HAND AND ORTHO ARTICLES

Grasp

2012-11-16T20:03:00.001-08:00

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Proc (Bayl Univ Med Cent). 2000 October; 13(4): 343–348.

PMCID: PMC1312228

Grasp

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In seeking a short, sharp title for this essay, I vacillated between grip and grasp. When consulting Dr. Dorland's Dictionary, I was surprised to find the primary definition of grip was “French, grippe influenza.” I therefore chose grasp, even though it does not appear in the good doctor's dictionary.

Despite the fact that the skeletal and muscular elements of the human hand are very nearly matched in many species, praise of our own human hand and its abilities is a very natural human weakness. In fact, the history of human civilization is replete with special studies of the hand. Galen (AD 129–199) devoted a large part of his De Usu Partium to the anatomy and physiology of the hand. Throughout the centuries, mystical properties have been imputed to the hand, and many gullible people have had their lives directed by the pronouncements of palmists.

Sir Charles Bell, in the first chapter of his fascinating fourth Bridgewater treatise—written >160 years ago—asserted that there is in the hand “a universal plan extending through all animated nature and which has prevailed in the earliest condition of the world, and that on the most comprehensive study of those subjects, we everywhere behold prospective design” (1).

In the second half of the 20th century, the writings of John R. Napier, an anthropologist-physician, are preeminent. His book Hands, first published in 1980 and now in its third edition, is the book to be recommended to nonspecialists interested in the evolutionary, functional, and behavioral aspects of the hand.

The best comparison and differentiation between nonhuman primates' hands and our own lies in the manner in which the hand is able to grasp something. The anthropoids' grip is strong and secure, but its range of function will remain small because of its less developed thumb. It is at best a “power grip,” but it does not have the “precision grip” of the human hand, which has achieved excellent refinement in prehensility.

This, however, does not mean that the human hand has lost the more primitive ability of the power grip or any other movement of the primate foot-hand. Essentially, the anatomical structure of our hand is no different from that in a gorilla, with the exception of the opposability of the thumb. What has changed is that over time, a strong hand remained strong but acquired more intricate capabilities. Monkeys are basically quadrupedal; man is fully bipedal. Our upright walk makes all the difference. During the last century, many discoveries have led to the understanding of the origins of our hands and their capabilities.

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ORIGINS

In 1650, Archbishop James Ussher determined to his satisfaction that the earth was created on the evening of October 22, 4004 BC. John Lightfoot, another divine, claimed that the correct time was 9:00am on October 26, 4004 bc. We now know they were off by many millions of years.

Precursors of the skeleton of our human hand can be traced back at least 370 million years to the pectoral fin of an extinct fish. The basic pentadactyl (5-digit) hand is found in skeletons of mammal-like reptiles that lived 200 million years ago. Sixtyfive million years ago, the basic hand skeleton became a fixed mammalian characteristic. Around 25 million years ago, the apes living in the forests began to develop more mobile forelimbs and hands with longer, stronger fingers. Their thumb was short and lacked both long flexor and extensor tendons, and the fingers and nails were curved to aid in grasping tree limbs. Our first unequivocal ape ancestor lived 19 million years ago. Named Proconsulitous, it was about the size of a fox terrier and had fingers that were flat nailed and had a pseudo opposable thumb. Some apes developed a knuckle-walking gait similar to that of modern chimpanzees.

About 5 million years ago, future man split off from the apes, and between 3 and 4 million years ago “Lucy” developed. Properly named Australopithecus afarensis, her given name was derived from the Beatles' song “Lucy in the Sky with Diamonds,” which was popular at the time her bones were discovered (2). Lucy was 3¹/2' tall with arms longer than modern man and small, strong hands. Thus, around 3 million years ago we have the first evidence of a true bipedal hominid. It was another million years before tool use developed. There is now evidence that modern man has existed for at least 100,000 years and that he used tools made of stone, bone, horn, and wood. The science of molecular genetics has now vindicated Darwinism and, no doubt to the discomfort of some, has shown that almost 99% of our DNA is identical to that of the chimpanzee.

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STRUCTURE AND FUNCTION

Skin is the most ancient sense organ of our body, and the skin of our hand is highly specialized to provide detailed sensory feedback. Since mobility is concentrated toward the concavity of the palm, its nerve endings are far more numerous than are those on the dorsum. The most sensitive area is the central whorl or loop of the fingertips in which the threshold of touch is 2 g per mm². In contrast, the threshold is 33 g in the forearm and 26 g in the abdomen. This acute sensibility is explained by the presence of some 2400 to 2500 nerve endings in each 9-mm² area. Deeper sensibility in the fingers is supplied by a rich nerve plexus in which, among many nerve endings, are >800 of the estimated 2000 Pacinian corpuscles in the whole body.

On the dorsal extensor surface the skin of our hand is thin and loose, and on the palmar aspect it is thicker and tethered to the deep fascia by strands passing from the flexion creases. The palmar creases or “skin joints” do not correspond to the underlying bony joints but anchor the skin during grasp. Subsidiary creases on the fingers fold up the skin that balloons up when the fingers are flexed (see your own proximal interphalangeal joint).

These creases are not the result of use; they are present in the newborn baby's hands. Many other minor creases are present, and throughout the palmar aspect papillary ridges carry sweat glands which open along the ridge crests. The sweat provides an adhesive quality, preventing slippage of tools, and enhances the appreciation of pain and touch. The pattern of these ridges is unique and unchanging and is established by the 12th week of intrauterine life.

John Napier has written, “I suppose we all have our heroes. I have three—Hunter, Bell, and Darwin. John Hunter turned our attention from the structure of the hand to its function; Bell related the function of the hand to the environment; and Darwin demonstrated that the environment, by the process of natural selection, gave birth to structure” (3).

I would add a fourth hero, a general practitioner from Boulogne, France, Gulliaume Duchenne, who in his book Physiology of Motion published in 1855 made the forthright statement, “The hand as understood physiologically is nothing but an unsightly paw more awkward than useful.” Despite this stricture, he comprehensively described the normal and abnormal motions of the hand. His great contribution was to use electrical stimulation to demonstrate the complexity of motion during grasp, pointing out that many muscles participate, some as direct motors, some as moderators, some as restrainers, and some as antagonists.

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THE MUSCLES

Mechanically, the grasping hand is a 2-sided chuck with the mobile thumb on 1 side and the fingers on the other. This chuck provides our refined and powerful pinch and grasp mechanism. The fingers on the opposite side of the grasping chuck are each capable of independent action. Opposing the powerful flexor mechanism is the weak extensor apparatus, whose major function is to open the fist and lift the digits against gravity.

The power of grasp is derived from 2 groups of muscles: the extrinsic and the intrinsic. The extrinsic muscles in the forearm provide the major power of the hand. The intrinsic muscles within the hand are of fundamental importance, since they are largely responsible for the refinement and delicate control of digital movements. These small muscles achieve their control by modifying and moderating the actions of the long extrinsic muscles.

Opening the hand and then closing it around an object is a very complicated motion. Simultaneous contraction to varying degrees of the 35 muscles in the forearm and hand will create a grasping motion. If you are among the 20% of humans who do not have a palmaris longus muscle, then you have only 34 muscles working for you. Unfortunately, you lack a muscle that can be used in reconstructive surgery. Its absence does not hinder you. To test if you own one, press your thumb tip against your little fingertip and flex your wrist against resistance. The palmaris tendon will stand out under the skin in the middle of the wrist crease.

Three phases operate when grasping large objects. In the first the hand opens widely from action of both the long extensors and the intrinsics. Then the object is surrounded largely by intrinsic action. Closure and firm grasp result from the strong action of the extrinsic flexors and the intrinsics of both the thumb and fingers. Finally, slight extension of the wrist tightens the grip even more.

The great variability in the postures of grasp would seem to exclude easy classification. But in 1956 Napier in his classic paper “The prehensile movements of the human hand” showed that all forms of grasp can be grouped as either power or precision grasp, with a third category combining elements of both (Figure (Figure11) (4).

Figure 1

Power grasp and precision grip. In grasp the object is pulled into the hand and rests on the thenar muscles. In precise actions the object is usually held away from the palm. Reprinted with permission from Napier JR. The prehensile movements of the human ...

Power grip is thought to have developed early in humans and consists of a prehensile movement in which the object is grasped by the fingers and pressed against the buttress of the thumb and its intrinsic muscles. This is a powerful movement with little skill involved. Precision grip is thought to be the most recent adaptation of the evolving human hand. It is an accurate prehensile action in which the object may be held away from the palm between thumb and fingertips. Some activities require features of both grips, as in tying 2 pieces of string together; the power fingers (ring and small) hold the string, and the precision digits (thumb, index, and long) do the precise activity of creating the knot. The so-called hook grip, while of great use to the apes suspended in trees, is only of use in humans when carrying suitcases.

Formerly 3 clinical models could be used for the study of grasp. Nowadays, with the conquest of poliomyelitis, only the rheumatoid hand and the leprosy hand are available. Practically every biomechanical imbalance that afflicts the hand occurs in one or the other of these 2 diseases.

Studies show that a power grasp of about 5 lbs per in² will keep a hammer handle from slipping out of the palm. However, if skin sensory feedback is impaired, then strength has to be increased to provide deeper sensory feedback. In the extreme case of the “blind” hand of Hansen's disease (leprosy), the neurological changes cause a collapsed posture of grasp and a concentration of force at the tips of the digits. The normal palmar surface grip area in an adult is about 10 in². The intrinsic minus posture of leprosy allows only fingertip grip, concentrating the force of grip into an area of about 1 in² (Figure (Figure22).The final resultant force in this small area is huge and reaches about 250 lbs per in²:

Figure 2

Intrinsic minus hand. The metacarpophalangeal joints are hyperextended, and the interphalangeal joints are flexed. Note that the tip of the long finger is shortened and rounded; absorption of the terminal phalanx has already started.

5 lbs per in²	×	5	×	10 in²	=	250 lbs per in²
normal pressure		increase for lack of sensibility		adjustment in surface area^*		actual pressure during grasp

*Pressure usually applied in an area of 10 in² is now in an area of 1 in².

The high grip pressure causes persistent microfractures, bone absorption, and ultimately disappearance of the digits (Figure (Figure33).

Figure 3

Hansen's disease. (a) Late stage. The fingers have absorbed and only a flipper of a hand is left. (b) X-ray of late stage.

Just as in leprosy, in which the internal forces of grasp destroy the skeleton, so in rheumatoid disease the aberrant forces produced by soft tissue disease disarray the normal forces of grasp. The more the patient increases the force of grasp, the greater the self-destruction of the normal postures of grasp.

Many factors influence the strength of grasp. Studies show that grip strength is greatest around 3:00 PM each day (5). Actual strength will vary with age and sex. A strong grasp reflex is present at birth. A baby begins to develop control of strength around the age of 2 as appreciation of the friction between skin and object develops. Progress is slow and early on is compensated for by excessive use of force (6). Gloves produce a significant drop in grip strength. Ordinary working gloves cause a reduction of 14% to 28%, while the inflated gloves of the astronaut produce a 37% reduction in strength.

Proper grasp is dependent upon appropriate lengths of the constituent bones of the palm and digits. These lengths are in fact proportionally related and determine the form and shape of grasp. The different lengths of the fingers disappear when a sphere is grasped; the fingers abduct and rotate and the tips line up. When grasping a cylinder, there is a normal inclination of palmar grasp, a fact unfortunately not well known to the manufacturers of crutches, who still copy the ancient Roman model. If only they would slope the handle, it would not force the wrist into a painful end position(Figure (Figure44).

Figure 4

The inclination of grasp. (a) Horizontal crutch handles force the wrist into an uncomfortable position. (b) With a sloped handle, the wrist is comfortably in line with the forearm. Reproduced with permission from Geriatrics 1960;15:733–745. Copyright ...

Our work has shown that regardless of wrist position, the percentage of total grasp force allocated to each finger is constant. The long finger shows the greatest amount of force, with approximately 33% of the total force. The index and ring fingers have about 25% each, and the small finger has approximately 16% of the total force (7).

The type of grip used in any given activity is a function of purposeful action and is not dependent on the shape or size of the object grasped. Humans have now moved beyond using rocks and fallen branches as tools, and as Benjamin Franklin said, “The tool user has become a tool maker.” Unfortunately, the current— cosmetically attractive—tendency to make digital profiles on tool handles severely restricts the range of hand sizes that can comfortably grasp the tool. The size and shape of tool handles should be such that the digital joints are near mid-flexion so that tool retention is high and the muscles are only partially stretched. Recent “ergonomic” designs show a great improvement. In surgery a round handle for the scalpel blade is wonderful; one can readily adjust the blade angle. The regular thin flat handle was probably invented by the Romans!

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RESTORATION

In the latter part of World War II the American army set up 10 hospitals in the USA for the exclusive treatment of upperlimb injuries. Thirty-five young surgeons were trained in reconstructive hand surgery, and what is now a worldwide specialty was born.

The basic objective of the specialty is the restoration of skilled function to a hand disabled by congenital defects, trauma, or disease. The fundamental functions are that of precision grip or power grasp. Two factors are paramount in their restoration: a thumb that moves or can be stabilized and fingers that flex. In massive injury, particularly when it is bilateral, restoration of both power and precision grips to both hands may not be possible. It may well be that the remaining serviceable parts will restore precision grip to the nondominant hand and power grip to the remnants of the dominant side. This is far better than attempting to restore both functions to both hands using inadequate resources.

