammatory cytokine chemotaxis attracts extrinsic cells from the
synovial sheath and other peritendinous tissues surrounding the
zone of injury, including fibroblasts and macrophages. They de-
posit type III collagen and organise granulation tissue, filling the
gap and providing biomechanical stability, respectively [26,27]. Ca-
nine models, including the landmark experiments by Lundborg
et al., have revolutionised our understanding of intrinsic healing

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O. Pearce, M.T. Brown, K. Fraser et al.
[28,29]. The specialised fibroblasts (tenocytes) from the epitenon
and endotenon, lead intrinsic tendon healing during the prolifer-
ative and remodelling phases through the synthesis, longitudinal
orientation and crosslinking of collagen fibrils. In general, intrin-
sic healing is associated with enhanced biomechanical outcomes,
whereas extrinsic healing contributes to adhesion formation [30].
Tendon repair aims to minimise extrinsic processes and maximise
intrinsic healing. Early post-operative mobilisation aims to coun-
teract adhesion formation and enhance intrinsic remodelling. Of
note, remodelling never achieves complete tendon regeneration or
‘normalisation’, with thinner collagen fibrils resulting in inferior
tendon strength and mechanical properties compared to the pre-
injury state [27,31].
Clinical evaluation
Suspected flexor tendon injuries require a thorough clinical as-
sessment and often are not isolated injuries. The history should
elicit general patient characteristics including age, handedness, oc-
cupation, hobbies, general health (including medications and aller-
gies), previous hand injuries and home circumstances (rehabilita-
tion is prolonged and restrictive). Always clarify the timing, loca-
tion and mechanism of injury, with penetrating or open injuries
requiring a judgement regarding soft tissue contamination. En-
quire regarding current symptoms and any changes since the in-
jury, including pain (location and nature), altered sensation (dis-
tribution) and functional deficits (loss of movement or disability).
If the patient has sought previous medical review (i.e. emergency
department) or if the presentation is delayed, ascertain treatments
received, including wound care, splinting, antibiotics and tetanus
status.
Apply the orthopaedic examination principles of look, feel and
move. Inspect for wounds, swelling, scars and asymmetry. Assess
the digital cascade: a resting injured digit that appears extended
compared to its neighbours suggests a complete FDP injury. Open
injuries necessitate an assessment of neurovascular status, soft tis-
sue viability or loss, and the risk of joint cavity and/or flexor
sheath inoculation. Palpate along the proximal path of the injured
tendon; tenderness proximal to the zone of injury commonly sug-
gests the level of tendon retraction in complete injuries. Assess the
vascular status by considering skin colour, temperature, turgor and
capillary refill time. Assess neurological status using light touch
and two-point discrimination.
Review the broad range and quality of tendon motion by asking
the patient to make a fist, assessing the tenodesis effect upon pas-
sive wrist motion, and, finally, examining FDP and FDS separately
in each digit. FDP is assessed through active DIPJ flexion range and
power whilst stabilising the middle phalanx in extension. FDS is
assessed by immobilising the neighbouring digits in full extension
(cancelling the effect of FDP) and asking the patient to flex the
digit: normal or partial injuries will permit MCPJ and PIPJ flexion.
Alternatively, ask the patient to flex PIPJ whilst stabilising the prox-
imal phalanx in extension: active PIPJ flexion with DIPJ extension
represents intact FDS function. Consider partial tendon injury with
painful active flexion, triggering or neurovascular deficits. FPL func-
tion is assessed by stabilising the proximal phalanx of the thumb
and asking the patient to flex at the IPJ. Pre-morbid limitations
to movement are assessed through passive motion. Remember to
compare suspected deficits with uninjured digits.
Little finger assessment is complicated by an absent FDS in 21%
of individuals, with right and left hand asymmetry existing in 26%
[35]. In addition, some individuals have a reduced active range of
movement of the little finger DIPJ. The Linburg–Comstock anomaly
describes a tendinous connection between FPL and FDP of the in-
dex finger, which may exist in 21% of patients [36]. On examina-
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Injury 52 (2021) 2053–2067
tion, active IPJ flexion of the thumb will cause simultaneous flexion
of the index finger DIPJ [37].
