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Intrinsic Anatomy
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Intrinsic Anatomy
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Language: EN.
Segment:0 .
PAUL C. DELL: The objectives of this presentation are to review the anatomy of extrinsic and intrinsic musculature of the hand as well as mechanisms of action. Also included are intrinsic related to pathology such as boutonniere
PAUL C. DELL: swan necks, describe provocative positions to evaluate dysfunction such as ulnar plus ulnar negative. We have borrowed liberally from Richard J Smith's landmark article on intrinsic anatomy, which was published in the AAOS instructional course lectures, volume 24, 1975. I would encourage everyone to read this article several times during their residency.
PAUL C. DELL: The extrinsic extensors are organized in six dorsal compartments. The EDC's, which we are particularly focused on are in the fourth compartment. As the EDC's approach the metacarpophalangeal joint, there are oblique fibers that come off at about a 30 to 45 degree angle.
PAUL C. DELL: These are typically arising from the ring finger spanning out to the adjacent, middle and small. These are the juncturae tendinae. The index does not have a juncturae tendinae. There are some transverse fibers that are loosely connected, which are called the superficial transverse fascia. The juncturae tendinae stabilize the metacarpal, stabilize the dorsal hood over the MCP joint during flexion.
PAUL C. DELL: There are seven interosseous muscles in the hand, four dorsal, which are principally involved in abduction of the fingers and three volar, which are principally adductors of the fingers. These seven muscles are principally innervated by the ulnar nerve. The exceptions are, if there is a median to ulnar anastomosis either in the forearm, which is called Martin Gruber or in the hand called [?].
PAUL C. DELL: The first, second and fourth dorsal interossei have two bellies which arise from adjacent metacarpals. The deep belly passes superficial to the sagittal bands and inserts on the dorsal hood. So the function of the deep belly is not only to flex the MCP joint, but it can also extend the PIP joint.
PAUL C. DELL: The superficial belly, on the other hand, passes deep to the sagittal bands. It inserts on the tubercle of the proximal phalanx so that its function is principally an abduction. It does not contribute to the hood, so therefore it cannot extend the PIP joints. There are some variations to the dorsal interossei.
PAUL C. DELL: First of all, in the first dorsal interosseous, the superficial belly which can be seen with a red arrow is the principal muscle belly. It is much bigger than the deep, deep belly. Why is that? Because it is to provide abduction strength of the index finger to resist the thumb.
PAUL C. DELL: The third dorsal interosseous, which is on the ulnar side of the middle finger, has only a single muscle belly. This inserts onto the dorsal hood. It has no insertion on the bone so that there's little contribution to abduction of the middle finger. This muscle is primarily an extensor of the PIP joint.
PAUL C. DELL: The little finger actually doesn't have a dorsal interosseous. There is a volar interosseous that attaches to the radial side. On the ulnar side, however, the abductor Digiti Quinti replaces the interosseous and is the lateral band on, on that on the medial side of the little finger.
PAUL C. DELL: There are three volar interossei. They also originate from contiguous metacarpal shafts. They lie superficial to the sagittal bands and insert onto the dorsal hood as the lateral bands. They are extensors primarily of the IP joints.
PAUL C. DELL: In summary, there are seven dorsal and volar interossei. Most dorsal interossei have two muscle bellies have two functions. The third dorsal interosseous and the three volar interossei have a single belly, single insertion and single function. The lumbricals are very unique muscles.
PAUL C. DELL: They originate on their antagonists, the flexor digitorum profundus and insert on the radial aspect of the, of each dorsal hood. They can initiate MCP joint flexion, which is controversial, but they are said to be the, the workhorse of the intrinsics and are primarily extensors of the IP joint independent of MCP joint position.
PAUL C. DELL: This is a classic illustration from Dick Smith's article, the, it shows that there's an interplay between the intrinsic and extrinsic musculature that sometimes blends together. We will try to break this apart in the next few slides. As the EDC passes over the metacarpophalangeal joint, transverse fibers can be seen arising from the edge of the tendon to insert on the sagittal on the volar plate as the sagittal bands.
PAUL C. DELL: The sagittal bands are the extensor mechanism of the MCP joint. They also stabilize the EDC tendon over the joint during flexion. Immediately adjacent to the sagittal bands are the transverse fibers. These are fibers that arise from the intrinsic tendon on either side of the finger.
PAUL C. DELL: They arch over the EDC and flex the finger. That is, they flex the MCP joint. So immediately adjacent to each other are the extensor and flexor mechanisms of the MCP joint, hence the term dorsal hood. So diagrammatically you can appreciate that the EDC extends the MCP joint through the sagittal bands.