Destruction of the individual nerve supply within the forearm or hand, such as the median, ulna, or radial nerves, produces recognizable patterns of function loss. Standard plans of effective tendon transfers have evolved, and such surgery has now become routine. When >1 nerve is involved, functional restoration becomes more difficult and the results are less efficient. Precision activities are lost first and, depending on the extent of damage, only grossly controlled motions may be possible.

During the days of poliomyelitis, paralysis of thumb opposition was a frequent occurrence. Since this is a fundamental component of grasp, a great many operations have been suggested for its restoration. Unfortunately, many of these procedures failed to appreciate that the thumb is, in effect, a post projecting into space with a very mobile joint at its base. Accordingly, a thumb has to be supplied with at least 3 “guy ropes” distributed around its circumference to hold the thumb erect. The flexor pollicis longus, the extensor pollicis longus, and the abductor pollicis longus usually supply the necessary stability. Once stability is achieved, then a fourth muscle can be transferred to move the thumb into opposition.

The prime mover into opposition is usually made from the flexor superficialis of the ring finger. Its removal does not interfere with grip in the presence of an intact flexor profundus tendon. A pulley is made in the region of the pisiform bone, and the transfer is attached near the metacarpophalangeal joint. After 3 weeks of immobilization, the transfer can be taught to produce opposition in an astonishingly short time—usually about 10 minutes.

Since the conquest of poliomyelitis, this operation is still in use to provide opposition when its absence is caused by trauma or neurological disease. For patients with progressive neurological conditions, a positive “can-do” attitude will provide, through an operation lasting an hour to an hour and a half, significant temporary improvement in grasp. Some of these individuals have been among my most grateful patients, even though they know the result cannot be permanent.

When trauma has amputated the thumb or one is born with an absent thumb, the hand is reduced to a virtual hook and no form of opposition is possible. Indeed, Napier has written, “Without the thumb the hand is put back 60 million years in evolutionary terms to the stage when the thumb had no independent movement and was just another digit” (8). Such a state is unacceptable, and a thumb has to be provided. The best substitution is one of the fingers, and technically it is possible to move any of the fingers across onto the base of the destroyed thumb. However, the use of any finger other than the index produces an indifferent thumb and is best regarded as a surgical triumph and a functional disaster.

The translation of an index finger onto a thumb stump is a relatively easy procedure and gives a highly functional result (Figure (Figure55). The cerebral cortex readily adjusts to its new responsibilities, but at first the new thumb is often inadvertently used by its owner as a pointer. This patient's insurance company kept writing to me demanding to know whether he should be compensated for loss of thumb or loss of index finger. My reply? Both!

Figure 5

An electrical accident burned off both thumbs in this adult man. Parts a, b, and c show 3 different views of the transposition of both index fingers, which restored grasp. The man returned to work on power lines.

In infants born with 4 fingers but no thumb, a thumb can be readily made from the index finger. However, the conversion of an index finger to a thumb necessitates some shortening since in the normal hand the tip of the thumb usually reaches just proximal to the line of the proximal interphalangeal joint of the index finger. This shortening is accomplished by removal of most of the metacarpal shaft, but the head is retained since it will become a new trapezium (Figure (Figure66). The key to this shortening is destruction of the growth plate of the metacarpal head. This arrests longitudinal growth at the base of the new thumb and prevents the development of the grotesque thumbs made by earlier methods (Figure(Figure77). This operation should be done early so that the child uses the thumb normally and is never aware of its original absence. I usually do it at about 6 months of age and believe it should always be done before the first birthday.

Figure 6

Pollicization—joint distribution. The 3 joints of the index finger become the 3 joints of the thumb, but the index metacarpophalangeal (MP) joint becomes the carpometacarpal (CMC) joint of the thumb. Reprinted with permission from Flatt AE.The ...

Figure 7

Pollicization. In the early development of this operation, the growth center in the index metacarpal head was not destroyed. It continued to grow, producing a grotesque digit. Reprinted with permission from Buck-Gramcko D. Pollicization of the index figure. ...

Infants born with webbed hands in which their thumb is tightly adducted to the index finger can have full restoration of grasp by liberation of their thumb. Three rotation flaps can be moved down the forearm to completely cover the thumb with sensate skin, and no skin grafting is necessary (Figure (Figure88).

Figure 8

(a) Adducted thumb. (b, c) By judicious use of rotating skin flaps, the thumb can be liberated and clothed with full-thickness skin. Vascular supply and cutaneous nerves are carried in the flaps. Reprinted with permission from Flatt AE, Wood VE. Multiple ...

Even patients with high spinal cord lesions, which leave only 1 forearm muscle under voluntary control, can be given significant improvement of function. For the patient illustrated in Figure Figure99 a 2-stage operation was used. The first procedure anchored the finger flexor tendons to the radius with the lengths arranged so that there was a normal cadence of flexion with the least in the index and the most in the small finger. When the wrist was extended by the sole working muscle (extensor carpi radialis longus), the fingers would close in grasp. However, the paralyzed thumb intruded into the palm, blocking grasp. The second-stage operation shortened the thumb by removing the proximal phalanx and fusing the distal phalanx to the metacarpal head. The phalanx was used as a bone graft, fixing the thumb in abduction and radial deviation from the hand. This provided a variety of useful functions for a previously flaccid hand. I first published this operation in 1964 and have used it ever since for patients with high neurological loss and for spastic patients. Surprisingly, these hands do not appear grotesque, and most lay people do not realize the thumb has been shortened.

Figure 9

Quadriplegia. The ability of limited grasp can be restored with only 1 functioning muscle in the forearm. (a) The thumb is shortened and stabilized. (b) A variety of functions are supplied by the operation. Reprinted with permission from Flatt AE. Indications ...

The field of hand surgery has grown exponentially since World War II. The original 35 military hand surgeons founded the American Society for Surgery of the Hand in Chicago on January 20, 1946. Today there are 1213 active members of this society dedicated to the improvement of and education in restoration of functions to the hand. A major effort has been the training for the next generation of surgeons; I have trained 50 hand surgeons from 11 different countries and many of my colleagues have similar records, so that now 49 countries have trained hand surgeons who are members of the International Federation of Hand Surgery.

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References

1. Bell C. The Hand, Its Mechanism and Vital Endowments as Evincing Design. London: William Pickering; 1834.

2. Johanson DC, Edey MA. Lucy. New York: Warner Books; 1982. p. 18.

3. Napier JR, Tuttle RH. Hands. Princeton: Princeton University Press; 1993. p. 9.

4. Napier JR. The prehensile movements of the human hand. J Bone Joint Surg. 1956;(38B):902–913.

5. Business Week October 2, 1995.

6. Wilson FR. The Hand. New York: Pantheon Books; 1998. p. 121.

7. Hazelton FT, Study of the Influence of Wrist Position on the Force Produced by the Finger Flexors[master's thesis]. Iowa City: University of Iowa, 1972.

8. Napier JR. Hands: 55.

Articles from Proceedings (Baylor University. Medical Center) are provided here courtesy of Baylor Health Care System

Congenital clasped thumb

2012-11-16T19:28:00.002-08:00

J Child Orthop. 2007 November; 1(5): 313–322.

Published online 2007 October 17. doi: 10.1007/s11832-007-0057-x

PMCID: PMC2656739

Characteristics of patients with congenital clasped thumb: a prospective study of 40 patients with the results of treatment

Hisham Abdel Ghani,¹ Ahmed El-Naggar,¹ Mohamad Hegazy,¹ Atef Hanna,¹ Yehia Tarraf,¹ and Samia Temtamy²

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Abstract

Purpose

Congenital clasped thumb is a deformity that is associated with heterogeneous congenital anomalies and it has been addressed in many congenital syndromes. The aim of this study was to diagnose and evaluate cases of clasped thumb as regards the associated congenital anomalies and syndromes, and evaluation of the results of treatment of such cases.

Methods

A prospective study on 40 patients with 73 clasped thumbs was done. All the patients’ data regarding their personal, family, pregnancy and developmental histories were recorded. All the patients were exposed to thorough clinical and radiological examination and genetic assessment. The cases were classified using the Tsuyuguchi et al. (J Hand Surg [Am] 10:613–618, 1985) classification into three types. Conservative treatment was adopted in ten hands, and surgical treatment was performed for 28 hands in 17 patients, with an average follow-up of 26 months.

Results

Positive consanguinity was recorded in 57.5% of cases. Associated anomalies were recorded in 77.5% of cases. Type I was the most common one, followed by type III and then type II. Conservative treatment is effective in type I cases when presented early, and all patients were satisfied with the results of surgical treatment.

Conclusions

We reported associated anomalies which are to our knowledge have not mentioned before in the literature which include; congenital blindness, radial deviation of the index finger and ventricular septal defect. We found that 68% of the patients had associated syndromes, and this has not been mentioned before. In this study, we found that there were no difference between type II and type III clasped thumb as regards the pathological findings, severity, the operative procedures, the treatment protocol and the operative results. Properly planned treatment gives satisfactory results.

Keywords: Thumb, Clasped thumb, Thumb contracture, Flexed adducted thumb

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Introduction

A persistent flexed adducted thumb after the 3rd or 4th month of life is called congenital clasped thumb [1]. It is due to deficiency of the extensor pollicis brevis or longus or both. The deformity is usually accompanied with a variable degree of narrowing and contracture of the first web space [2]. This deformity is usually associated with other generalized musculo-skeletal malformations, commonly; arthrogryposis, digitotalar dysmorphism and Freeman–Sheldon syndrome.

Most of the literature has discussed a surgical technique or case reports of associated anomalies or syndromes. Little has been written about the epidemiology of the deformity.

The aim of this study is to characterize a group of patients describing the associated anomalies and syndromes, the possible predisposing factors and results of treatment.

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Patients and methods

Forty patients with 73 congenital clasped thumbs were prospectively studied. There were 29 males and 11 females, with an average age at presentation of 27 months (range from 3 months to 11.5 years). The condition was bilateral in 33 cases.

The patients were exposed to thorough assessment, including recording of the family history, pregnancy history and full clinical assessment performed by a paediatrician. Genetic assessment was intended to be done for all cases by a paediatric geneticist (last author). Radiographic examinations of the extremities, skull, spine, and the pelvis and abdominal ultrasonography were conducted for all the patients. Echocardiography was done when recommended by the paediatrician.

The deformed thumbs were classified according to Tsuyuguchi et al. [3] into three types (Fig. 1).

Fig. 1

a Type I: supple clasped thumb. The thumb could be passively abducted and extended against the resistance of thumb flexors, without other digital anomalies. b Type II: clasped thumb with hand contractures. The thumb could not be passively extended and...

Thirty-eight hands were treated. Non-operative treatment was followed in ten hands in five patients who presented before the age of 1 year (eight hands type I and two hands type II). Surgical treatment was done in 28 hands in 17 patients (cases presented later than 1 year of age or which had not responded to non-operative treatment) (Tables 1, ,22).

Table 1

The distribution of the operated patients with regard to sex and bilaterality

Table 2

The number of different types of clasped thumb operated upon

The cases which were not treated were; nine hands waiting for surgery, 16 hands where the patients did not return for surgery, and ten hands where the parents refused surgery.

Treatment protocol

Non-operative treatment: full time splinting of the thumb in extension for at least 6 months, followed by night splinting for further 6 months after achieving active extension of the thumb.
Operative treatment: surgical procedures for every case were variable according to the degree of narrowing of the first web, stability of the metacarpophalangeal (MP) joint and muscle deficiency.

Surgery aims at widening the narrow first web space, including the skin and deep tight structures. Skin widening was done through either simple Z-plasty, four-flap Z-plasty [], butterfly flap [], dorsal rotational advancement flap [6] and modified dorsal rotational advancement flap [7]. The choice of the technique is variable according to the degree of narrowing. Through the skin incision designed to widen the web, the dissection is deepened through underlying fascia over the intrinsic muscles, protecting the distal arborisation of the superficial radial nerve, the flexor tendon and neurovascular bundles to the index finger. The tight structures are identified to be released; the origin of adductor pollicis muscle is released from the third metacarpus. If necessary, the first dorsal interosseous muscle is elevated from the first metacarpus. The thumb is then manipulated into extension and abduction. If necessary, the carpometacarpal joint capsule is released. After achieving full release, the first metacarpus is maintained in full abduction with two crossed k-wires across the first web space.

A markedly unstable MP joint necessitated chondrodesis, but in cases of mild laxity of the ulnar collateral ligament, double breasting of the capsule was done. In either case, the MP joint was transfixed with a single or two crossed k-wires.

Tendon transfer was done to restore active extension of the MP joint when it was stable or after achieving stability with reconstruction of the ulnar collateral ligament. The extensor indicis was the preferred tendon for transfer, and if it was absent, one slip of the flexor digitorum superficialis muscle is transferred to the vestigial remnant of the deficient thumb extensors (Table 3).

Table 3

The different surgical procedures done

An above-elbow splint was applied immediately. The k-wires were removed after 6 weeks of surgery. The position was maintained in a night splint with the thumb extended for at least 6 months post-operatively, with daytime active use of the thumb being encouraged. The average duration of follow-up was 26 months (range from 16 to 60 months).