When the patient first presents, open contaminated wounds (or
those sustained in agricultural, aquatic, animal or sewage environ-
ments) should be cleansed in an antiseptic solution and appropri-
ate prophylactic antibiotic therapy should be commenced. Infected
wounds should be managed empirically, with wound swabs taken
for microbiological analysis before commencing antibiotics. Estab-
lish tetanus status and administer a booster if indicated by local
guidance. Supplementary clinical assessment should be achieved
with plain radiographs, ultrasound or magnetic resonance imag-
ing depending on the nature of the injury, particularly in blunt
trauma and closed injuries [38–42]. Plain radiographs help to ex-
clude concurrent fractures, avulsion injuries, joint dislocations and
pre-morbid joint pathology that may explain limited movement
range. Ultrasound facilitates a dynamic assessment, making it a su-
perior imaging modality.
General repair principles
Principles of flexor tendon repair include a strong suture con-
struct, minimising gap formation between tendon ends, preserving
tendon blood supply and providing a smooth repair interface. Ade-
quate exposure of the zone of injury using full-thickness skin flaps
and preservation of neurovascular and pulley structures is essen-
tial. Direct tendon handling with instruments should be minimised
to avoid iatrogenic injury, which predisposes to adhesion forma-
tion. Non-toothed forceps are used to grasp the cut ends of the
tendon at the radial or ulnar corners. Tendons that have retracted
from the zone of injury (due to muscle tone and delays) may be
secured ready for tension-free repair using a hypodermic needle
(e.g., 25 Fr gauge) once retrieved. The chosen approach should seek
to present the zone of injury and incorporate any skin lacerations
in the design of the incisions. A zig-zag Bruner incision is com-
monly used to approach the flexor tendons (Fig. 6) [43]. Less di-
rect digital access is afforded by the lateral approaches (mid-lateral
or mid-axial), which raise radial- or ulnar-based full thickness skin
flaps (Fig. 6) [44]. The mid-lateral and mid-axial approaches utilise
longitudinal skin incisions that run parallel, and volar or dorsal, to
the neurovascular bundles, respectively. A combination of the two
approaches can be used, especially when incorporating wounds.
Tendon stump retraction within the sheath may require distal or
proximal extension or secondary incisions to facilitate retrieval.
The strength of the repair is dependent on the choice of suture
material, number of core strands and repair techniques applied.
Traditionally, techniques involve a core suture augmented with
an epitendinous circumferential running suture. Suture choice and
technique help to minimise repair site elongation, or gap forma-
tion, which is a key detrimental factor to repair site integrity. Im-
mediately following tendon repair, Tang et al. recommends intra-
operative assessment using the ‘extension-flexion’ test: passive fin-
ger extension checks for gapping, moderate passive flexion con-
firms smooth gliding, and, finally, pushing the digit to almost full
flexion will permit assessment of sheath or pulley impingement
[45]. During the first 21 days post-repair, tensile strength remains
static, with ultimate tensile strength increasing significantly there-
after as the tendon remodels [46]. The in vivo canine study by Gel-
berman et al. demonstrated that healing of tendon repairs with no
gaps or gaps <3mm acquired strength six weeks post-repair and
that gaps >3mm did not accrue strength with time [46].
Suture Material
The optimal suture material for flexor tendon repair must be
easy to use and manipulate, minimise gap formation, maintain
O. Pearce, M.T. Brown, K. Fraser et al. Injury 52 (2021) 2053–2067

Fig. 6. Common surgical approaches to the flexor tendons. A. A traditional Bruner incision (dashed green line) provides a direct volar approach to the flexor tendons. Distally,
Bruner incisions should stop at the pulp centre to avoid scar sensitivity during pinch grip. Mid-lateral or mid-axial incisions may be combined with the Bruner (dashed blue
line), especially when incorporating wounds. B. The mid-axial longitudinal incisions (dotted yellow line) are sited parallel and dorsal to the neurovascular bundle (red line),
utilising the dorsal apex of the digital palmar creases during flexion (yellow dots). The mid-lateral incision (not shown) is sited at the mid-point between the volar and
dorsal surfaces (volar to the neurovascular bundle).

its tensile strength until intrinsic tendon strength is achieved,
and provide good biocompatibility to prevent immune-mediated
adhesion formation or granulomatous reactions. Non-absorbable
monofilament sutures are often used, including polypropylene
(Prolene®) angggggd nylon (Ethilon®). These synthetic monofila-
ment sutures should be manually stretched, or pretensioned, be-
fore use to prevent post-operative elongation and gap formation
[47]. Monofilament sutures, polypropylene in particular, have rela-
tively poor knot security and can be more difficult to handle due
to their inherent memory. Non-absorbable polyester (Ethibond® or
Ethibond Excel®) sutures are a braided alternative with high ten-
sile strength, superior knot security and no tendency to elongate,
but glide less and can be more difficult to evenly tension. Regard-
less of material, a non-cutting, or ‘taper point’, needle will avoid
the potentially catastrophic risk of cutting through buried suture
material.