PAUL C. DELL: This is extrinsic function. The intrinsic function is demonstrated by the transverse fibers. These flex the MCP joint. Beyond the transverse fibers, the intrinsic mechanism continues as the oblique fibers, the oblique fibers, as they pass more distally, bifurcate into medial bands and lateral bands.
PAUL C. DELL: The medial bands continue to the dorsum of the proximal phalanx where they aid in PIP joint extension through the central slip. The lateral bands continue to distally to form part of the conjoined lateral band. As the intrinsics are bifurcating, the extrinsic EDC is trifurcating over the dorsum of the proximal phalanx.
PAUL C. DELL: The trifurcation includes the central slip and two lateral slips. The central slip continues distally to form the central slip to extend the PIP joint. The lateral slips combine with the intrinsic tendon to form the conjoint lateral band.
PAUL C. DELL: Nomenclature often gets confusing when determining the various structures of the dorsal hood. The lateral bands are the oblique fibers of the dorsal apparatus, which are an extension of the intrinsic tendon. The central slip, the extensor mechanism of the PIP joint is a combination of extrinsic and intrinsic fibers.
PAUL C. DELL: The conjoined lateral bands are a merging of the extrinsic and intrinsic tendons. They form at the level of the PIP joint and continue distally to form the terminal tendon. The terminal tendon inserts at the dorsal base of the distal phalanx, extends the DIP joint through its attachment.
PAUL C. DELL: There's a thin fascial triangular shaped ligament that is just distal to the central slip that is just distal to the PIP joint. The triangular ligament maintains the conjoined lateral bands in a dorsal position. As the PIP joint flexes and extends, there is a 3 to 4 millimeter excursion of the conjoined lateral band.
PAUL C. DELL: The triangular ligament maintains the conjoined lateral band dorsally. To maintain the proper positioning of the conjoined lateral bands, there is another structure called the transverse retinacular ligament, which arises on the volar edge of the band. It inserts on the flexor tendon sheath.
PAUL C. DELL: The function of the transverse retinacular ligament is to maintain the conjoined lateral bands in a volar position to prevent dorsal subluxation. The oblique retinacular ligament or landsmeer ligament is a link ligament between the PIP and the DIP joints. It originates on the volar aspect of the proximal phalanx and inserts on the distal phalanx
PAUL C. DELL: dorsally. The function is an active tenodesis so that as the PIP joint extends, the oblique retinacular ligament starts, initiates extension at the DIP joint through an active tenodesis. The test for oblique retinacular ligament tightness is to evaluate passive flexion of the DIP joint relative to the position of the PIP joint. On the left,
PAUL C. DELL: the PIP joint is flexed, the ligament is relaxed, the DIP joint flexes fully, passively. On the right, the PIP joint is extended, there is increased tension on the ligament. The DIP joint passively cannot be flexed. This is an example of tightness of the oblique retinacular ligament.
PAUL C. DELL: Cleland's ligament, not a part of the intrinsic mechanism, are part of dermatofascial fibers that run between the skeleton and the skin. They help stabilize the skin as the joint is flexing, they run the full length of the finger, are mostly condensed near the flexion creases of the IP joint.
PAUL C. DELL: Dorsal to the neurovascular bundle are Cleland's, volar to the neurovascular bundle are Grayson's ligaments. Intrinsic tightness is a common cause of hand impairment after trauma. Causes are typically from swelling. The, the muscle, the intrinsic muscles become fibrotic or they go into spasm and they become tight.
PAUL C. DELL: Other examples are stroke or paradoxical extension to be discussed later. The intrinsic tightness test, originally described by Finochietto in 1920, is a comparison of passive PIP joint flexion with varying degrees of MCP joint extension. With the MCP joint extended,
PAUL C. DELL: the intrinsic tendon, which is volar to the axis of the MCP joint, is on stretch. Therefore, its contribution to the dorsal hood is going to be tight. If there's intrinsic tightness, then passively the PIP joint will be limited when the MCP joint is held in extension. Obviously the, there has to be full passive motion of both joints to successfully do this test.
PAUL C. DELL: If there is intrinsic tightness that fails to respond to non-operative care, which includes therapy stretching program, then there's a simple procedure to weaken the intrinsic mechanism on the ulnar aspect. The oblique fibers of the hood are excised under local anesthesia through a dorsal incision. The patient is then actively allowed to flex with the MCP joint in extension and in flexion.
PAUL C. DELL: Swan neck deformity of the finger is a clinical diagnosis with many different etiologies. Probably the most common is mallet finger that's undertreated, other causes are listed in the slide. We see this frequently with intrinsic tightness or EDC subluxation. Common to all causes are dorsal subluxation of the conjoined lateral band.