The criteria used to assess results of treatment were:

I: Parents’ satisfaction: regarding cosmetic appearance and function.
II: Thumb position and appearance: degree of abduction and rotation.
III: Stability of MP joint.
IV: Thumb function: degree of opposition and the ability to grasp different objects.

The degree of abduction, rotation, stability and opposition were graded into four grades according to Gilbert (personal communication) (Table 4).

Table 4

Gilbert’s method of assessment of thumb function (personal communication)

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Results

The results will be discussed under the following headings:

I: Clinical findings
II: Operative findings
III: Results of treatment

Clinical findings

Family history

Twenty-three patients had positive consanguinity. First-degree consanguinity was found in 13 patients and far relationship in ten patients. Parents’ anomalies were found in six patients; the most common parents’ anomalies were club feet (two patients) and windblown deformity of the hands (two patients).

Seven patients had either the brother or the sister affected with other congenital anomalies. One patient had a sister with clasped thumb, and another one had three brothers who had other congenital anomalies but they could not be assessed. One patient had the mother, the aunt and the grandfather with windblown deformity, and his cousin had clasped thumb.

Prenatal history

Positive history of fever during pregnancy was reported in seven patients, but the mothers could not specify the type of infections they had had. One patient had a history of radiation exposure during pregnancy. Drug intake during the first trimester was found in 12 patients. Most of the mothers could not specify the types of medication they received (Table 5).

Table 5

Types of drugs taken during the first trimester of pregnancy in 12 patients

General examination

The distribution of different types of clasped thumb and their sex distribution are mentioned in Table 6. Thirty-one patients (58 hands) were found to have associated anomalies.

Table 6

The different types of clasped thumb with sex distribution

Facial abnormalities were found in 18 patients; ptosis, antimongoloid obliquity of the palpebral fissure, cleft palate, broad bossed forehead, flat face, depressed nasal bridge and long philtrum. Whistling face was diagnosed in six patients. Two patients had congenital blindness. Four patients had short neck, and one had additional webbing. Congenital heart anomalies were found in two patients; one had atrial septal defect and the other had ventricular septal defect. Scoliosis was found in one patient with arthrogryposis, but MRI was not done. No abdominal anomalies were found in any patient, but accidentally discovered renal stones were found in two patients (Tables 7, ,8,8, ,99).

Table 7

Lower limb anomalies associated with clasped thumb

Table 8

Upper limb anomalies associated with clasped thumb

Table 9

Associated hand anomalies

Associated syndromes

In 11 patients, genetic assessment was refused by the parents, and their associated syndromes were not diagnosed; two of them had congenital blindness with clasped thumb. Different syndromes were present in 20 patients out of the 29 patients assessed (68%) (Table 10).

Table 10

Associated syndromes

Patterns of inheritance among genetically assessed cases

Autosomal dominant inheritance: there was variable expressivity of the autosomal dominant inheritance in one parent and sibs of 13 patients. These patients had isolated Freeman–Sheldon syndrome (four patients), clasped thumb deformity (three patients), arthrogryposis multiplex congenita (two patients), clasped thumb club foot syndrome (two patients), congenital contracture arachnodactyly (one patient) and digitotalar dysmorphism (one patient).

Suspected autosomal recessive inheritance: 13 patients had positive family history of consanguinity without a family history of similar conditions. These patients have isolated clasped thumb deformity (six patients), arthrogryposis multiplex congenita (three patients), multiple pterygium syndrome (three patients), and Emery–Nelson syndrome (one patient).

Sporadic hands: three patients had no consanguinity or similar familial anomaly; two of them have Freeman–Sheldon syndrome, and the other have digitotalar dysmorphism.

Operative findings

Abnormal pathological anatomy

Attenuated extensor pollicis longus and brevis were found in all hands, and they appeared as vestigial strands of tendon-like structures measuring about a millimeter in diameter. Absent extensor indicis was detected in one out of eight hands with tendon transfer.

Contracture of adductor pollicis muscle was found in 13 hands (seven hands had Type III and six hands had Type II clasped thumb). Meanwhile, first dorsal interosseous muscle was contracted in nine hands (six hands had Type III and three hands had Type II clasped thumb).

Global instability of the MP joint was present in 18 hands. Laxity of ulnar collateral ligament of the MP joint was detected in two hands (Type III clasped thumb). The true nature of instability was identified after release of the web space.

Abnormal articular surface of the first MP joint was detected in six hands (four hands had Type II and two hands had Type III clasped thumb) with hypoplasia of the volar aspect of the first metacarpal head. The dorsal capsule of the MP joint was adherent to the cartilage of the metacarpal head and sharp dissection was needed to separate it in eight hands (four hands Type II and four hands Type III clasped thumb). Flexion contracture of the MP joint was present in eight hands (four hands Type II and four hands Type III).

Post operative complications

Superficial necrosis of the tip of the modified dorsal rotational advancement flap with venous congestion occurred in one hand Type II, and it was treated with repeated dressings without effect on the result. Proximal retraction of the tip of the dorsal rotational advancement flap was noticed in all cases. This produced some re-narrowing of the web, which was avoided in later cases by using the modification of this flap []. Non-union of chondrodesis of MP joint occurred in two hands (Figs. 2, ,33).

Fig. 2

Ulnar drift hand

Fig. 3

Radial deviation of the index finger associated with flexion deformity of the lateral four fingers

Results of treatment

Results of operative treatment

Twenty-eight hands were assessed postoperatively with regard to:

(1) Parent’s satisfaction. The parents of all the patients were satisfied with the results (Fig. 4).

Fig. 4

a Severe type III clasped thumb in patient with arthrogryposis treated surgically with release of the first web, widening the web with modified dorsal rotational advancement flap and chondrodesis of the MP joint of the thumb. b Result of surgical treatment ...

(2) Cosmetic appearance. The simple Z-plasty deepened the web, transforming it into a slit, and did not give the normal rounded appearance of the web. The appearance of the first web space was better with the other techniques. The modified dorsal rotational advancement flap allowed maximal degree of widening more than the other techniques used. Twenty-four thumbs had excellent abduction, and four thumbs had good abduction. Twenty-six thumbs had excellent rotation, and two had good rotation.

(3) Stability of the MP joint. The stability of the MP joint of the thumbs operated upon was excellent in 24 cases. In the two hands with non-union of the chondrodesis, revision of chondrodesis was needed in one thumb with poor stability, while in the other the stability was fair and there was no need for surgery; otherwise, the rest of cases with chondrodesis had excellent stability (Fig. 4). The stability of two cases with ligamentous reconstruction of the ulnar collateral ligament was graded as good.

(4) Thumb functions. Active extension of the thumb was full in all cases for which tendon transfer was done (Fig. 5).

Fig. 5

a Type I clasped thumb. b Result of surgical treatment after transfer of extensor indicis to remnant of the extensor tendons

Ten thumbs had excellent opposition, 14 thumbs had good opposition and two thumbs had fair opposition. Two thumbs were unable to oppose, and opponensplasty was needed. In all the hands for which muscle transfer to the extensors of the thumb was done, the opposition were excellent. There was improvement of the grasp pattern in all the operated thumbs. Twenty-five hands were able to pick up a pen and a key and were able to grasp a ball. Two hands (one patient) wer able to pick up a key and a pen between the thumb and the middle finger because of the severe flexion deformity of the index finger. In one hand, the ability to grasp and pick up an object could not be assessed.

Results of non-operative treatment

Non-operative treatment was successful in eight hands type I, with achievement of full active extension of all joints of the thumb. There was no improvement in the two hands of type II that will need surgical treatment.

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Discussion

Congenital clasped thumb is a deformity that is associated with heterogeneous congenital anomalies and syndromes [1]. The incidence of these anomalies and syndromes vary, and are based on study of small groups of patients. Little has been written about the distribution and epidemiology of clasped thumb. Also, the characteristics of the patients with clasped thumb are not well described in the literature.

The clinical evaluation of the patients in this study revealed that the male-to-female ratio is 2.5:1, which is similar to the reported ratio by Lin et al. [8], and is near to the estimated ratio reported by Flatt [9]. However, it differs from the 1:1 ratio reported by Tsuyuguchi et al. [3]. This difference can be attributed to the wide variety of syndromes associated with clasped thumb and their different modes of inheritance, and also the small number of reports in the literature that document the sex ratio of the affected cases.

With regard to the possible predisposing factors, the incidence of positive consanguinity is 60% and positive family history in our study is 32.5%, which is much higher than the 10% positive family history that was reported by Tsuyuguchi et al. [3], who also did not mention the incidence of consanguinity.

The high percentage of positive consanguinity and family history in about one-third of our cases, and the high incidence of bilateral cases, strongly suggest that the genetic defect is an important causative factor []. However, there may be an underestimation of the percentage of drug intake. We noticed that mothers might deny intake of drugs taken to abort babies. Also, the drug may be in the form of a herbal extract, which may be taken for the same purpose. In the majority of cases, other therapeutics were taken without knowing the existence of pregnancy.

One-third of cases were sporadic. This agrees with the literature regarding the causative factors for such an anomaly [3]. However, the exact causative factors are not yet known.

This study confirms the previously reported high incidence of associated congenital anomalies with clasped thumb [1, 3, –]. About 77.5% of our patients were found to have associated anomalies; this value differs according to the number of syndromes included in the literature, and no previous literature studied the incidence of congenital anomalies with clasped thumb, as the different syndromes were studied separately or the literature contains case reports of certain syndromes. The incidence of upper limb anomalies in our patients (15%) agrees with reported cases of Temtamy and McKusick [1].

Other anomalies encountered included congenital heart disease in the form of ventricular septal defect—which was detected in one patient who had no other anomalies except unilateral type I clasped thumb—and this association was not found to be reported in the literature. We reported other anomalies, which to our knowledge have not been mentioned before which include two patients with congenital blindness in association with bilateral clasped thumb, and a case with radial deviation and rotation of the index finger. No abdominal anomalies were encountered in this study, and this agrees with the literature [1, 17,].

Associated syndromes were encountered in 68% of patients, and this percentage was not studied before in the literature.

We used the classification suggested by Tsuyuguchi et al. [3]. This classification was also used by Mih []. We found that there was no difference between type II and type III clasped thumb with regard to the pathological findings, severity, the operative procedures, the treatment protocol and the operative results; thus, it was wiser to classify the clasped thumb into supple and complex types, as McCarroll [] did.

The distribution of different types of clasped thumb and the male to female distribution was almost the same as reported by Tsuyuguchi et al. [3] (Table 11).

Table 11

Comparison between the distributions of different types of clasped thumb in the present study and the study presented by Tsuyuguchi et al. [3]

Our protocol of management is similar to that followed by Weckesser et al. [], Lipskeir and Weizenbluth [29] and McCarroll [], who divided the clasped thumb into two types (supple and complex), and treated the supple type with splinting and tendon transfer if splinting failed, while the complex type was treated by correction of the fixed contractures and reconstruction of lax ligaments and tight skin as appropriate. Tsuyuguchi et al. [3] cases were treated by splinting for types I and II cases and operative treatment for type III and type II cases which didn’t respond to conservative management.

In this study, 50% of operated cases were type III clasped thumb; 29% of cases were type II, and only 21% were type I cases who were presented at an age older than 1 year. This differs from the cases presented by Tsuyuguchi et al. [3], where 50% of the patients were type I and 50% were type II; this can be explained by the young age at presentation of their type I cases, as all their patients were within their first 7 months of life.

The operative findings agreed with Crawford et al. [2] and McCarroll [], in that the extensor tendons were not absent but attenuated in the three types. Our findings also agreed with McCarroll [], in that the complex type of clasped thumb (types II and III) have contractures in the soft tissues in the volar surface of the digit, involving all tissues including skin, subcutaneous fascia, periarticular structures and in the radial collateral ligament–volar plate complex of the MP joint. The dorsal capsule of the MP joint is adherent to the cartilage of the metacarpal head, and there is abnormality of the articular surface of the metacarpal head in some cases of types II and III clasped thumb. The shortening of the flexor pollicis longus muscle was present in cases of types II and III, but Z-lengthening was needed in few cases because in the majority of cases we did chondrodesis of the MP joint.

We noted that the severity of these pathological findings is variable, and dependent on the age of the patient at the time of surgery. We also noted that these findings were present in types II and III clasped thumbs, and there was no difference in these pathological findings in both types.

We used different skin incisions in this study to widen the web space. No technique can be standardized for release of the web as this depends on the severity of web narrowing and degree of contracture; as a result, it is difficult to compare the different methods used for release.

There were no universal criteria for the evaluation of the results of management of clasped thumb, due to the difficulty in assessing the thumb function at that young age, and other authors used different systems for evaluation of their results. Some authors used the degree of active extension of first MP joint as the reference for evaluation [8, ]. Tsuyuguchi et al. [3] added the degree of active radial abduction of the trapeziometacarpal joint to their system of evaluation. Lipskeir and Weizenbluth [29] added the width of the first web space to their scoring system, and they mentioned that active extension of first MP joint is the most important factor for the apprehension of large objects.