Suture Configuration
Core sutures can be divided into three primary components:
longitudinal, transverse and link segments [48]. The link compo-
nent usually comes to lie outside the tendon (epitenon) and vari-
ably connects the longitudinal and transverse segments. Variations
in the link component (constructed as an arc, loop or knot) will
produce either a sliding grasping or locking suture configuration,
representing a hierarchy of increasing grip at the suture-tendon
interface. Locking configurations are favoured as they facilitate in-
creased transmission of axial tension and will impact repair sur-
vival and overall strength [49]. Non-grasping (sliding) techniques
(e.g. Bunnell) have anchor points which are aligned perpendicular
to the fibre orientation, and integrate a small portion of epitenon.
Grasping techniques (e.g. cruciate, most modified Kessler) include
non-closed suture loops (arcs) around the epitenon and tendon fi-
bres that loosely constrict the tendon substance on loading [50].
The Pennington repair is a further modification of the Kessler
technique that maintains a grasping (sliding) configuration; how-
ever, it utilises a loop link to provide increased tendon hold [51].
Locking techniques (e.g. Adelaide) possess closed loops that be-
have as a noose to more effectively anchor or trap the contained
fibres [52].
Core Suture
Numerous ex vivo studies have demonstrated that repair
strength is proportional to the number of strands crossing the re-
pair site, with studies consistently supporting a minimum of four
core suture strands [53–58]. However, high strand numbers con-
tribute to increased bulk and deformed repair zones leading to
increased friction during tendon excursion [58,59]. Overall repair
strength and resistance to gap formation is critically influenced
by increasing core suture purchase length (distance from the cut
tendon end to the core suture limb farthest away from the lacer-
ation site) and the use of higher calibre sutures [60,61]. Biome-
chanical studies support core tendon purchase of 7-10 mm with
dorsal suture placement (closer to the bone) [62,63]. The modi-
fied Kessler core suture technique is associated with less adhesion
formation on meta-analysis; however, many techniques remain

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O. Pearce, M.T. Brown, K. Fraser et al.
Fig. 7. Common suture techniques for core and epitendinous repair.
popular (Fig. 7) [57]. A 3/0 or 4/0 polypropylene (Prolene®), ny-
lon (Ethilon®) or polyester (Ethibond®) core suture may be reli-
ably used.
Epitendinous Circumferential Suture
Epitendinous circumferential repair aims to prevent gap for-
mation, reduce repair site bulk and may increase overall repair
2059
Injury 52 (2021) 2053–2067
strength by 10-50% [64,65]. Strength may be further increased with
suture purchase of 2-3mm from tendon ends and increasing the
depth of engagement [66,67]. A 6/0 polypropylene (Prolene®) or
nylon (Ethilon®) epitendinous suture is commonly used. The use
of a taper point needle is key to minimising the risk of accidental
damage to the core suture. Access can be optimised by complet-
ing the dorsal and volar epitendinous repairs before and after the
O. Pearce, M.T. Brown, K. Fraser et al.
core repair, respectively. Simple continuous or Silfverskiold suture
techniques are described (Fig. 7).
Flexor tendon repair
Partial tendon injury
The treatment of partial flexor tendon injuries remains contro-
versial. Concerns regarding untreated partial tendon injuries in-
clude complete rupture, symptomatic triggering and loss of excur-
sion. It remains common practice to manage injuries less than 50%
of tendon cross-sectional area with debridement alone [68]. Har-
iharan et al. reported that threshold load levels of partial tendon
injuries were higher than physiological loads experienced during
active motion, concluding that partial tendon injuries can with-
stand forces applied during active mobilisation rehabilitation [69].
In vivo suture repair of partial lacerations results in reduced tensile
strength, higher rates of rupturing, and inferior excursion proper-
ties when compared to non-sutured tendon [70–72].
Flexor tendon injuries less than 50% cross-sectional area may
be debrided or repaired with a running epitendinous suture to
avoid triggering [73]. Near complete injuries are managed similar
to complete lacerations, with core suture placement and a supple-
mentary running epitendinous suture. Therefore, partial tendon in-
juries undergoing suture repair should be protected and rehabili-
tated using the same active mobilisation regimes as for complete
repairs.