PAUL C. DELL: There is attenuation of the transverse retinacular ligament, there is contracture of the triangular ligament which maintains the conjoined lateral band dorsally and prevents them from laterally and volarly displacing as the finger tries to flex. The nail buff, Edward nail buff has an excellent classification, which starts with a swan neck that is asymptomatic and is a clinical presentation to one that is stiff and doesn't flex at all with a distorted joint.
PAUL C. DELL: Obviously treatment is dependent upon the various stage that you, your patient presents in. Boutonniere deformity is the opposite of swan neck. It occurs when the conjoined lateral bands have subluxated volar to the axis of the PIP joint so that the triangular ligament is attenuated, the transverse retinacular ligament is contracted, maintaining the bands in a volar displacement.
PAUL C. DELL: In the full blown boutonniere,
PAUL C. DELL: there is hyperextension of the DIP joint because of the, the pathologic course of the band. The most common causes are central slip rupture, but many times is seen when there's a chronic PIP joint flexion contracture. Why does this happen? Because the central slip is very thin and can be attenuated very quickly. Lumbrical plus is a very distinct form of intrinsic tightness, remembering that the lumbrical originates on the profundus.
PAUL C. DELL: If there is rupture of the profundus such as you would see with a Jersey finger or with a DIP joint disarticulation, the profundus retracts proximally. The resting tension in the lumbrical muscle and tendon is then increased. When the patient goes to make a fist, the, the FDP glides more proximally,
PAUL C. DELL: there's more tension on the lumbrical and there is what has been called paradoxical extension. Most of the time you do not see paradoxical extension, but you do appreciate the lack of PIP joint full flexion because of the increased tightness in the lumbrical tendon. Intrinsic minus hand results from ulnar nerve chronic compression or from ulnar nerve laceration.
PAUL C. DELL: The fingers become asynchronous, so they're not able to flex simultaneously at the MCP joint and IP joint. The claw deformity has developed because of paralysis of the intrinsics. You've lost your main flexor of the MCP joint and the main extensor. There's loss of pinch strength because the thumb is also compromised as the adductor is innervated.
PAUL C. DELL: So ulnar nerve palsy is characterized by a claw deformity, intrinsic wasting, Wartenberg and flattened palmar arch. To understand claw deformity of the fingers, typically it's ring in small, there is an a imbalance between the EDC, which is radial nerve innervated. The intrinsic musculature, which is the flexor of the MCP joint, is deficient
PAUL C. DELL: so the MCP joint assumes a extended position. At the PIP joint, the ulnar nerve deficiency is manifest as intrinsic absence, so no extension at the IP joint, but the FDS is still intact so the finger assumes a flexed position. Now if the FDS is denervated such as in a median nerve associated injury, then the clawing is going to be significantly less because the the the malalignment will be just at the MCP joint and it will not be as profound.
PAUL C. DELL: So we talked about the claw deformity as a as an imbalance of muscle at the MCP and PIP joint levels. Another way of understanding it is that the hyperextension created by unopposed pull of the EDC renders slight laxity in the dorsal hood overlying the proximal phalanx. If that occurs, then there's not enough tension at the central slip to extend the PIP joint.
PAUL C. DELL: Remembering that the extrinsic extensor has contributions to the central slip, that extension is compromised because of the hyperextension deformity at the MCP joint. Therefore, many of our surgical procedures are to rebalance the the tension in the dorsal hood by blocking hyperextension at the MCP joint.
PAUL C. DELL: Bouvier Maneuver evaluates whether the central slip is intact. As we talked about previously in long standing flexion contractures of the PIP joint, the central slip, which is relatively thin, can be attenuated. The same thing can happen with a long standing ulnar nerve claw deformity. If the central slip is attenuated when you block hyperextension of the MCP joint,
PAUL C. DELL: the IP joint will not be able to extend. This maneuver shown in these slides shows the hyperextension of the MCP joint being blocked passively. The patient is then asked to actively extend the PIP joint. If the PIP joint central slip is intact, then this is a negative Bouvier Maneuver.
PAUL C. DELL: Wartenberg sign is simply a muscle tendoness imbalance. The extensor digiti quinti inserts on the ulnar aspect of the dorsal hood of the small finger. If the volar interosseous is out on the radial side, then the EDQ has is unopposed and will produce an abduction of the little finger.
PAUL C. DELL: The, if this is persistent, it can be easily corrected by taking the EDQ off of the ulnar aspect, passing it underneath the intermetacarpal ligament, inserting it on the radial side to negate the abduction force. These images show the result of a long standing ulnar nerve injury. The first dorsal interosseous is wasted.