We used a combination of criteria to evaluate the thumb function, because it is of no benefit to achieve active thumb extension without achieving stability of the MP joint or without widening of the web. It is very important to consider the stability of the MP joint. Using the active extension as the sole criteria for assessment is possible in type I cases where this is the only deficient function.

The results of splinting in this study were excellent in type I clasped thumb [3, 8]. The small number of patients that followed the non-operative treatment in this study is attributed to the delayed presentation of the patients until after the age of 1 year.

In this study, the results of tendon transfers done for type I clasped thumb were excellent. We did not use an osseous tunnel in the proximal phalanx for the extensor indicis tendon as originally described [], and instead we sutured it to the attenuated extensor tendon of extensor pollicis brevis, as described by Mih [].

In the case of ulnar collateral ligament instability of the MP joint, ligamentous stabilization is a prerequisite for tendon transfer. Although the ligament reconstruction did not give excellent stability, the residual instability did not interfere with thumb function. In the case of global instability of the MP joint, chondrodesis is the best way to achieve stability, and at the same time it obviates the need for tendon transfer. The results of chondrodesis are better than that reported by Tsuyuguchi et al. [3] and Lipskeir and Weizenbluth [29].

In this study, we found that properly planned treatment according to the type of the deformity improves the cosmetic appearance and functional capabilities of the hand.

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References

1. Temtamy S, McKusick V (1978) The genetics of hand malformation. Alan R. Liss, New York .

2. Crawford H, Horton C, Adamson J (1966) Congenital aplasia or hypoplasia of thumb and fingers extensor tendons. J Bone Joint Surg Am 48:82–91 .

3. Tsuyuguchi Y, Masda K, Kawabata H, Kawai H, Keiro Ono (1985) Congenital clasped thumb: a review of forty-three cases. J Hand Surg [Am] 10:613–618 .

4. Broadbent TR, Woolf RM (1964) Flexion-adduction deformity of the thumb—congenital clasped thumb. Plast Reconstr Surg 34:612–616. [PubMed]

5. Shaw DT, Ricky DG, Nahigian JH (1973) Interdigital butterfly flap in the hand (the double-opposing Z-plasty). J Bone Joint Surg Am 55:1677. [PubMed]

6. Buck-Gramcko D (1998) Congenital malformations of the hand and forearm. Churchill Livingstone, London .

7. Abdel Ghani H (2006) Modified dorsal rotational advancement flap for release of thumb web space. J Hand Surg [Br] 31(2):226–229 .

8. Lin SC, Hung TH, Hsu HY, Lin CG, Chiu HY (1999) A simple splinting method for correction of supple congenital clasped thumbs in infants. J Hand Surg [Br] 24:612–614 .

9. Flatt AE (1994) The care of congenital hand anomalies. 2nd ed. Quality Medical Publishing, St. Louis .

10. Weckesser EC, Reed JR, Heiple KG (1968) Congenital clasped thumb (congenital flexion-adduction deformity of the thumb). J Bone Joint Surg Am 50:1417–1428. [PubMed]

11. Beals RK (1973) Trico-rhino-phalangeal dysplasia. report of kindred. J Bone Joint Surg Am 55:821–826. [PubMed]

12. Cervenka j, Figalová P, Gorlin RJ (1969) Cranio-carpo-tarsal dysplasia, or the whistling face syndrome II. Oral intercommissural distance in children. Am J Dis Child 117:434–435. [PubMed]

13. Christian JC, Andrews PA, Conneally PM, Muller J (1971) The adducted thumbs syndrome. Clin Genet 2:95–103. [PubMed]

14. Freeman EA, Sheldon JH (1938) Cranio-carpo-tarsal dystrophy. An undescribed congenital malformation. Arch Dis Child 13:277–238 .

15. Gilly RJ, Cotton S, Farouz A, Nairet A, Maclet M (1971) Hydrocéphalie congénitale et anomalie bilatérale des pouces: Syndrome malformatif lié au chromosome “X”. Pediatrie 26: 365–378. [PubMed]

16. Janecke AR, Unsinn K, Krecxy A (2001) Adducted thumb-club foot syndrome in sibs of a consanguineous Austrian family. J Med Genet 138:265–269. [PMC free article] [PubMed]

17. McCarroll HR, Manske PR (1998) The windswept hand. In: Buck-Gramcko D (ed) Congenital malformations of the hand and forearm. Churchill Livingstone, London, pp 313–325 .

18. O’Keefe M, Crawford JS, Young JDH, Macrae WG (1986) Ocular abnormalities in the Freeman–Sheldon syndrome. Am J Ophthalmol 102:346–348. [PubMed]

19. Senrui H (1998) Congenital Contractures. In: Buck-Gramcko D (ed) Congenital malformations of the hand and forearm. Churchill Livingstone, London, pp 295–309 .

20. Weinstein S, Grolin RJ (1969) Cranio-carpo-tarsal dysplasia or the whistling face syndrome. Am J Dis Child 117:427–433. [PubMed]

21. Wood VE (1994) Another look at the causes of the windblown hand. J Hand Surg [Br] 19:679–682 .

22. Dundar M, Demiryikmaz F, Demiryikmaz I (1997) An autosomal recessive adducted thumb-club foot syndrome observed in Turkish cousins. Clin Gene 51:61–64 .

23. Hall J (1981) An approach to congenital contractures (arthrogryposis). Pediatr Ann 10:15. [PubMed]

24. Pozanski AK, LaRowe PC (1970) Radiographic manifestations of arthrogryposis syndrome. Radiology 95:353. [PubMed]

25. Sonoda T, Kouno K (2000) Two brothers with distal arthrogryposis, peculiar facial appearance, cleft palate, short stature, hydronephrosis, retentio testis and normal intelligence: a new type of distal arthrogryposis? Am J Med Genet 10:280–285. [PubMed]

26. Fitch N, Levy EP (1975) Adducted thumb syndromes. Clin Genet 8:190–198. [PubMed]

27. Mih AD (1998) Congenital clasped thumb. Hand Clinics 14:77–84. [PubMed]

28. McCarroll HR (1985) Congenital flexion deformities of the thumb. Hand Clin 1:567–575. [PubMed]

29. Lipskeir E, Weizenbluth M (1989) Surgical treatment of clasped thumb. J Hand Surg [Br] 14:72–79 .

snake bite

2012-06-11T08:41:00.002-07:00

Snake Bites

Received 5 May 2010; accepted 5 July 2010.

Article Outline

There are thousands of snake species worldwide, and approximately 15% are considered dangerous to humans.¹ The American Association of Poison Control Centers has recently reported that the United States averages approximately 6,000 snake bites every year, of which 2,000 are from venomous snakes.¹, ², ³, ⁴ However, the exact incidence of snake bites is unknown because most bites are not reported and receive no medical treatment. Most snake bites occur when humans and snakes are likely to be in the same environment, from April to October.⁵, ⁶ No more than 12 annual snake bite fatalities have been reported from 1960 to 1990.⁵

Educational Objectives

Few of the native snake species in the United States are venomous.¹ The most common offenders are pit vipers, such as rattlesnakes (Fig. 1A), cottonmouths (Fig. 1B), and copperheads (Fig. 1C). Coral snakes also cause some bites. All states except Alaska, Maine, and Hawaii have native venomous snake species.¹, ³ Snakes should never be handled because many have an inherent bite reflex that renders even decapitated snakes dangerous.¹, ⁷ Even when snake bites occur, up to 25% do not result in envenomation.¹, ⁸ Signs of envenomation include nausea/vomiting, paresthesias, pain, edema, erythema, ecchymosis, lymphangitis, bullae, altered taste, hypotension, delirium, respiratory distress, and/or coagulopathy.¹These symptoms can manifest in minutes to hours and often result in a visit to medical professionals.

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FIGURE 1.

Venomous snakes. A Rattlesnake. B Cottonmouth. C Copperhead.

Printed with permission from Public Health Image Library (PHIL). Centers for Disease Control and Prevention Web site. http://phil.cdc.gov/phil(image ID 8131, 8125, and 8130, respectively). Accessed July 19, 2010.

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Treatment

Initial first aid principles include first moving the patient away from the snake, and then transporting the patient to the nearest medical facility. Immobilization of the affected extremity should be in a functional position. Electric shock, cryotherapy, incision/suction, and tourniquets are no longer recommended.¹ Airway, breathing, and circulation are the first priorities, followed by a thorough history and physical examination. The bite site should be measured circumferentially above and below. These measurements should be repeated every 15 to 30 minutes, and the leading edge of swelling should be marked.¹ Standard laboratory blood tests should be checked. Suspected snake bites should be observed for at least 8 to 12 hours.⁵, ⁹ Antivenin such as antivenin Crotalidae polyvalent or Crotalidae polyvalent immune Fab antivenom should be administered as indicated. All wounds should be cleaned and properly dressed. Tetanus immunization should be updated. Numerous regional poison control centers are available for assistance through nationally available 24-hour call centers.⁶

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Complications

Care for snake bites can be complicated by problems with local wound management, lacerated deep structures, or rarely, compartment syndrome (Fig. 2). All wounds should be cleaned and dressed. Necrotic tissue at times requires debridement. Infections at the bite site are not common, and antibiotics should be used only when there are signs of local infection. Bites can damage deep structures, such as nerves, vessels, and tendons, which necessitates surgical intervention. Compartment syndrome can be difficult to diagnose because the reaction to the venom can mimic signs of compartment syndrome. Often, compartment pressures help in making the diagnosis. Some physicians recommend elevation of extremity and administration of Crotalidae polyvalent immune Fab antivenom before any surgical intervention.¹, ¹⁰ Fasciotomies are not the standard of care for all snake bites, but they are performed when indicated. There is a lack of evidence-based literature on the role of antivenin and the need for fasciotomies.

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FIGURE 2.

Patient with compartment syndrome of upper extremity, just before fasciotomies were performed. A, B The fasciotomy surgical sites are marked and the ecchymosis and swelling are noted. C The puncture wounds from the bite are seen.

Courtesy of Dr. John Elfar, University of Rochester Orthopaedics.

Snake bites are common and can affect the extremities. These often do not result in a hand surgery specialist consultation, and there is a resulting lack of literature on the topic. A basic understanding of the etiology, treatment recommendations, and complications of such bites can improve the effectiveness of patient care.

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References

Gold BS, Dart RC, Barish RA. Bites of venomous snakes. N Engl J Med. 2002;347:347–356
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- CrossRef

Litovitz TL, Klein-Schwartz W, White S, Cobaugh DJ, Youniss J, Omslaer JC, et al. 2000 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2001;19:337–395

Litovitz TL, Klein-Schwartz W, White S, Cobaugh DJ, Youniss J, Drab A, et al. 1999 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2000;18:517–574

Parrish HM. Incidence of treated snakebites in the United States. Public Health Rep. 1966;81:269–276
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Consroe P, Egen NB, Russell FE, Gerrish K, Smith DC, Sidki A, et al. Comparison of a new ovine antigen binding fragment (Fab) antivenin for United States Crotalidae with the commercial antivenin for protection against venom-induced lethality in mice. Am J Trop Med Hyg. 1995;53:507–510
- View In Article
- MEDLINE

Juckett G, Hancox JG. Venomous snakebites in the United States: management review and update. Am Fam Physician.2002;65:1367–1374
- View In Article

Gold BS, Barish RA. Venomous snakebites (Current concepts in diagnosis, treatment, and management). Emerg Med Clin North Am. 1992;10:249–267
- View In Article
- MEDLINE

Kitchens CS, Van Mierop LH. Envenomation by the Eastern coral snake (Micrurus fulvius fulvius) (A study of 39 victims).JAMA. 1987;258:1615–1618
- View In Article
- MEDLINE

Walter FG, Bilden EF, Gibly RL. Envenomations. Crit Care Clin. 1999;15:353–386ix

Garfin SR, Castilonia RR, Mubarak SJ, Hargens AR, Akeson WH, Russell FE. The effect of antivenin on intramuscular pressure elevations induced by rattlesnake venom. Toxicon. 1985;23:677–680

No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.

PII: S0363-5023(10)00789-6

doi:10.1016/j.jhsa.2010.07.005

chemo extravasation

2012-06-11T07:37:00.001-07:00

http://www.uic.edu/classes/pmpr/pmpr652/Final/bressler/extrainj.html

http://www.jhandsurg.org/article/S0363-5023(11)01243-3/fulltext

flaps

2012-06-08T15:29:00.001-07:00

http://www.msdlatinamerica.com/ebooks/HandSurgery/sid806116.html

stsg

2012-06-04T12:50:00.001-07:00

http://cdn.intechopen.com/pdfs/18924/InTech-Split_thickness_skin_grafts.pdf

hook test biceps

2012-06-04T12:27:00.002-07:00

The Hook Test for Distal Biceps Tendon Avulsion

+Author Affiliations

From the ^†Mayo Clinic, Rochester, Minnesota, ^‡Hospital Madre Teresa, Belo Horizonte, Brazil, and ^§Hospital Base Osorno, Osorno, Chile

Address correspondence to Shawn W. O’Driscoll, PhD, MD, Mayo Clinic, 200 1st Street SW, MSB 3-69, Rochester, MN 55905 (e-mail: odriscoll.shawn@mayo.edu).