Two low volume prospective clinical studies have advocated a
conservative approach to partial tendon injury in zone 2, specifi-
cally. Wray et al. studied partial tendon lacerations with a median
cross-sectional area of 60%, demonstrating excellent function with
no reports of complete rupture. They concluded that partial in-
juries should not be repaired, and early active motion should com-
mence in the absence of ‘bevelling’ or ‘bunching’. A more recent
prospective study with 5-year follow-up further supported non-
repair of tendons with major injury (>50%), who replicated man-
agement principals recommended by Wray [68,74]. This included
exploration under digital block anaesthesia, pulley excision for im-
pingement, and chamfering of prominent tendon edges.
Complete tendon injury: Zones 1-5
Zone 1
Zone 1 injuries include only the FDP tendon, and can result
from either penetrating injuries or closed avulsions. Zone 1 avul-
sion injuries, or jersey finger, are relatively uncommon and presen-
tation is often delayed. They occur mostly in young adults when
the distal phalanx is subjected to forced extension during active
flexion [75,76], and can involve the enthesis alone or the avul-
sion of a fragment of distal phalanx with the tendon. The ring fin-
ger is the most commonly affected. Treatment is often challenging,
with reports suggesting variable outcomes [77]. Three main fac-
tors influence the prognosis of zone 1 injuries, including length
of diagnostic delay, characteristics of the avulsed bone fragment
and, most importantly, the degree of proximal stump retraction
and subsequent disruption to the vincula vascular system. The de-
gree of retraction influences the overall management of avulsion
injuries and may be referenced according to the Leddy and Packer
classification (Table 2) [78].
Although early repair is preferred for all flexor tendon injuries,
Leddy and Packer type 1 injuries require surgical repair within
three weeks due to the risks of tendon devascularisation (vincula
system disruption), pulley collapse and fibrosis, and muscle con-
tracture preventing advancement. Type 2 and 3 injuries may be
treated up to three months with good results. Type 3 may be
treated with K-wire or mini screw and/or plate fixation [82]. Type
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Injury 52 (2021) 2053–2067
Fig. 8. Moiemen & Elliott sub-classification of zone 1 flexor tendon injuries.
4 injuries were recognised separately, and fracture fixation usually
precedes tendon repair. In some cases, it may be necessary to ex-
cise small bone fragments [79,80]. Type 5 represents a FDP avul-
sion with an attached bone fragment combined with a concomi-
tant significant fracture of the distal phalanx [81].
Zone 1 pure tendinous lacerations have been classified by
Moiemen and Elliot into three subtypes: type 1a occur distal to
the A5 pulley, type 1b occur between the distal edges of the A4
and A5 pulleys, and type 1c occur beneath the A4 pulley (Fig. 8)
[77]. Type 1a lacerations are not amenable to core suture repair
and are managed like avulsion injuries. Type 1b and 1c injuries
can be repaired with conventional suture techniques. Moderate re-
pair bulk is acceptable in zone 1 and some authors suggest direct
repair with many more core sutures to maximise tensile strength
[45].
For injuries not amenable to tendon-to-tendon repair, either
closed avulsions or Moieman and Eliot type 1a injuries, external
and internal anchoring techniques have been described. First re-
ported by Bunnell, the pull-out button external fixation technique,
involves placement of a proximal stump core suture (e.g. 4-strand),
which is passed through the distal phalanx and nail plate via paral-
lel transosseous tunnels [83–85]. The monofilament suture is ten-
sioned and secured to the tendon stump prior to transosseous pas-
sage, and tied externally over a plastic button (Fig. 9). Alternatively,
the sutures may be passed around the distal phalanx to avoid vi-
olating bone. At 6-8 weeks the button is removed and the suture
material is pulled out. Polypropylene sutures are the most easily
removed, but a higher number of knots is advisable. Some authors
report high complication rates with the pull-out technique, includ-
ing infection (22%), nail fold necrosis, nail plate deformity (35%)
and DIPJ stiffness [86]. Complications can be minimised by placing
the nail plate exit point well distal to the lunula and using a small
button with the convex surface in contact with the nail. Alterna-
tively, the nailbed can be avoided entirely using a coronal osseous
tunnel [87,88].
Internal fixation techniques avoid bulky external constructs and
broadly involve 2- or 4-strand trans-osseous or multi-strand bone
anchor fixation [88–92].