PAUL C. DELL: The intermetacarpal interosseous are non-visible, not visible. The little finger is abducted. On the right side, you can appreciate loss of the hypothenar eminence as well as flattening of the arch of the of the hand. With paralysis of the adductor pollicis,
PAUL C. DELL: there is a substitutional pattern characterized by utilization of the flexor pollicis longus instead of the adductor. The test is done by asking the patient to hold a piece of paper between their thumb and their index finger with the IP joint extended. The examiner is trying to pull the piece of paper out of their pinch.
PAUL C. DELL: If the adductor is not working, they will substitute their FPL to hold on to the piece. The the positive sign is flexion of the IP joint. Froment's sign is going to be present the night of the injury. This is a interoperative picture of a, an image where the motor branch of the ulnar nerve has been lacerated sharply.
PAUL C. DELL: It's important to evaluate both motor and ulnar sensory function when evaluating these palmar lacerations. You can appreciate the lacerated motor branch. The intact sensory branch is immediately to the ulnar aspect of it. If you were to evaluate just sensibility, you might miss the presence of a of a Froment's sign, which is going to be present right from the get go.
PAUL C. DELL: Also, as an incidental finding that branch coming from the ulnar sensory going across obliquely towards the index finger is a Riche-Cannieu Anastomosis Thomas sign is a subconscious positioning of the wrist inflection. Little do they know that this is only going to exacerbate their hyperextension of the MCP joint and increase their dysfunction.
PAUL C. DELL: So what's the ideal treatment of a ulnar negative hand? The, the objective should be to block MCP joint hyperextension, provide IP joint extension and provide active MCP joint flexion. As in all long standing nerve issues involving the upper extremity, there should be a full passive range of motion of all joints involved.
PAUL C. DELL: This may be achieved with splinting, serial cast capsulotomy to set the stage for return to function. In regards to specifically ulnar nerve and specifically low ulnar nerve problems, the simplest thing to do is put a lumbrical bar on. This is a splint that is fabricated or is prefabbed in therapy.
PAUL C. DELL: The, it blocks hyperextension of the MCP joint and retensions the dorsal hood. Many times this is suitable if someone is hopeful of ulnar nerve recovery after repair. Other things to consider are dermodesis, which essentially excises skin to create a shortage of skin, keeping the MCP joint flexed.
PAUL C. DELL: This can be combined with a volar capsulorrhaphy which is called a Zancolli. In some cases, a two can be released to cause a bowstring across the MCP joint. There are other tenodesis described by Parkes and Reardon. All of these procedures that we talked about so far do not bring any active tendon transfers into the hand to restore strength.
PAUL C. DELL: So active transfers to restore strength would include taking a tendon like superficialis and moving it to an intrinsic position. To restore active MCP joint flexion, various transfers have been outlined in in the literature. The simplest one, I think, is the modified Stiles-Bunnell.
PAUL C. DELL: This is an operation where the, the superficialis of the ring finger is removed from its sheath, split into two and inserted into the lateral band of the ring and small. This is done to block hyperextension because the, and works because the route of the FDS is volar to the axis of the MCP joint passes through the lumbrical tunnel and flexes the MCP joint.
PAUL C. DELL: This is good for low ulnar nerve palsy only. High ulnar nerve palsy, which implies that the nerve has been cut at or near the elbow, is a different animal entirely because the FDS of the ring, nor any of the FDS, are available for this transfer because they are the only thing working in the, in the finger because of the loss of FDP function.
PAUL C. DELL: So a more appropriate operation for someone requiring active MCP joint flexion in a high ulnar nerve palsy may be a brand transfer which is extensor carpi radialis brevis prolonged with graft inserted into the lateral band of the appropriate fingers. Bill Burkhalter described putting the tendon transfer into the proximal phalanx.
PAUL C. DELL: This works well. You have to have a negative Bouvier sign for that to be functional. The, the FCR transfer may be a transfer to consider if you have a Thomas sign to weaken wrist flexion, which is compromising or enhancing your MCP joint hyperextension.
PAUL C. DELL: So the bottom line is that you need to thoroughly evaluate the patient's needs. A truck driver may not have clawing because he already has a dermodeses from heavy use of his hands and may not be bothered by it, by ulnar nerve palsy at all. And maybe his principal problem is lack of pinch strength. You have to make sure the level of injury is thoroughly assessed in your equation, in your plan, because of muscles that may be dennervated that will compromise finger function if this if another tendon is removed.