Abstract

Background: Complete biceps tendon avulsions are frequently missed on clinical examination, suggesting the need for a reliable diagnostic test.

Hypothesis: Complete distal biceps avulsions can be reliably detected with the Hook test.

Study Design: Cohort study (diagnosis); Level of evidence, 2.

Methods: The hook test was performed by a single surgeon in a cohort of 45 patients undergoing surgical exploration of the distal biceps tendon. While the patient actively supinates with the elbow flexed 90°, an intact hook test permits the examiner to hook his or her index finger under the intact biceps tendon from the lateral side. With an abnormal hook test, indicating distal avulsion, there is no cord-like structure under which the examiner may hook a finger.

Results: Thirty-three patients had an avulsion and 12 had a partial tear. The hook test was abnormal in 33 of 33 (100%) patients with complete biceps avulsions, and intact in 12 of 12 with partial detachments. However, it was painful in 9 of those 12. In the noninjured contralateral arms, which served as the normal control group, 45 of 45 (100%) had a normal hook test. Magnetic resonance imaging (MRI) diagnosed a complete tear in 11 of 12 patients with partial tears and in 11 of 13 with complete lesions. The sensitivity and specificity were both higher with the hook test (both 100%) than with MRI (92% and 85%, respectively).

Conclusions: The hook test is a highly sensitive and specific test for assessment of distal biceps tendon avulsions.

Keywords:

Footnotes

No potential conflict of interest declared.
Copyright 2007 by American Orthopaedic Society for Sports Medicine

tendon relative strengths

2012-06-04T12:06:00.003-07:00

. With the FCR muscle as the reference it is well known that the relative strengths of the FCU, flexor pollicis longus, each of the digital flexors, extensor carpi radialis longus, extensor carpi radialis brevis, extensor carpi ulnaris, and each of the digital extensors are 2, 1, 0.5, 1, 1, 1, and 0.5, respectively.⁸ When one takes the ratio of all the flexors to all the extensors the flexion/extension ratio is essentially 8 divided by 6 and is approximately 1.33 based on the cross-sectional area of the muscle bellies, suggesting that the total flexion force generated will be greater than the extension force.

Elbow instability

2012-06-04T12:05:00.000-07:00

http://www.bonepit.com/Lectures/Elbow%20instability%20Matthew%20James%20Sharp.pdf

cp

2012-05-31T13:00:00.000-07:00

macs

TABLE 1. Summary of the MACS

MACS Level	Description
I	Handles objects easily and successfully.
II	Handles most objects but with somewhat reduced quality or speed of achievement.
III	Handles objects with difficulty; needs help to prepare or modify activities.
IV	Handles a limited selection of easily managed objects in adapted situations.
V	Does not handle objects and has severely limited ability to perform even simple actions.

house

TABLE 2. House Functional Classification

Grade	Designation	Activity Level
0	Does not use	Does not use
1	Poor passive assist	Uses as stabilizing weight only
2	Fair passive assist	Can hold on to object placed in hand
3	Good passive assist	Can hold on to object and stabilize it for use by the other hand
4	Poor active assist	Can actively grasp object and hold it weakly
5	Fair active assist	Can actively grasp object and stabilize it well
6	Good active assist	Can actively grasp object and then manipulate it against other hand
7	Spontaneous use, partial	Can perform bimanual activities easily and occasionally uses the hand spontaneously
8	Spontaneous use, complete	Uses hand completely independently without reference to the other hand

tetraplegia ue

2012-05-31T09:51:00.000-07:00

A group of hand surgeons realized in the 1970s that the level of injury did not predict the number of available muscles in the upper limb very well. Therefore the international classification was established in 1979, at the Edinburgh meeting. It was called “The international classification (IC) of hand surgery in tetraplegic patients” (table 2) and it describes the number of possible transferable muscles. To measure and evaluate hand strength each muscle is tested and all muscles with a BMRC grade of M4 or more are recorded.^[3]
Table 2: International Classification of Hand surgery in Tetraplegic Patients^[3]

	Group	M4 (BMRC) Muscles
	IC 0	No muscle below the elbow
High-level Tetraplegia
	IC 1	m. brachioradialis
	IC 2	m. extensor carpi radialis longus
Mid-level tetraplegia
	IC 3	m. extensor carpi radialis brevis
	IC 4	m. pronator teres
	IC 5	m. flexor carpi radialis
Low-level tetraplegia
	IC 6	finger extensors
	IC 7	thumb extensor
	IC 8	partial digital flexors
	IC 9	lack only intrinsics
	IC X	exceptions

A muscle not included in the International Classification, but of great importance, is the triceps muscle. When assessing a patient pre-operatively the triceps strength must also be recorded. An active triceps means a patient can reach in space, and the elbow can be stabilized against gravity and against other muscles to be transferred. (see further)^[3]

Furthermore, to classify patients it is essential to record sensation in at least the thumb and index pulpa. Patients with a two point discrimination of less than 10mm are classified as cutaneous sensation (OCu) and patients with a two point discrimination of more than 10mm are classified as ocular sensation (O) (meaning that control of the to be operated limb cannot be performed by normal sensation, but is controlled visually).^[28]

Therefore patients are classified as: O or OCu, IC gr(0-X), Triceps + or –

For example: a patient has sensation of 8 mm in thumb and index pulpa, and has a good brachioradialis, extensor carpi radialis longus and brevis and a pronator teres (all of M4) but no Triceps. This patient is classified as OCu 4, Tr -.

The Role of the Upper Extremity Surgeon in the Management ofTetraplegia

TABLE 1. International Classification for Surgery of the Hand in Tetraplegia (Edinburgh 1978, Modified—Giens, 1984)

Reprinted with permission from Kuz JE, Van Heest AE, House JH. Biceps-to-triceps transfer in tetraplegic patients: report of the medial routing technique and follow-up of three cases. J Hand Surg 1999;24A:161–172.

Grade	Lowest Motor Description	Muscle Function Below the Elbow
0	ElbowFlexion/supination	None
1	Forearmneutralization	BR
2	Weakwristextension	ECRL
3	Strongwristextension	ECRB
4	Forearmpronation	PT
5	Wristflexion	FCR
6	Fingerextension	EDC
7	Thumbextension	EPL
8	Weakdigitalflexion	FDS
9	StrongdigitalFlexion(lacksonlyintrinsics)	FDP
X	Exceptions	Variable

[edit]

nerve/ vein conduit digital nerves

2012-05-31T06:49:00.001-07:00

http://journals.lww.com/plasreconsurg/Abstract/2000/10000/A_Randomized_Prospective_Study_of_Polyglycolic.13.aspx

A Randomized Prospective Study of Polyglycolic Acid Conduits for Digital Nerve Reconstruction in Humans

Weber, Robert A. M.D.; Breidenbach, Warren C. M.D.; Brown, Richard E. M.D.; Jabaley, Michael E. M.D.; Mass, Daniel P. M.D.

Abstract

This article reports the first randomized prospective multicenter evaluation of a bioabsorbable conduit for nerve repair. The study enrolled 98 subjects with 136 nerve transections in the hand and prospectively randomized the repair to two groups: standard repair, either end-to-end or with a nerve graft, or repair using a polyglycolic acid conduit. Two-point discrimination was measured by a blinded observer at 3, 6, 9, and 12 months after repair. There were 56 nerves repaired in the control group and 46 nerves repaired with a conduit available for follow-up. Three patients had a partial conduit extrusion as a result of loss of the initially crushed skin flap.

The overall results showed no significant difference between the two groups as a whole. In the control group, excellent results were obtained in 43 percent of repairs, good results in 43 percent, and poor results in 14 percent. In those nerves repaired with a conduit, excellent results were obtained in 44 percent, good results in 30 percent, and poor results in 26 percent (p = 0.46). When the sensory recovery was examined with regard to length of nerve gap, however, nerves with gaps of 4 mm or less had better sensation when repaired with a conduit; the mean moving two-point discrimination was 3.7 ± 1.4 mm for polyglycolic acid tube repair and 6.1 ± 3.3 mm for end-to-end repairs (p = 0.03). All injured nerves with deficits of 8 mm or greater were reconstructed with either a nerve graft or a conduit. This subgroup also demonstrated a significant difference in favor of the polyglycolic acid tube. The mean moving two-point discrimination for the conduit was 6.8 ± 3.8 mm, with excellent results obtained in 7 of 17 nerves, whereas the mean moving two-point discrimination for the graft repair was 12.9 ± 2.4 mm, with excellent results obtained in none of the eight nerves (p < 0.001 and p = 0.06, respectively).

This investigation demonstrates improved sensation when a conduit repair is used for nerve gaps of 4 mm or less, compared with end-to-end repair of digital nerves. Polyglycolic acid conduit repair also produces results superior to those of a nerve graft for larger nerve gaps and eliminates the donor-site morbidity associated with nerve-graft harvesting.

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Bassini operation
Clinical Article

Secondary nerve reconstruction using vein conduit grafts for neglected digital nerve injuries ^†

Yen-Hsun Lee M.D.^1,2,

Shyh-Jou Shieh M.D., Ph.D.^1,*

Article first published online: 11 JUL 2008

DOI: 10.1002/micr.20517

Copyright © 2008 Wiley-Liss, Inc.

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Microsurgery

Volume 28, Issue 6, pages 436–440, 2008

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Presented at the Annual Scientific Meeting of the Taiwan Surgical Association, March 25, 2007, Kaohsiung, Taiwan.
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Abstract

Digital nerve defects can result from neglected nerve injuries. The standard method of reconstruction is nerve grafting, but donor-site morbidity encourages searching for alternative graft materials, including vein conduit grafts. From 1995–2005, three patients with neglected digital nerve injuries received vein conduit grafting for digital nerve reconstruction in our hospital. The interval between the injury and the reconstructive procedure ranged from 17 days to 2 years, and the length of the defects ranged from 0.8 to 2.5 cm. All the vein grafts were harvested from the distal forearm. Patient 1 had a moving and a static two-point discrimination (M2PD and S2PD) of 3 and 4 mm, respectively, at a 12-year follow-up. Patient 2 had an M2PD of 5 mm and S2PD of 6 mm at an 11-year follow-up, and the patient 3 had both an M2PD and S2PD of 4 mm at a near 3-year follow-up. They all achieved useful sensory function (S3 and S3+) by modified Highet and Sander criteria. Although previous studies showed secondary repair using vein grafts yielded worse sensory recovery than that of primary repair, in our cases, secondary digital nerve reconstruction with vein conduit grafts gives excellent results at the long-term sensory evaluation, two of them with more than 10 years' follow-up. To the best of our knowledge, this might be the longest follow-up after secondary digital nerve reconstruction using a vein conduit graft. It bears the advantages of readily accessible, no donor-site morbidity, and compatible in size with digital nerves. © 2008 Wiley-Liss, Inc. Microsurgery, 2008.

http://www.bjjprocs.boneandjoint.org.uk/content/91-B/SUPP_I/97.1.short

DIGITAL NERVE RECONSTRUCTION IN THE HAND USING BIODEGRADABLE POLYGLYCOLIC ACID CONDUITS

D.N. Pafilas,

M. Vekris,

D. Gartzonikas,

A.V. Korompilias and

A. Beris

Abstract

Introduction: Digital nerve lesions with nerve gaps require reconstruction with the use of some form of graft or guide. Neurotube, a bioabsorbable polyglycolic acid (PGA) conduit, has been proposed as an effective solution for this kind of defect in emergency and planned surgery.

Methods: Nineteen posttraumatic lesions of common (5 cases) or proper (14 cases) palmar digital nerves were repaired by means of Neurotube from January 2003 till January 2006. The nerve gap size averaged 22 mm (range 15–35 mm). Thirteen lesions had associated vascular, tendon or osseous injury.

Results: Nerve regeneration was evaluated at a mean of 17 months postoperative interval. Positive results in recovery of sensibility were noticed in 73 % of the cases; static and moving two point discrimination was excellent (less than 6mm and 4mm respectively) in 9 cases and fair in 5 (7–15mm and 5–7mm respectively). Dysesthesia was present in 6 patients, cold intolerance in two, delayed wound healing in one and one patient complained for painful scar. There was no infection, conduit extrusion or allergic reaction.

Discussion and Conclusion: Bioabsorbable polyglycolic acid conduit presents an attractive and useful alternative for the reconstruction of digital nerve lesions with a small nerve gap, especially when a direct anastomosis of the two stumps is not possible, or when the suture appears to be in tension. Its use is simple, safe and also eliminates the donorsite morbidity associated with nerve-graft harvesting

The Stiff Elbow

2012-05-30T10:52:00.004-07:00

download bonefeed an ios app for orthopedics

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787214/

The Stiff Elbow

Sumon Nandi,¹ Steven Maschke,² Peter J. Evans,² and Jeffrey N. Lawton²

Author information ► Article notes ► Copyright and License information ►

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Abstract

Elbow motion is essential for upper extremity function to position the hand in space. Unfortunately, the elbow joint is prone to stiffness following a multitude of traumatic and atraumatic etiologies. Elbow stiffness can be diagnosed with a complete history and physical exam, supplemented with appropriate imaging studies. The stiff elbow is challenging to treat, and thus, its prevention is of paramount importance. When this approach fails, non-operative followed by operative treatment modalities should be pursued. Upon initial presentation in those who have minimal contractures of 6-month duration or less, static and dynamic splinting, serial casting, continuous passive motion, occupational/physical therapy, and manipulation are non-operative treatment modalities that may be attempted. A stiff elbow that is refractory to non-operative management can be treated surgically, either arthroscopically or open, to eliminate soft tissue or bony blocks to motion. In the future, efforts to prevent and treat elbow stiffness may target the basic science mechanisms involved. Our purpose was to review the etiologies, classification, evaluation, prevention, operative, and non-operative treatment of the stiff elbow.