Advances in bone anchor design make them an attractive al-
ternative to the pull-out technique. Anchor fixation is associated
with reduced rates of infection, nail deformity, and an earlier re-
turn to work [93]. The FDP is secured to its footprint using a mod-
ified Bunnell or Becker suture technique. The cadaveric study by
Brustein et al. identified greater load to failure when using two
Mitek micro QuickAnchor® anchors (4-strand repair with 4/0 Ethi-
bond) when compared to a single Mitek mini anchor (2-strands).
Four-strand repair with two anchors was also stronger than 2-
strand repairs with a pull-out suture [94]. Retrograde anchor place-
ment angled towards the DIPJ may be employed; however, load to
failure is not affected [95]. Care should be taken to avoid dorsal
cortex violation (to protect the nail matrix), with retrograde an-
gulation (45 degrees) recommended in the little finger [96]. Fluo-
roscopy may be used to confirm anchor position. The anchor tech-
nique might have higher failure risks in osteoporotic bone, and be
O. Pearce, M.T. Brown, K. Fraser et al. Injury 52 (2021) 2053–2067

Table 2
Leddy & Packer classification of zone 1 FDP avulsion injuries.

Type Level of Retraction Blood Supply

Type 1
Palm Disruption of vinculum
longus and brevis

Type 2
Level of A3 pulley (PIPJ) Vinculum longus intact

Type 3
Level of A4 pulley (DIPJ). Large Vincula both intact
avulsion fracture limits retraction.

Type 4 [79,80]
Variable retraction within pulley Variable
system or palm. Large avulsion
fracture detached from retracted
FDP.

Type 5 [81]
Level of A4 pulley (DIPJ). Avulsion Variable
fragment with concomitant distal
phalanx fracture.

2061
O. Pearce, M.T. Brown, K. Fraser et al.
Fig. 9. Pull-out and internal fixation techniques for zone 1 injuries. A| Bunnell pull-out suture button technique. B| Internal fixation with distal phalanx bone anchors (usually
two).
contraindicated in avulsions of large fragments or distal phalanx
fractures.
Zone 1 tendon repairs risk FDP overtightening and advance-
ment. Advancement greater than 1cm risks significant flexion con-
tracture or a ‘quadrigia’ effect on the intact FDP tendons [97].
Quadrigia is a flexion lag in digits neighbouring a shortened FDP,
affecting the middle, ring and little fingers, which are connected
by a common muscle belly.
Zone 2
Bunnell (1948) once referred to this unforgiving zone as ‘no
man’s land’ due to the higher risk of post-operative tendon ad-
hesions and stiffness [98]. In recent decades, outcomes follow-
ing zone 2 repairs have improved significantly with advances in
repair technique, suture material and early controlled rehabilita-
tion regimes. For complete FDP and FDS zone 2 injuries, dual re-
pair may cause overcrowding, which risks triggering, adhesion for-
mation, reduced excursion and increased rupture rate [99–103].
Therefore, three operative strategies exist: (1) repair of FDP alone
with debridement of the FDS stump; (2) repair of FDP and a sin-
gle slip of FDS; (3) repair of FDP and both FDS slips. If both FDS
and FDP are repaired, it is essential to avoid malrotation and re-
store the correct anatomical relationship between both tendons.
The level of FDS injury relative to the A2 pulley often dictates the
repair strategy. If repair of both slips encroaches on the A2 pul-
ley, one or both slips may be excised. If the repair is proximal to
slip decussation, and does not encroach on A2 during excursion,
2-strand FDS core suture repair is appropriate. Partial division, or
venting, of the A2 pulley (up to 50%) and A4 (up to 100%) does not
substantially increase the work of flexion and can permit improved
access and prevent triggering [104,105].
Zones 3-5
More proximal zones receive little attention in the literature.
Surgical concepts of optimal tendon repair described previously
can be applied to tendon injuries within these zones. Concurrent
injury of adjacent neurovascular structures including the super-
ficial palmar arterial arch (zone 3), median nerve (zone 4) and
proximal neurovascular structures within the forearm of zone 5
may complicate post-operative rehabilitation. Furthermore, zone
3 includes the lumbrical origins along FDP, thus risking flexor-
lumbrical adhesions. Zone 3 triggering may warrant a preventive
A1 pulley release.
Flexor Pollicis Longus
Complete zone 1 and 2 FPL injuries are frequently associated
with early proximal stump retraction, found either deep to the
thenar musculature or within the carpal tunnel. The FPL has no
lumbrical to help limit retraction. Historically, zone 2 rupture rates
were highest in the thumb, approaching 8% in studies reviewing
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Injury 52 (2021) 2053–2067
Table 3
Boyes pre-operative injury classification for tendon grafting.