PAUL C. DELL: So you have to make sure of what's available for transfer.
Segment:0 .
PAUL C. DELL: The objectives of this presentation are to review the anatomy of extrinsic and intrinsic musculature of the hand as well as mechanisms of action. Also included are intrinsic related to pathology such as boutonniere
PAUL C. DELL: swan necks, describe provocative positions to evaluate dysfunction such as ulnar plus ulnar negative. We have borrowed liberally from Richard J Smith's landmark article on intrinsic anatomy, which was published in the AAOS instructional course lectures, volume 24, 1975. I would encourage everyone to read this article several times during their residency.
PAUL C. DELL: The extrinsic extensors are organized in six dorsal compartments. The EDC's, which we are particularly focused on are in the fourth compartment. As the EDC's approach the metacarpophalangeal joint, there are oblique fibers that come off at about a 30 to 45 degree angle.
PAUL C. DELL: These are typically arising from the ring finger spanning out to the adjacent, middle and small. These are the juncturae tendinae. The index does not have a juncturae tendinae. There are some transverse fibers that are loosely connected, which are called the superficial transverse fascia. The juncturae tendinae stabilize the metacarpal, stabilize the dorsal hood over the MCP joint during flexion.
PAUL C. DELL: There are seven interosseous muscles in the hand, four dorsal, which are principally involved in abduction of the fingers and three volar, which are principally adductors of the fingers. These seven muscles are principally innervated by the ulnar nerve. The exceptions are, if there is a median to ulnar anastomosis either in the forearm, which is called Martin Gruber or in the hand called [?].
PAUL C. DELL: The first, second and fourth dorsal interossei have two bellies which arise from adjacent metacarpals. The deep belly passes superficial to the sagittal bands and inserts on the dorsal hood. So the function of the deep belly is not only to flex the MCP joint, but it can also extend the PIP joint.
PAUL C. DELL: The superficial belly, on the other hand, passes deep to the sagittal bands. It inserts on the tubercle of the proximal phalanx so that its function is principally an abduction. It does not contribute to the hood, so therefore it cannot extend the PIP joints. There are some variations to the dorsal interossei.
PAUL C. DELL: First of all, in the first dorsal interosseous, the superficial belly which can be seen with a red arrow is the principal muscle belly. It is much bigger than the deep, deep belly. Why is that? Because it is to provide abduction strength of the index finger to resist the thumb.
PAUL C. DELL: The third dorsal interosseous, which is on the ulnar side of the middle finger, has only a single muscle belly. This inserts onto the dorsal hood. It has no insertion on the bone so that there's little contribution to abduction of the middle finger. This muscle is primarily an extensor of the PIP joint.
PAUL C. DELL: The little finger actually doesn't have a dorsal interosseous. There is a volar interosseous that attaches to the radial side. On the ulnar side, however, the abductor Digiti Quinti replaces the interosseous and is the lateral band on, on that on the medial side of the little finger.
PAUL C. DELL: There are three volar interossei. They also originate from contiguous metacarpal shafts. They lie superficial to the sagittal bands and insert onto the dorsal hood as the lateral bands. They are extensors primarily of the IP joints.
PAUL C. DELL: In summary, there are seven dorsal and volar interossei. Most dorsal interossei have two muscle bellies have two functions. The third dorsal interosseous and the three volar interossei have a single belly, single insertion and single function. The lumbricals are very unique muscles.
PAUL C. DELL: They originate on their antagonists, the flexor digitorum profundus and insert on the radial aspect of the, of each dorsal hood. They can initiate MCP joint flexion, which is controversial, but they are said to be the, the workhorse of the intrinsics and are primarily extensors of the IP joint independent of MCP joint position.
PAUL C. DELL: This is a classic illustration from Dick Smith's article, the, it shows that there's an interplay between the intrinsic and extrinsic musculature that sometimes blends together. We will try to break this apart in the next few slides. As the EDC passes over the metacarpophalangeal joint, transverse fibers can be seen arising from the edge of the tendon to insert on the sagittal on the volar plate as the sagittal bands.
PAUL C. DELL: The sagittal bands are the extensor mechanism of the MCP joint. They also stabilize the EDC tendon over the joint during flexion. Immediately adjacent to the sagittal bands are the transverse fibers. These are fibers that arise from the intrinsic tendon on either side of the finger.
PAUL C. DELL: They arch over the EDC and flex the finger. That is, they flex the MCP joint. So immediately adjacent to each other are the extensor and flexor mechanisms of the MCP joint, hence the term dorsal hood. So diagrammatically you can appreciate that the EDC extends the MCP joint through the sagittal bands.