Keywords: Elbow, Stiff, Contracture, Capsulectomy

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Introduction

The elbow is a highly constrained synovial hinge joint, intolerant of trauma, with a high propensity for stiffness and degeneration. Articulations between the trochlea and capitellum of the humerus with the trochlear notch of the ulna and radial head, respectively, are the bony foundation of the elbow joint (Fig. 1a, b). The soft tissue boundary of the elbow joint is the articular capsule, which is weakest anteriorly and posteriorly but has well-defined lateral and medial ligamentous complexes (Fig. 1c, d).

Figure 1

Anterior (a) and lateral (b) views of elbow bony anatomy. Anterior (c) and lateral (d) views of elbow ligamentous anatomy.

Elbow motion serves to position the hand in space. Morrey et al. [46] found the functional arc of elbow motion during activities of daily living to be 100° for both flexion–extension (30° to 130°) and pronation–supination (50° in either direction). Although functional limitations can be seen with less severe loss of motion, a stiff elbow has been defined as one with loss of extension of greater than 30° and flexion of less than 120° []. Elbow stiffness results from perturbations of bone, soft tissue, or a combination of both that may or may not follow a traumatic event. The etiology of elbow stiffness is the basis of its classification, diagnosis, prevention, and treatment. Given the multitude of atraumatic etiologies of elbow stiffness and at least a 5% incidence following elbow trauma, elbow stiffness is a condition affecting numerous patients who will certainly be encountered by the clinician treating upper extremity pathology []. Early rehabilitation, minimal immobilization, advances in surgical management, and basic science investigation are efforts to improve outcomes in the management of the stiff elbow. Our purpose was to review the etiologies, classification, evaluation, prevention, operative, and non-operative treatment of the stiff elbow.

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Etiologies

There are numerous and varied inciting events ultimately resulting in a stiff elbow that can be broadly categorized as either traumatic or atraumatic. Trauma, burns, and head injury are known causes of elbow contractures that are directly proportional to the severity of the insult []. Elbow surgery involves controlled trauma to the tissues and may be complicated by postoperative stiffness. Atraumatic causes of elbow stiffness include osteoarthritis and inflammatory arthritis, post-septic arthritis, multiple hemarthroses in hemophiliacs, and congenital contractures found in arthrogryposis and congenital radial head dislocation.

Bone and soft tissue are what ultimately provide mechanical blocks to motion resulting in elbow stiffness. Intra-articular fracture, osteochondral defects, and arthritic changes alter the geometry of the elbow joint, leading to stiffness. Heterotopic ossification occurs commonly about the elbow in response to tissue trauma; this acts as a physical block to elbow motion (Fig. 2). Heterotopic ossification can also create a synostosis between the radius and ulna, eliminating forearm pronation/supination. Approximately 3% of simple elbow dislocations and up to 20% of elbow fracture–dislocations are complicated by heterotopic ossification [, , ]. Five percent to 10% of patients with isolated closed head injury form heterotopic ossification, as do patients with spinal cord injuries below the level of their injury [18, , 58, ]. Those patients who have sustained both head injury and elbow trauma develop heterotopic ossification at a rate of 76% to 89% and are thus at highest risk for its formation [17, , 61]. Thermal and electric burns cause elbow heterotopic ossification formation in proportion to their degree and severity [, , , ]. Additional reported risk factors for the development of heterotopic ossification include: (1) two-incision distal biceps repair [11], (2) elbow arthroscopy [], and (3) multiple surgeries within 7 to 14 days after trauma [].

Figure 2

Plain radiograph, A-P and lateral view, of elbow with heterotopic ossification.

Trauma has immediate effects on the elbow that are direct causes of stiffness, but may also lead to elbow stiffness through secondary processes [37]. A poorly aligned articular surface following intra-articular fracture impedes elbow motion [37]. Similarly, osteochondral defects can prevent smooth motion at the articular surface, especially if a loose fragment remains within the joint. Trauma to the elbow articular surface results in its degeneration long after the initial insult in posttraumatic arthritis [37]. Once again, an incongruous articular surface hinders elbow motion, as does osteophyte formation, a hallmark of the arthritic process. Articular surface degeneration and osteophyte formation are the end result of all arthritic processes such as inflammatory arthritis, septic arthritis, as well as arthritis secondary to multiple hemarthroses in hemophiliacs.

Soft tissue contractures lead to stiffness by physically restricting elbow motion. These soft tissue changes typically occur with the bony pathology described above. More specifically, intra-articular elbow pathology is often followed by contracture of the articular capsule, collateral ligaments, and muscles [, ]. If skin overlying the elbow is no longer supple following a burn, motion is again compromised (Fig. 3) [].

Figure 3

Elbow with soft tissue contracture secondary to burn.

Some of the mechanisms of elbow stiffness have been elucidated at the basic science level. The formation of heterotopic ossification is thought to require an osteo-inductive agent acting upon mesenchymal progenitor cells in an environment that is favorable to osteogenesis [, , ]. Patients with closed head injuries, who are more likely to develop heterotopic ossification, have increased levels of circulating osteoblastic growth factors [4, ]. It has been shown that the number of myofibroblasts and levels of alpha-smooth muscle actin in the articular capsule of elbows with posttraumatic contractures are increased as compared to elbows without contractures [23]. The level of joint capsule matrix turnover was also found to be higher in elbows with posttraumatic contractures as compared to controls [].

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Classification

The two primary elbow stiffness classification systems are those of Kay and Morrey [, 47]. While Kay’s classification is based on the structure impeding elbow motion, Morrey’s classification is based on the etiology and its anatomic location []. Kay’s five-part classification system includes soft tissue contracture (type I), soft tissue contracture with ossification (type II), non-displaced articular fracture with soft tissue contracture (type III), displaced intra-articular fracture with soft tissue contracture (type IV), and posttraumatic bony bars (type V) [].

Morrey’s three-part system classifies elbow stiffness as extrinsic, intrinsic, or mixed [, 47]. Extrinsic stiffness is due to extra-articular causes, including capsular, collateral ligament, and muscle contractures as well as heterotopic ossification and extra-articular malunions. Intrinsic stiffness is due to intra-articular adhesions, loose bodies, osteophyte formation, or malalignment of the articular surface. Extrinsic contractures developing as a result of intrinsic pathology are classified as mixed.

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Evaluation

A thorough history and physical examination complimented by imaging studies comprise the requisite evaluation for elbow stiffness. The history should include the onset, duration, character, and progression of symptoms. Inquiries should be made into elbow trauma or pathology, especially infection, and prior non-surgical or surgical treatments. Comorbid conditions should be investigated, as they may have implications on the elbow such as hemophilia with resulting hemarthroses or neurologic conditions involving spasticity. The patient’s vocational and recreational pursuits should be established in order to determine the level of demand that will be placed on the elbow.

Physical examination should begin with a neurovascular exam with particular attention to ulnar nerve function. Not only is the ulnar nerve commonly involved in elbow trauma, but if operative treatment for the elbow is necessary, preoperative ulnar nerve function should be known [, 13, , 22, 28, , , 40,42–, 49, , , , 74, ]. Active and passive elbow range of motion, for both flexion–extension and pronation–supination, should be examined. The character of the endpoint at the extremes of motion should be noted. While a firm endpoint suggests a bony block to motion, a soft endpoint is indicative of a soft tissue contracture. Crepitus appreciated during elbow range of motion may signify degenerative changes, synovitis, or fracture.

The first imaging studies to evaluate a stiff elbow should be plain radiographs, including anterior–posterior, lateral, and two oblique views. Bony blocks to motion can often be detected using this modality. Should further detail of the articular surface be required, computed tomography of the elbow with two- and sometimes three-dimensional reconstructions should be performed which will aid in surgical planning for the removal of extensive heterotopic ossification. Live fluoroscopy can be used to distinguish between a bony block and soft tissue contracture.

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Prevention

The stiff elbow is challenging to treat, and thus, its prevention is of paramount importance. The loss of soft tissue compliance that leads to elbow contracture results from bleeding, edema, granulation tissue formation, and ultimately fibrosis []. Splinting the elbow in full extension postoperatively creates sufficient pressure within tissues around the elbow to minimize bleeding and resist extravasation of fluid [, , ]. Continuous passive motion (CPM) applied to the elbow immediately postoperatively and continued for 3 to 4 weeks until soft tissue swelling is controlled drives fluids away from the joint and periarticular tissues, thus minimizing the cascade of events leading to soft tissue contracture [, ]. However, a requisite for splinting in extension and postoperative CPM is stable postoperative bony and soft tissue support of the elbow.

Elbow stiffness is also prevented with the effective treatment of disease processes that damage the elbow articular surface and compromise motion. The underlying processes involved in inflammatory arthropathies should be medically controlled with a rheumatologist-prescribed anti-inflammatory/disease-modifying/biologic regimen to slow joint destruction. Hemophiliacs should receive appropriate blood factor repletion to prevent multiple hemarthroses. Joint degeneration may also be avoided with the emergent irrigation and debridement of a septic elbow, which halts cartilage destruction by proteolytic enzymes found in purulent material.

Heterotopic ossification, a potential bony block to elbow motion, may be prevented following surgical release of stiff elbows with the use of radiation postoperatively [60]. While nonselective non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin have been used effectively to prevent formation of heterotopic ossification around the hip, further investigation is required to elucidate the role of NSAIDs in preventing elbow heterotopic ossification [37].

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Treatment

The goals in treating the stiff elbow are to provide patients with a pain-free, functional, and stable elbow. Both non-operative and operative treatment modalities are available. Timing, severity, patient specific factors, and underlying pathology guide the selection of specific treatment protocols. Non-operative treatment is considered upon initial presentation in those who have minimal contractures of 6-month duration or less [27, , ]. Operative treatment is appropriate for those patients who have failed to achieve adequate pain relief or functional range of motion after initial non-operative management.

Non-operative treatments for elbow stiffness include static and dynamic splinting, serial casting, CPM, occupational/physical therapy, and manipulation [5, 8, 21, , , 47, , , , 76]. These treatment modalities have yielded variable results, with some patients gaining motion and others, ironically, losing motion [, 73].

Soft tissue contractures that result in moderate loss of elbow flexion or extension have been treated effectively by Sojbjerg [] using a dynamic splint. The contractures must be less than a year old in adults, but can be of indefinite duration in children. Once a stiff elbow is pain-free, this splint can be applied at night with serial increases in the tension of its adjustable spring. The patient must remain pain-free while the tension of the spring is increased, or the splint will not be tolerated. Non-steroidal anti-inflammatories are administered to minimize joint inflammation. Reversed dynamic slings were shown by Shewring et al. [] to increase the range of motion in elbows with posttraumatic flexion contractures by 39%. However, patients often complain of pain and discomfort with dynamic splinting (resulting in non-compliance), likely from increased co-contraction of elbow flexors and extensors due to constant tension on the soft tissues [].

Static progressive adjustable splints (Fig. 4), such as the turnbuckle splint, commercially available flexion–extension and pronation–supination splints, and serial above-the-elbow casts, have been shown to help recover elbow range of motion. Bonutti et al. [5], Green and McCoy [21], and Gelinas et al. [19] have reported a 25° to 43° increase in range of motion in contracted elbows following static progressive splinting. Zander and Healy [76] have shown that elbow flexion contractures can be reduced by 33° with the use of serial casting. Some of these devices may be more cumbersome for the patient than a dynamic splint, but offer more comfort due to the inherent stress relaxation of the tissues [, ].

Figure 4

Static progressive elbow splint.

Manipulation of the stiff elbow can be beneficial, but the procedure is not without risks. Duke et al. [8] found an increase in elbow motion in 55% of patients; the only complications reported were in two out of 11 patients who had transient sensory ulnar neuropathies. Additional complications, such as periarticular fracture and heterotopic ossification formation/exacerbation, have been reported by others [, , ].

Children with upper brachial plexus palsy suffer from elbow flexion contractures. Non-operative treatment modalities such as electrical stimulation and physical therapy are the mainstays of treatment. Basciani and Intiso [] have shown that in children who have failed serial cast treatment, botulinum toxin type A injection followed by plaster casting has improved active elbow extension by approximately 27°.

A stiff elbow that is refractory to non-operative management can be treated surgically, either arthroscopically or open. The decision to operate is based on elbow function, patient factors, and surgeon preference. Flexion contractures/extensor lag greater than 30° or the inability to flex the elbow to at least 130° is often an indication for surgery. However, surgery may be pursued for smaller deficiencies in elbow motion if a patient’s lifestyle or vocation is significantly impaired. Patient factors that may influence the decision to operate are comorbidities and willingness or ability to comply with a rigorous postoperative rehabilitation program. Surgeon comfort with a procedure and the reliability and efficacy of a procedure in a surgeon’s hands may also determine the type of surgery pursued []. All surgical procedures must: (1) respect the close proximity of critical neurovascular structures; (2) minimize soft tissue trauma by exploiting defined soft tissue planes/intervals; and (3) critically evaluate fracture reduction, stability, and intraoperative gains in range of motion. With that said, the technique for surgical release of elbow contractures should follow the pathology, the site/direction of loss of motion, and the presence or absence of ulnar nerve symptoms/signs.