Grade Description
1 Good: minimal scar, supple joints, no trophic changes
2 Cicatrix: scar limiting gliding of graft (heavy skin scarring or
deep scarring from failed primary repair or infection)
3 Joint damage: loss of passive joint motion
4 Nerve damage: digital nerve injury with trophic changes
5 Multiple damage: multiple fingers with combination of above
2-strand core repair [106,107]. Significant improvements have ac-
companied the adoption of 4-strand repairs [107]. Of note, the FPL
is relatively avascular at the level of the MCPJ which might con-
tribute to increased rupture rates (i.e. within zone 2) [108]. The
retrieval of retracted tendons may be aided by proximal-to-distal
massage, passive thumb and wrist flexion, gentle pulley dilatation
or venting and secondary incisions at the carpal tunnel or distal
forearm. Distal passage may be aided by using a tendon passer or
a paediatric feeding tube [109].
Special consideration: Single- or two-stage tendon reconstruction
Single-stage free tendon graft reconstruction may be required
for segmental tendon loss or delayed presentations (i.e. >4 weeks
post-injury when retraction impedes primary repair). If the tendon
stumps almost approximate, consider tendon lengthening (i.e. Le
Viet lengthening within the muscle) [110]. A single small diameter
primary palm-to-fingertip graft is sometimes performed for FDP or
combined FDS and FDP injuries in zone 2, which avoids repair bulk
within the most unforgiving section of the pulley system by posi-
tioning the repairs outwith [111]. The graft is secured distally us-
ing established zone 1 techniques and proximally using a weave
technique (i.e. Pulvertaft) after tensioning. Prerequisites for single-
stage reconstruction include mobile joints with full passive mobil-
ity and no wound or joint contractures, an intact flexor pulley sys-
tem with a minimally scarred or contaminated bed (i.e. no infec-
tion), no neurovascular impairment (Boyes’ grade 1) and a patient
who is willing to cooperate with post-op rehabilitation [112,113].
Boyes outlined these prerequisites in his classification for tendon
grafting, with grades 2-5 often managed with staged reconstruc-
tion (Table 3).
Two-stage reconstruction options include the Hunter-Salisbury
(donor graft) technique and, less frequently, the modified Paneva-
Holevich (remnant FDS transposition) technique [114,115]. Both
techniques involve a first stage comprising debridement of the in-
jured tendon (maintaining a 1cm distal FDP stump if possible) and
placement of a temporary flexible silicone rod spacer in the space
of the obliterated sheath to develop a smooth gliding bed, or pseu-
dosheath. The silicone rod is sutured distally to the FDP stump to
prevent migration and should extended proximally into the palm
or distal forearm. If bowstringing occurs during flexion, the pul-
O. Pearce, M.T. Brown, K. Fraser et al.
leys, A2 in particular, are reconstructed. Additionally, the modified
Paneva-Holevich first stage requires the proximal tendon stumps
of FDS and FDP of the injured digit to be sutured together in
the palm to create a loop (4-strand end-to-end repair). Immedi-
ate post-operative rehabilitation maintains joint mobility. A min-
imum of three months between stages helps to optimise move-
ment range and scar maturity that reduce the risks of stiffness and
tendon rupture, respectively. The Hunter-Salisbury second stage in-
volves extrinsic free tendon graft placement, with donor options
including palmaris longus, plantaris, extensor indicis proprius, ex-
tensor digiti minimi, or extensor digitorum longus to the second
toe. The distal and proximal repair techniques are performed sim-
ilarly to those used in single-stage reconstruction. The modified
Paneva-Holevich second stage involves loop retrieval, cutting the
FDS tendon proximally at its musculocutaneous junction, and tun-
nelling it up through the pseudosheath to the remnant FDP stump
[115]. Regardless of technique, a post-operative early active reha-
bilitation protocol should follow.
Flexor rehabilitation
An ideal rehabilitation protocol promotes intrinsic tendon heal-
ing, minimises adhesion formation and optimises tendon glide to
restore a functional range of movement without significant forces
which could compromise the repair [116,117]. Irrespective of the
rehabilitation protocol, post-operative rupture rates can approach
4-6% [118–121]. Appropriate rehabilitation and compliance to ther-
apy have a significant impact on repair outcomes. Communication
between the surgeon and the hand therapist is essential, with doc-
umentation of zone of injury, repair quality and number of core
strands helping to guide therapy. Underlying fractures, significant
soft-tissue injuries and neurovascular repair may also influence de-
cision making.