PAUL C. DELL: This is extrinsic function. The intrinsic function is demonstrated by the transverse fibers. These flex the MCP joint. Beyond the transverse fibers, the intrinsic mechanism continues as the oblique fibers, the oblique fibers, as they pass more distally, bifurcate into medial bands and lateral bands.
PAUL C. DELL: The medial bands continue to the dorsum of the proximal phalanx where they aid in PIP joint extension through the central slip. The lateral bands continue to distally to form part of the conjoined lateral band. As the intrinsics are bifurcating, the extrinsic EDC is trifurcating over the dorsum of the proximal phalanx.
PAUL C. DELL: The trifurcation includes the central slip and two lateral slips. The central slip continues distally to form the central slip to extend the PIP joint. The lateral slips combine with the intrinsic tendon to form the conjoint lateral band.
PAUL C. DELL: Nomenclature often gets confusing when determining the various structures of the dorsal hood. The lateral bands are the oblique fibers of the dorsal apparatus, which are an extension of the intrinsic tendon. The central slip, the extensor mechanism of the PIP joint is a combination of extrinsic and intrinsic fibers.
PAUL C. DELL: The conjoined lateral bands are a merging of the extrinsic and intrinsic tendons. They form at the level of the PIP joint and continue distally to form the terminal tendon. The terminal tendon inserts at the dorsal base of the distal phalanx, extends the DIP joint through its attachment.
PAUL C. DELL: There's a thin fascial triangular shaped ligament that is just distal to the central slip that is just distal to the PIP joint. The triangular ligament maintains the conjoined lateral bands in a dorsal position. As the PIP joint flexes and extends, there is a 3 to 4 millimeter excursion of the conjoined lateral band.
PAUL C. DELL: The triangular ligament maintains the conjoined lateral band dorsally. To maintain the proper positioning of the conjoined lateral bands, there is another structure called the transverse retinacular ligament, which arises on the volar edge of the band. It inserts on the flexor tendon sheath.
PAUL C. DELL: The function of the transverse retinacular ligament is to maintain the conjoined lateral bands in a volar position to prevent dorsal subluxation. The oblique retinacular ligament or landsmeer ligament is a link ligament between the PIP and the DIP joints. It originates on the volar aspect of the proximal phalanx and inserts on the distal phalanx
PAUL C. DELL: dorsally. The function is an active tenodesis so that as the PIP joint extends, the oblique retinacular ligament starts, initiates extension at the DIP joint through an active tenodesis. The test for oblique retinacular ligament tightness is to evaluate passive flexion of the DIP joint relative to the position of the PIP joint. On the left,
PAUL C. DELL: the PIP joint is flexed, the ligament is relaxed, the DIP joint flexes fully, passively. On the right, the PIP joint is extended, there is increased tension on the ligament. The DIP joint passively cannot be flexed. This is an example of tightness of the oblique retinacular ligament.
PAUL C. DELL: Cleland's ligament, not a part of the intrinsic mechanism, are part of dermatofascial fibers that run between the skeleton and the skin. They help stabilize the skin as the joint is flexing, they run the full length of the finger, are mostly condensed near the flexion creases of the IP joint.
PAUL C. DELL: Dorsal to the neurovascular bundle are Cleland's, volar to the neurovascular bundle are Grayson's ligaments. Intrinsic tightness is a common cause of hand impairment after trauma. Causes are typically from swelling. The, the muscle, the intrinsic muscles become fibrotic or they go into spasm and they become tight.
PAUL C. DELL: Other examples are stroke or paradoxical extension to be discussed later. The intrinsic tightness test, originally described by Finochietto in 1920, is a comparison of passive PIP joint flexion with varying degrees of MCP joint extension. With the MCP joint extended,
PAUL C. DELL: the intrinsic tendon, which is volar to the axis of the MCP joint, is on stretch. Therefore, its contribution to the dorsal hood is going to be tight. If there's intrinsic tightness, then passively the PIP joint will be limited when the MCP joint is held in extension. Obviously the, there has to be full passive motion of both joints to successfully do this test.
PAUL C. DELL: If there is intrinsic tightness that fails to respond to non-operative care, which includes therapy stretching program, then there's a simple procedure to weaken the intrinsic mechanism on the ulnar aspect. The oblique fibers of the hood are excised under local anesthesia through a dorsal incision. The patient is then actively allowed to flex with the MCP joint in extension and in flexion.
PAUL C. DELL: Swan neck deformity of the finger is a clinical diagnosis with many different etiologies. Probably the most common is mallet finger that's undertreated, other causes are listed in the slide. We see this frequently with intrinsic tightness or EDC subluxation. Common to all causes are dorsal subluxation of the conjoined lateral band.