Open surgery using a lateral approach to the stiff elbow as described by Morrey has been termed “the column procedure” (Fig. 5a) [, 38]. Hotchkiss et al. described the medial over-the-top (MOTT) approach (Fig. 5b) []. Both involve anterior and posterior capsulectomy and preservation of collateral ligaments and consideration of partial release only in severe contractures. Flexion contractures greater than 100° require ulnar nerve decompression (we also prefer transposition), as cubital tunnel retinaculum and posterior band of the medial collateral ligament (pMCL) contracture and changes intrinsic to the nerve may result in a stretch injury of the nerve with gains in flexion [, 49].

Figure 5

Lateral column approach (a). Skin incision (a-1). Anterior and posterior inter-muscular intervals (a-2). Anterior and posterior intervals carried down to joint capsule (a-3). Anterior interval carried down to capsular incision anterior to lateral radial (more ...)

Arthroscopy can be used to address both bony blocks to motion and soft tissue contracture about the elbow (Fig. 6a–c). However, capsular contracture causes decreased intra-articular volume; Gallay et al. [] reported the capacity of the normal elbow joint as 14 mL and that of the stiff elbow as only 6 mL. This makes arthroscopic access and visualization difficult [, ]. There is also potential for injury to neurovascular structures, which lie particularly close to arthroscopic portals in the stiff elbow with low intracapsular volume []. The use of retractors greatly facilitates arthroscopic visualization of the stiff elbow [, 33]. The risk of injury to anterior neurovascular structures also increases with a more extensive capsular excision []. Osteophytes at the tip of the olecranon or coronoid process and loose bodies have been removed arthroscopically with good results and few complications [, ].

Figure 6

Arthroscopic view of elbow with abundant soft tissue adhesions (a). Arthroscopic lysis of adhesions (b) and debridement (c).

In our hands, the technique for elbow release starts with the determination of whether the loss of motion is flexion, extension, flexion and extension, and whether osteophytes or heterotopic bone contributes (Table 1). Patients that lack elbow flexion have significant thickening and contracture of the pMCL and medial joint capsule, and these structures require resection at the time of surgery. The pMCL lies on the floor of the cubital tunnel, and excessive scarring can also lead to ulnar nerve compression and symptoms. If a patient cannot passively flex greater than 90–100°, then open release of the ulnar nerve and resection of the pMCL should be performed [, 33]. After that is done, the remainder of the release could be all arthroscopic, posterior open plus anterior arthroscopic, or all open via a MOTT procedure (see below). Our choice is to transpose the ulnar nerve subcutaneously when the nerve is required to be released.

Table 1

Algorithm for surgical release of elbow contracture.

If a patient has acceptable flexion and only lacks extension, then the release can be done either all arthroscopic, open via a lateral column (see below), or a MOTT technique. For patients with combined flexion and extension contractures, if a patient lacks flexion but can flex more than 100°, then it is surgeon preference as to technique, but one should be prepared to perform an adjuvant open medial incision to resect the pMCL. Patients with osteophyte formation can be treated as above with debridement of any bony blocks to motion, but when heterotopic bone is required to be removed, we generally prefer open resection only.

Many of the above arthroscopic techniques are employed in arthroscopic osteocapsular arthroplasty, as described by O’Driscoll [51]. This technique uses arthroscopic osteophyte excision, loose body removal, and capsulectomy to improve function and alleviate pain in those suffering from arthritis with contracture. Contraindications to this procedure include submuscular ulnar nerve transposition, which places the nerve at risk for injury during the procedure, posttraumatic arthritis with severe joint surface irregularities, and non-hypertrophic osteoarthritis in patients older than 65 years. While O’Driscoll [51] reports reliable success with this procedure, he warns that it should only be performed by experienced elbow arthroscopic surgeons. Of particular concern is any attempt to release the pMCL arthroscopically, as the ulnar nerve can be scarred directly to it.

When elbow stiffness is a result of the destruction of at least 50% of the articular surface, interposition arthroplasty is a viable option in the young, high-demand patient [10]. This procedure first involves contouring the ulno-humeral joint so that the surfaces are complementary (Fig. 7a). The joint is then resurfaced with a biologic material, such as autograft fascia lata or cutis (Fig. 7b–d) [14] or allograft Achilles or dermal graft (graft jacket). Following extensive soft tissue release and excision of bone to regain motion in a stiff elbow, the joint may be rendered unstable. External fixation (hinged) can be used in this situation to provide sufficient stability to allow for soft tissue healing without limiting early postoperative motion (Fig. 8) [56, ]. Joint distraction can also be applied across the joint using the hinged external fixator to minimize insult to the interposed tissue during early postoperative motion [,10]. It has been reported in the literature that distraction interposition arthroplasty yields satisfactory results 69–92% of the time [6, 14, 48, , ]. However, the need for external fixation following a stable contracture release without interposition was shown to offer no added benefit and in fact causes increased numbers of complications [57].

Figure 7

En face view of distal humerus with severe degenerative disease (a). Cutis graft preparation from abdomen (b, c). Distal humerus following cutis soft tissue resurfacing (d).

Figure 8

Plain radiograph, lateral view, of elbow with external fixator.

Recently, the role of botulinum toxin-A in preventing posttraumatic elbow stiffness in adults has been explored. In patients who underwent open reduction and internal fixation following elbow fracture or fracture dislocation, intraoperative injection of botulinum toxin-A into the elbow flexors resulted in improved postoperative range-of-motion and function [34]. Presumably, this limits the overpowering flexor muscle spasticity that sets up a cycle of co-contraction with the triceps across the joint. Similarly, botulinum toxin-A in the triceps postoperatively has had promising results in our hands for patients undergoing pMCL and posterior capsular release to gain flexion.

While focus is largely placed on loss of elbow flexion and extension, loss of pronation and supination (forearm rotation) can also be disabling. Heterotopic ossification resulting in proximal radioulnar synostosis greatly limits forearm rotation and is a difficult problem to treat surgically given the close proximity of neurovascular structures. Proximal radial resection at a point just distal to the radioulnar synostosis, creating a pseudo joint, has shown to have favorable outcomes with an increase in average arc of forearm rotation from 0° to 98° [30]. In patients with congenital proximal radioulnar synostosis, it has been reported that acute elbow flexion contracture induced by forced hyperflexion resolves after excision of a hypoplastic annular ligament-like structure [41].

When the ulnohumeral joint surface cannot be salvaged (greater than 50% involvement of the articular surface) following surgical release of a severely contracted or ankylosed elbow, total elbow arthroplasty is considered in patients greater than 60 years (Fig. 9a, b). Instability often results following operative release of a stiff elbow, so a semi-constrained implant is recommended. Figgie et al. [12] reported a significant increase in mean arc of motion (0° preoperatively to 80° postoperatively) following total elbow arthroplasty using semi-constrained and custom prostheses in completely ankylosed elbows. Mansat and Morrey [39] showed a significant increase in mean arc of motion (7° preoperatively to 67° postoperatively) following total elbow arthroplasty without the use of custom implants in patients with stiff and ankylosed elbows. These are difficult procedures and high complication rates were reported.

Figure 9

Plain radiographs, A-P (a) and lateral (b) views, of total elbow arthroplasty.

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Summary

The elbow joint is critical to upper extremity function as it positions the hand in space. With a stiff elbow, the entire upper extremity range of motion is diminished and function suffers. While there are multiple non-operative and operative treatment options available to address the bony and/or soft tissue basis of elbow stiffness, prevention is of paramount importance, as this is a difficult condition to treat. In the future, efforts to prevent elbow stiffness may target mechanisms involved at the basic science level.

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References

1. Apfelberg DB, Larson SJ. Dynamic anatomy of the ulnar nerve at the elbow. Plast Reconstr Surg. 1973;51(1):79–81. doi:10.1097/00006534-197301000-00014. [PubMed]

2. Bain GI, Mehta JA, Heptinstall RJ. The dynamic elbow suspension splint. J Shoulder Elbow Surg. 1998;7(4):419–21. doi:10.1016/S1058-2746(98)90035-0. [PubMed]

3. Basciani M, Intiso D. Botulinum toxin type-A and plaster cast treatment in children with upper brachial plexus palsy. Pediatr Rehabil. 2006;9(2):165–70. doi:10.1080/13693780500402229. [PubMed]

4. Bidner SM, Rubins IM, Desjardins JV, Zukor DJ, Goltzman D. Evidence for a humoral mechanism for enhanced osteogenesis after head injury. J Bone Jt Surg Am. 1990;72(8):1144–9.

5. Bonutti PM, Windau JE, Ables BA, Miller BG. Static progressive stretch to reestablish elbow range of motion. Clin Orthop Relat Res. 1994;(303):128–34.

6. Cheng SL, Morrey BF. Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J Bone Jt Surg Br. 2000;82(2):233–8. doi:10.1302/0301-620X.82B2.9507.

7. Cheung EV, Adams R, Morrey BF. Primary osteoarthritis of the elbow: current treatment options. J Am Acad Orthop Surg. 2008;16(2):77–87. [PubMed]

8. Duke JB, Tessler RH, Dell PC. Manipulation of the stiff elbow with patient under anesthesia. J Hand Surg [Am]. 1991;16(1):19–24.

9. Ellerin BE, Helfet D, Parikh S, Hotchkiss RN, Levin N, Nisce L, et al. Current therapy in the management of heterotopic ossification of the elbow: a review with case studies. Am J Phys Med Rehabil. 1999;78(3):259–71. doi:10.1097/00002060-199905000-00016. [PubMed]

10. Evans PJ. Elbow interposition/distraction arthroplasty. In: Yamaguchi K, King GJW, McKee MD, O’Driscoll SWM, editors. Advanced reconstruction elbow. 1st ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007. p. 435.

11. Failla JM, Amadio PC, Morrey BF, Beckenbaugh RD. Proximal radioulnar synostosis after repair of distal biceps brachii rupture by the two-incision technique. report of four cases. Clin Orthop Relat Res. 1990;(253):133–6.

12. Figgie MP, Inglis AE, Mow CS, Figgie HE 3rd. Total elbow arthroplasty for complete ankylosis of the elbow. J Bone Jt Surg Am. 1989;71(4):513–20.

13. Froimson AI, Anouchi YS, Seitz WH Jr, Winsberg DD. Ulnar nerve decompression with medial epicondylectomy for neuropathy at the elbow. Clin Orthop Relat Res. 1991;(265):200–6.

14. Froimson AI, Morrey BF. Interposition arthroplasty of the elbow. In: Morrey BF, editor. Master techniques in orthopaedic surgery: the elbow. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2002. p. 391.

15. Galbraith KA, McCullough CJ. Acute nerve injury as a complication of closed fractures or dislocations of the elbow. Injury 1979;11(2):159–64. doi:10.1016/S0020-1383(79)80015-7. [PubMed]

16. Gallay SH, Richards RR, O’Driscoll SW. Intraarticular capacity and compliance of stiff and normal elbows. Arthroscopy 1993;9(1):9–13. doi:10.1016/S0749-8063(05)80336-6. [PubMed]

17. Garland DE, O’Hollaren RM. Fractures and dislocations about the elbow in the head-injured adult. Clin Orthop Relat Res. 1982;(168):38–41.

18. Garland DE. A clinical perspective on common forms of acquired heterotopic ossification. Clin Orthop Relat Res. 1991;(263):13–29.

19. Gelinas JJ, Faber KJ, Patterson SD, King GJ. The effectiveness of turnbuckle splinting for elbow contractures. J Bone Jt Surg Br. 2000;82(1):74–8. doi:10.1302/0301-620X.82B1.9792.

20. Gofton WT, King GJ. Heterotopic ossification following elbow arthroscopy. Arthroscopy 2001;17(1):E2. doi:10.1053/jars.2001.16283. [PubMed]

21. Green DP, McCoy H. Turnbuckle orthotic correction of elbow-flexion contractures after acute injuries. J Bone Jt Surg Am. 1979;61(7):1092–5.

22. Heithoff SJ, Millender LH, Nalebuff EA, Petruska AJ Jr. Medial epicondylectomy for the treatment of ulnar nerve compression at the elbow. J Hand Surg [Am]. 1990;15(1):22–9.

23. Hildebrand KA, Zhang M, van Snellenberg W, King GJ, Hart DA. Myofibroblast numbers are elevated in human elbow capsules after trauma. Clin Orthop Relat Res. 2004;(419):189–97.

24. Hildebrand KA, Zhang M, Hart DA. High rate of joint capsule matrix turnover in chronic human elbow contractures. Clin Orthop Relat Res. 2005;439:228–34. doi:10.1097/01.blo.0000177718.78028.5c. [PMC free article] [PubMed]

25. Hoffer MM, Brody G, Ferlic F. Excision of heterotopic ossification about elbows in patients with thermal injury. J Trauma. 1978;18(9):667–70. [PubMed]

26. Holguin PH, Rico AA, Garcia JP, Del Rio JL. Elbow ankylosis due to postburn heterotopic ossification. J Burn Care Rehabil. 1996;17(2):150–4. doi:10.1097/00004630-199603000-00009.[PubMed]

27. Husband JB, Hastings H 2nd. The lateral approach for operative release of post-traumatic contracture of the elbow. J Bone Jt Surg Am. 1990;72(9):1353–8.