Exercise regimes can be categorised into controlled passive
motion, place and hold, and controlled active motion. There re-
mains no absolute consensus or ‘gold standard’ regarding optimal
mobilisation strategy [122]; however, advances in surgical repair
techniques and materials have allowed rehabilitation protocols to
evolve towards early active mobilisation (EAM) [123–128]. All pro-
tocols aim to manage oedema and wound integrity. We present an
overview of historic and contemporary rehabilitation strategies.
The degree of tendon excursion (glide distance) to prevent ad-
hesion formation is 1.7 to 3.5mm [46,129]. Although this can be
achieved with passive rehabilitation protocols, active flexion con-
fers additional mechanical strength [72]. Tendon tensile strength
remains static within the first three weeks of repair, while re-
pair site rigidity increases [72]. During post-operative days 1-4 the
resistance to gliding is increased secondary to increasing tendon
oedema, which resists smooth tendon gliding [130]. Therefore, re-
habilitation is commonly commenced on day 3-5 post-repair. The
different flexor rehabilitation protocols are unified by use of a
dorsal blocking splint, or hood, to minimise excessive extension
and repair site tension (Fig. 10). Traditional forearm-based splints
span the wrist and permit minimal or no active wrist extension
[131–134]. Originally supporting the wrist in flexion, splints have
evolved past neutral and towards wrist extension. Splints support
the MCPJs in flexion (30-45 degrees) and provide space to permit
full IPJ extension. Young children unable to adhere to protected re-
habilitation protocols (i.e. up to 5 or 6 years of age) are immo-
bilised in digital flexion for up to 4 weeks.
Passive motion regimes, including the Duran & Houser and
Kleinert protocols, were developed in the 1970s when 2-strand re-
pairs were standard practice [125,135]. Despite modifications, they
have limited capacity to preserve differential glide of FDS and FDP
within zone 2, which may explain greater adhesion formation and
compromised function [136]. The original Duran & Houser and
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Injury 52 (2021) 2053–2067
Fig. 10. Dorsal blocking splint, or ‘hood’. This traditional splint immobilises the
wrist in neutral or slight extension.
modified Duran protocols comprised controlled passive MCPJ, PIPJ
and DIPJ mobilisation [135,137]. The Kleinert protocol combines ac-
tive extension against rubber band resistance and passive flexion
through band recoil. Disadvantages of the Kleinert protocol include
the complex splint design and the risk of PIPJ flexion contractures
due to prolonged resting flexion [138]. Although rarely used in iso-
lation, the passive Duran exercises can support modern EAM pro-
tocols to achieve the extremes of movement.
EAM is considered routine for robust minimum 4-strand pri-
mary repairs in compliant patients [139]. Patient understanding,
motivation and compliance is key, whilst minimal swelling, soft-
tissue trauma and confidence in the repair are prerequisites [140].
Active motion should initiate from the DIPJ and progress through
the PIPJ to the MCPJ (restricting to the PIPJ alone will prevent dif-
ferential FDS and FDP glide). EAM was first developed in Belfast,
United Kingdom, for zone 2 repairs with active IPJ flexion starting
48 hours post-repair [141]. Emphasis was placed on DIPJ motion to
achieve differential tendon glide [141–143]. The early Belfast proto-
cols used a Kleinert-type splint (without rubber bands) to support
the wrist and MCPJs in flexion. Multiple modifications, including
supporting the wrist in extension, have contributed to heteroge-
neous contemporary EAM regimes.
A subcategory of EAM is ‘place and hold’ (or ‘active hold’) that
combines passive and active flexion and utilises the digital ten-
odesis effect seen with wrist movement [144]. Although it may be
used to support EAM protocols, it has otherwise fallen from favour
for flexor rehabilitation [145]. It is a popular early regime for other
hand injuries, including fracture rehabilitation. The exercise regime
is repeated hourly, as follows: (1) passive digital flexion to make a
fist combined with active wrist extension in the splint, (2) active
digital flexion to half a full fist (position held for a short period,
e.g. five seconds), and, finally, (3) active wrist flexion combined
with active digital extension. Full composite flexion is avoided as
this puts additional strain on the repair site [145].