PAUL C. DELL: There is attenuation of the transverse retinacular ligament, there is contracture of the triangular ligament which maintains the conjoined lateral band dorsally and prevents them from laterally and volarly displacing as the finger tries to flex. The nail buff, Edward nail buff has an excellent classification, which starts with a swan neck that is asymptomatic and is a clinical presentation to one that is stiff and doesn't flex at all with a distorted joint.
PAUL C. DELL: Obviously treatment is dependent upon the various stage that you, your patient presents in. Boutonniere deformity is the opposite of swan neck. It occurs when the conjoined lateral bands have subluxated volar to the axis of the PIP joint so that the triangular ligament is attenuated, the transverse retinacular ligament is contracted, maintaining the bands in a volar displacement.
PAUL C. DELL: In the full blown boutonniere,
PAUL C. DELL: there is hyperextension of the DIP joint because of the, the pathologic course of the band. The most common causes are central slip rupture, but many times is seen when there's a chronic PIP joint flexion contracture. Why does this happen? Because the central slip is very thin and can be attenuated very quickly. Lumbrical plus is a very distinct form of intrinsic tightness, remembering that the lumbrical originates on the profundus.
PAUL C. DELL: If there is rupture of the profundus such as you would see with a Jersey finger or with a DIP joint disarticulation, the profundus retracts proximally. The resting tension in the lumbrical muscle and tendon is then increased. When the patient goes to make a fist, the, the FDP glides more proximally,
PAUL C. DELL: there's more tension on the lumbrical and there is what has been called paradoxical extension. Most of the time you do not see paradoxical extension, but you do appreciate the lack of PIP joint full flexion because of the increased tightness in the lumbrical tendon. Intrinsic minus hand results from ulnar nerve chronic compression or from ulnar nerve laceration.
PAUL C. DELL: The fingers become asynchronous, so they're not able to flex simultaneously at the MCP joint and IP joint. The claw deformity has developed because of paralysis of the intrinsics. You've lost your main flexor of the MCP joint and the main extensor. There's loss of pinch strength because the thumb is also compromised as the adductor is innervated.
PAUL C. DELL: So ulnar nerve palsy is characterized by a claw deformity, intrinsic wasting, Wartenberg and flattened palmar arch. To understand claw deformity of the fingers, typically it's ring in small, there is an a imbalance between the EDC, which is radial nerve innervated. The intrinsic musculature, which is the flexor of the MCP joint, is deficient
PAUL C. DELL: so the MCP joint assumes a extended position. At the PIP joint, the ulnar nerve deficiency is manifest as intrinsic absence, so no extension at the IP joint, but the FDS is still intact so the finger assumes a flexed position. Now if the FDS is denervated such as in a median nerve associated injury, then the clawing is going to be significantly less because the the the malalignment will be just at the MCP joint and it will not be as profound.
PAUL C. DELL: So we talked about the claw deformity as a as an imbalance of muscle at the MCP and PIP joint levels. Another way of understanding it is that the hyperextension created by unopposed pull of the EDC renders slight laxity in the dorsal hood overlying the proximal phalanx. If that occurs, then there's not enough tension at the central slip to extend the PIP joint.
PAUL C. DELL: Remembering that the extrinsic extensor has contributions to the central slip, that extension is compromised because of the hyperextension deformity at the MCP joint. Therefore, many of our surgical procedures are to rebalance the the tension in the dorsal hood by blocking hyperextension at the MCP joint.
PAUL C. DELL: Bouvier Maneuver evaluates whether the central slip is intact. As we talked about previously in long standing flexion contractures of the PIP joint, the central slip, which is relatively thin, can be attenuated. The same thing can happen with a long standing ulnar nerve claw deformity. If the central slip is attenuated when you block hyperextension of the MCP joint,
PAUL C. DELL: the IP joint will not be able to extend. This maneuver shown in these slides shows the hyperextension of the MCP joint being blocked passively. The patient is then asked to actively extend the PIP joint. If the PIP joint central slip is intact, then this is a negative Bouvier Maneuver.
PAUL C. DELL: Wartenberg sign is simply a muscle tendoness imbalance. The extensor digiti quinti inserts on the ulnar aspect of the dorsal hood of the small finger. If the volar interosseous is out on the radial side, then the EDQ has is unopposed and will produce an abduction of the little finger.
PAUL C. DELL: The, if this is persistent, it can be easily corrected by taking the EDQ off of the ulnar aspect, passing it underneath the intermetacarpal ligament, inserting it on the radial side to negate the abduction force. These images show the result of a long standing ulnar nerve injury. The first dorsal interosseous is wasted.
PAUL C. DELL: The intermetacarpal interosseous are non-visible, not visible. The little finger is abducted. On the right side, you can appreciate loss of the hypothenar eminence as well as flattening of the arch of the of the hand. With paralysis of the adductor pollicis,
PAUL C. DELL: there is a substitutional pattern characterized by utilization of the flexor pollicis longus instead of the adductor. The test is done by asking the patient to hold a piece of paper between their thumb and their index finger with the IP joint extended. The examiner is trying to pull the piece of paper out of their pinch.
PAUL C. DELL: If the adductor is not working, they will substitute their FPL to hold on to the piece. The the positive sign is flexion of the IP joint. Froment's sign is going to be present the night of the injury. This is a interoperative picture of a, an image where the motor branch of the ulnar nerve has been lacerated sharply.
PAUL C. DELL: It's important to evaluate both motor and ulnar sensory function when evaluating these palmar lacerations. You can appreciate the lacerated motor branch. The intact sensory branch is immediately to the ulnar aspect of it. If you were to evaluate just sensibility, you might miss the presence of a of a Froment's sign, which is going to be present right from the get go.
PAUL C. DELL: Also, as an incidental finding that branch coming from the ulnar sensory going across obliquely towards the index finger is a Riche-Cannieu Anastomosis Thomas sign is a subconscious positioning of the wrist inflection. Little do they know that this is only going to exacerbate their hyperextension of the MCP joint and increase their dysfunction.
PAUL C. DELL: So what's the ideal treatment of a ulnar negative hand? The, the objective should be to block MCP joint hyperextension, provide IP joint extension and provide active MCP joint flexion. As in all long standing nerve issues involving the upper extremity, there should be a full passive range of motion of all joints involved.
PAUL C. DELL: This may be achieved with splinting, serial cast capsulotomy to set the stage for return to function. In regards to specifically ulnar nerve and specifically low ulnar nerve problems, the simplest thing to do is put a lumbrical bar on. This is a splint that is fabricated or is prefabbed in therapy.
PAUL C. DELL: The, it blocks hyperextension of the MCP joint and retensions the dorsal hood. Many times this is suitable if someone is hopeful of ulnar nerve recovery after repair. Other things to consider are dermodesis, which essentially excises skin to create a shortage of skin, keeping the MCP joint flexed.
PAUL C. DELL: This can be combined with a volar capsulorrhaphy which is called a Zancolli. In some cases, a two can be released to cause a bowstring across the MCP joint. There are other tenodesis described by Parkes and Reardon. All of these procedures that we talked about so far do not bring any active tendon transfers into the hand to restore strength.
PAUL C. DELL: So active transfers to restore strength would include taking a tendon like superficialis and moving it to an intrinsic position. To restore active MCP joint flexion, various transfers have been outlined in in the literature. The simplest one, I think, is the modified Stiles-Bunnell.
PAUL C. DELL: This is an operation where the, the superficialis of the ring finger is removed from its sheath, split into two and inserted into the lateral band of the ring and small. This is done to block hyperextension because the, and works because the route of the FDS is volar to the axis of the MCP joint passes through the lumbrical tunnel and flexes the MCP joint.
PAUL C. DELL: This is good for low ulnar nerve palsy only. High ulnar nerve palsy, which implies that the nerve has been cut at or near the elbow, is a different animal entirely because the FDS of the ring, nor any of the FDS, are available for this transfer because they are the only thing working in the, in the finger because of the loss of FDP function.
PAUL C. DELL: So a more appropriate operation for someone requiring active MCP joint flexion in a high ulnar nerve palsy may be a brand transfer which is extensor carpi radialis brevis prolonged with graft inserted into the lateral band of the appropriate fingers. Bill Burkhalter described putting the tendon transfer into the proximal phalanx.
PAUL C. DELL: This works well. You have to have a negative Bouvier sign for that to be functional. The, the FCR transfer may be a transfer to consider if you have a Thomas sign to weaken wrist flexion, which is compromising or enhancing your MCP joint hyperextension.
PAUL C. DELL: So the bottom line is that you need to thoroughly evaluate the patient's needs. A truck driver may not have clawing because he already has a dermodeses from heavy use of his hands and may not be bothered by it, by ulnar nerve palsy at all. And maybe his principal problem is lack of pinch strength. You have to make sure the level of injury is thoroughly assessed in your equation, in your plan, because of muscles that may be dennervated that will compromise finger function if this if another tendon is removed.
PAUL C. DELL: So you have to make sure of what's available for transfer.
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