The Manchester short splint EAM regime has gained popular-
ity for zone 1 and 2 repairs (excluding FPL) [146]. The Manchester
short splint permits unlimited wrist flexion and extension up to
45 degrees, which increases passive digital tendon excursion and
improves differential tendon gliding and DIPJ flexion arcs (Fig. 11)
[146]. MCPJ extension is limited to 30 degrees. In 1988, Savage
identified 45 degrees of wrist extension to be the optimal posi-
O. Pearce, M.T. Brown, K. Fraser et al.
Fig. 11. The Manchester short splint. This splint permits active wrist movement up
to 45 degrees extension.
tion for minimising the work of digital flexion for active regimes.
Peck et al. compared the Manchester short splint and traditional
forearm-based splints for zone 2 repairs (FDS and FDP) managed
with early passive and active motion and identified improved IPJ
flexion arcs at 12 weeks with the short splint (median 59 de-
grees versus 30 degrees; p<0.001) with no increased risk of rup-
ture [146]. From our experience, non-compliant patients, or those
unable to follow instruction, tend to fair better with the Manch-
ester short splint as it permits some hand function.
Rehabilitation of FPL repairs requires a dorsal forearm-based
splint, which often combines neutral wrist alignment, car-
pometacarpal joint abduction, MCPJ flexion (e.g. 20 degrees) and
a neutral IPJ to permit full extension. The splint is maintained
both day and night for six weeks with gradual weaning between
6-8 weeks. Zone 5 wrist flexor repairs (flexor carpi radialis and ul-
naris) are protected with dorsal wrist splintage (neutral) with no
digital restrictions until removal at six weeks.
Patients will often enquire regarding return to work, activities
of daily living, driving and recreation, including sports. Return to
light work (e.g. typing, administration, driving) or moderate work
(e.g. chef, hairdresser, cleaner, waiter) can be expected from 8-
10 weeks post-repair. Beyond 12 weeks a graded return to heavy
manual work (e.g. scaffolder, builder) or contact sports (e.g. rugby,
football, horse riding, sailing, racket sports) and unlimited hand
use is usually permissible. For FPL repairs, delaying these time-
frames by a further two weeks is often deemed sensible.
Discussion
Flexor tendon repair outcomes continue to improve as mate-
rials, techniques and rehabilitation protocols advance. In vivo and
ex vivo studies are fundamental to our understanding of tendon
physiology and for comparing management strategies. The devel-
opment of sutures with far greater tensile strengths may provide
future innovation [147,148]. Reporting outcomes following flexor
tendon repair should extend beyond mechanical indicators such
as rupture rate, movement range and grip strength, to include pa-
tient recorded outcome measures (PROMs) [149]. Commonly used
hand surgery PROMs include the Disabilities of the Arm, Shoulder
& Hand (DASH) questionnaire and the Michigan Hand Outcomes
Questionnaire (MHQ). Both are validated but neither are disease
2064
Injury 52 (2021) 2053–2067
specific. This article has endeavoured to provide an overview of
contemporary management strategies. Today’s hand surgeons and
therapists can choose from a variety of treatment options when
managing these important and potentially life-changing injuries.
CME Learning points
- Partial tendon lacerations <50% are commonly managed with
debridement alone. Partial lacerations >50% may be managed
with epitendinous repair to avoid triggering (+/- core repair).
Near complete lacerations are managed with core and epitendi-
nous repair.
- Minimise tendon handling with instruments to reduce the risk
of adhesions and optimise tendon healing.
- Zone 1 avulsion injuries are closed and often present late. They
are classified according to the Leddy and Packer classification.
- Zone 1 lacerations not amenable to primary end-to-end repair
may be secured using two micro suture anchors or traditional
pull-out button techniques. Anchors are associated with a re-
duced risk of infection and nail complications, and an earlier
return to work.
- Zone 2 injuries should be managed with core sutures (min-
imum 4-strands) and a running circumferential epitendinous
suture. Partial division of the A2 and A4 pulleys (up to 50%
and 100%, respectively) can permit improved access and pre-
vent triggering.
- Early active mobilisation (EAM) rehabilitation starting from 3-5
days post-repair increases the mechanical strength of the repair,
prevents adhesion formation and optimises movement range.
- The Manchester short splint is a popular contemporary EAM
protocol for zone 1 and 2 repairs.
- Tendon reconstruction using single-stage or two-stage (e.g.
Hunter-Salisbury technique) is indicated for delayed presenta-
tions or injuries with segmental tendon loss and/or tissues of
poor quality.
Conflict of interest
Authors confirm no conflicts of interest
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