28. Josefsson PO, Johnell O, Gentz CF. Long-term sequelae of simple dislocation of the elbow. J Bone Jt Surg Am. 1984;66(6):927–30.

29. Jupiter JB, O’Driscoll SW, Cohen MS. The assessment and management of the stiff elbow. Instr Course Lect. 2003;52:93–111. [PubMed]

30. Kamineni S, Maritz NG, Morrey BF. Proximal radial resection for posttraumatic radioulnar synostosis: a new technique to improve forearm rotation. J Bone Jt Surg Am. 2002;84-A(5):745–51.

31. Karachalios T, Maxwell-Armstrong C, Atkins RM. Treatment of post-traumatic fixed flexion deformity of the elbow using an intermittent compression garment. Injury 1994;25(5):313–5. doi:10.1016/0020-1383(94)90243-7. [PubMed]

32. Kasparyan NG, Hotchkiss RN. Dynamic skeletal fixation in the upper extremity. Hand Clin. 1997;13(4):643–63. [PubMed]

33. Kelly EW, Morrey BF, O’Driscoll SW. Complications of elbow arthroscopy. J Bone Jt Surg Am. 2001;83-A(1):25–34.

34. Kim P, Wolfe VM, McKean J, Jobin C, Strauch RJ, Rosenwasser MP. Intraoperative injection of botulinum toxin-A (Botox®) for prevention of post-traumatic elbow stiffness. Quebec: 2nd Combined Meeting of the American Orthopaedic Association and the Canadian Orthopaedic Association; 2008.

35. King GJ, Faber KJ. Posttraumatic elbow stiffness. Orthop Clin North Am. 2000;31(1):129–43. doi:10.1016/S0030-5898(05)70133-4. [PubMed]

36. Laurencin CT, Schwartz JT Jr, Koris MJ. Compression of the ulnar nerve at the elbow in association with synovial cysts. Orthop Rev. 1994;23(1):62–5. [PubMed]

37. Lindenhovius AL, Jupiter JB. The posttraumatic stiff elbow: a review of the literature. J Hand Surg [Am]. 2007;32(10):1605–23. doi:10.1016/j.jhsa.2007.09.015.

38. Mansat P, Morrey BF. The column procedure: a limited lateral approach for extrinsic contracture of the elbow. J Bone Jt Surg Am. 1998;80(11):1603–15.

39. Mansat P, Morrey BF. Semiconstrained total elbow arthroplasty for ankylosed and stiff elbows. J Bone Jt Surg Am. 2000;82(9):1260–8.

40. Manske PR, Johnston R, Pruitt DL, Strecker WB. Ulnar nerve decompression at the cubital tunnel. Clin Orthop Relat Res. 1992;(274):231–7.

41. Masuko T, Kato H, Minami A, Inoue M, Hirayama T. Surgical treatment of acute elbow flexion contracture in patients with congenital proximal radioulnar synostosis. A report of two cases. J Bone Jt Surg Am. 2004;86-A(7):1528–33.

42. McGowan AJ. The results of transposition of the ulnar nerve for traumatic ulnar neuritis. J Bone Jt Surg Br. 1950;32-B(3):293–301.

43. McKee M, Jupiter J, Toh CL, Wilson L, Colton C, Karras KK. Reconstruction after malunion and nonunion of intra-articular fractures of the distal humerus. methods and results in 13 adults. J Bone Jt Surg Br. 1994;76(4):614–21.

44. McKee MD, Jupiter JB. A contemporary approach to the management of complex fractures of the distal humerus and their sequelae. Hand Clin. 1994;10(3):479–94. [PubMed]

45. Mohan K. Myositis ossificans traumatica of the elbow. Int Surg. 1972;57(6):475–8. [PubMed]

46. Morrey BF, Askew LJ, Chao EY. A biomechanical study of normal functional elbow motion. J Bone Jt Surg Am. 1981;63(6):872–7.

47. Morrey BF. Post-traumatic contracture of the elbow. operative treatment, including distraction arthroplasty. J Bone Jt Surg Am. 1990;72(4):601–18.

48. Morrey BF. Distraction arthroplasty. clinical applications. Clin Orthop Relat Res. 1993;(293):46–54.

49. O’Driscoll SW, Horii E, Carmichael SW, Morrey BF. The cubital tunnel and ulnar neuropathy. J Bone Jt Surg Br. 1991;73(4):613–7.

50. O’Driscoll SW, Giori NJ. Continuous passive motion (CPM): theory and principles of clinical application. J Rehabil Res Dev. 2000;37(2):179–88. [PubMed]

51. O’Driscoll SW. Arthroscopic osteocapsular arthroplasty. In: Yamaguchi K, King GJW, McKee MD, O’Driscoll SWM, editors. Advanced reconstruction elbow. 1st ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007. p. 59.

52. Page C, Backus SI, Lenhoff MW. Electromyographic activity in stiff and normal elbows during elbow flexion and extension. J Hand Ther. 2003;16(1):5–11. [PubMed]

53. Peterson SL, Mani MM, Crawford CM, Neff JR, Hiebert JM. Postburn heterotopic ossification: insights for management decision making. J Trauma. 1989;29(3):365–9. doi:10.1097/00005373-198903000-00015. [PubMed]

54. Pignatti G, Ferrari D, Tigani D, Scardovi M, Trentanti P, Trentani F, et al. The treatment of post-traumatic stiffness of the elbow. Chir Organi Mov. 2000;85(4):381–7. [PubMed]

55. Rettig AC, Ebben JR. Anterior subcutaneous transfer of the ulnar nerve in the athlete. Am J Sports Med. 1993;21(6):836–9; discussion 839–40. [PubMed]

56. Ring D, Jupiter JB. Operative release of complete ankylosis of the elbow due to heterotopic bone in patients without severe injury of the central nervous system. J Bone Jt Surg Am. 2003;85-A(5):849–57.

57. Ring D, Hotchkiss RN, Guss D, Jupiter JB. Hinged elbow external fixation for severe elbow contracture. J Bone Jt Surg Am. 2005;87(6):1293–6. doi:10.2106/JBJS.D.02462.

58. Roberts JB, Pankratz DG. The surgical treatment of heterotopic ossification at the elbow following long-term coma. J Bone Jt Surg Am. 1979;61(5):760–3.

59. Roberts PH. Dislocation of the elbow. Br J Surg. 1969;56(11):806–15. doi:10.1002/bjs.1800561103.[PubMed]

60. Robinson C, Lyons J, Evans PJ, Lawton JN, Graham T, Polster J, et al. Postoperative single fraction radiation for prevention of heterotopic ossification after elbow surgery. Int J Radiat Oncol Biol Phys. 2007;69(3):S545. doi:10.1016/j.ijrobp.2007.07.1794.

61. Sazbon L, Najenson T, Tartakovsky M, Becker E, Grosswasser Z. Widespread periarticular new-bone formation in long-term comatose patients. J Bone Jt Surg Br. 1981;63-B(1):120–5.

62. Sharma RK, Covell NA. An unusual ulnar nerve injury associated with dislocation of the elbow. Injury 1976;8(2):145–7. doi:10.1016/0020-1383(76)90052-8. [PubMed]

63. Shewring DJ, Beaudet M, Carvell JE. Reversed dynamic slings: results of use in the treatment of post-traumatic flexion contractures of the elbow. Injury 1991;22(5):400–2. doi:10.1016/0020-1383(91)90105-N. [PubMed]

64. Sojbjerg JO. The stiff elbow. Acta Orthop Scand. 1996;67(6):626–31. [PubMed]

65. Stover SL, Hataway CJ, Zeiger HE. Heterotopic ossification in spinal cord-injured patients. Arch Phys Med Rehabil. 1975;56(5):199–204. [PubMed]

66. Summerfield SL, DiGiovanni C, Weiss AP. Heterotopic ossification of the elbow. J Shoulder Elbow Surg. 1997;6(3):321–32. doi:10.1016/S1058-2746(97)90025-2. [PubMed]

67. Tan V, Daluiski A, Capo J, Hotchkiss R. Hinged elbow external fixators: indications and uses. J Am Acad Orthop Surg. 2005;13(8):503–14. [PubMed]

68. Tan V, Daluiski A, Simic P, Hotchkiss RN. Outcome of open release for post-traumatic elbow stiffness. J Trauma. 2006;61(3):673–8. doi:10.1097/01.ta.0000196000.96056.51. [PubMed]

69. Thompson HC 3rd, Garcia A. Myositis ossificans: aftermath of elbow injuries. Clin Orthop Relat Res. 1967;50:129–34. doi:10.1097/00003086-196701000-00012. [PubMed]

70. Timmerman LA, Andrews JR. Arthroscopic treatment of posttraumatic elbow pain and stiffness. Am J Sports Med. 1994;22(2):230–5. doi:10.1177/036354659402200213. [PubMed]

71. Uchida Y, Sugioka Y. Ulnar nerve palsy after supracondylar humerus fracture. Acta Orthop Scand. 1990;61(2):118–9. [PubMed]

72. Vardakas DG, Varitimidis SE, Goebel F, Vogt MT, Sotereanos DG. Evaluating and treating the stiff elbow. Hand Clin. 2002;18(1):77–85, vi. [PubMed]

73. Viola RW, Hastings H, 2nd. Treatment of ectopic ossification about the elbow. Clin Orthop Relat Res. 2000;(370):65–86.

74. Wadsworth TG. The external compression syndrome of the ulnar nerve at the cubital tunnel. Clin Orthop Relat Res. 1977;(124):189–204.

75. Wang KC, Shih HN, Hsu KY, Shih CH. Intercondylar fractures of the distal humerus: routine anterior subcutaneous transposition of the ulnar nerve in a posterior operative approach. J Trauma. 1994;36(6):770–3. doi:10.1097/00005373-199406000-00003. [PubMed]

76. Zander CL, Healy NL. Elbow flexion contractures treated with serial casts and conservative therapy. J Hand Surg [Am]. 1992;17(4):694–7. doi:10.1016/0363-5023(92)90319-K.

Articles from Hand (New York, N.Y.) are provided here courtesy of American Association for Hand Surgery

Beighton Hypermobility Score

2012-05-30T10:52:00.000-07:00

http://www.shoulderdoc.co.uk/article.asp?article=645

Beighton Hypermobility Score

The Beighton score is a simple system to quantify joint laxity and hypermobility.

It uses a simple 9 point system, where the higher the score the higher the laxity.

The threshold for joint laxity in a young adult is ranges from 4-6. Thus a score above 6 indicates hypermobility, but not necessarily true BHJS (see below)

Joint	Finding	Points
left little (fifth) finger	passive dorsiflexion beyond 90°	1
	passive dorsiflexion <= 90°	0
right little (fifth) finger	passive dorsiflexion beyond 90°	1
	passive dorsiflexion <= 90°	0
left thumb	passive dorsiflexion to the flexor aspect of the forearm	1
	cannot passively dorsiflex thumb to flexor aspect of the forearm	0
right thumb	passive dorsiflexion to the flexor aspect of the forearm	1
	cannot passively dorsiflex thumb to flexor aspect of the forearm	0
left elbow	hyperextends beyonds 10°	1
	extends <= 10	0
right elbow	hyperextends beyonds 10°	1
	extends <= 10	0
left knee	hyperextends beyonds 10°	1
	extends <= 10	0
right knee	hyperextends beyonds 10°	1
	extends <= 10	0
forward flexion of trunk with knees full extended	palms and hands can rest flat on the floor	1
	palms and hands cannot rest flat on the floor	0

DIAGNOSTIC CRITERIA FOR THE BENIGN JOINT HYPERMOBILITY SYNDROME (BJHS)

Major Criteria

A Beighton score of 4/9 or greater (either currently or historically)
Arthralgia for longer than 3 months in 4 or more joints

Minor Criteria

A Beighton score of 1, 2 or 3/9 (0, 1, 2 or 3 if aged 50+)
Arthralgia (> 3 months) in one to three joints or back pain (> 3 months), spondylosis, spondylolysis/spondylolisthesis.
Dislocation/subluxation in more than one joint, or in one joint on more than one occasion.
Soft tissue rheumatism. > 3 lesions (e.g. epicondylitis, tenosynovitis, bursitis).
Marfanoid habitus (tall, slim, span/height ratio >1.03, upper: lower segment ratio less than 0.89, arachnodactily [positive Steinberg/wrist signs].
Abnormal skin: striae, hyperextensibility, thin skin, papyraceous scarring.
Eye signs: drooping eyelids or myopia or antimongoloid slant.
Varicose veins or hernia or uterine/rectal prolapse.

The BJHS is diagnosed in the presence two major criteria, or one major and two minor criteria, or four minor criteria. Two minor criteria will suffice where there is an unequivocally affected first-degree relative.
BJHS is excluded by presence of Marfan or Ehlers-Danlos syndromes

References:

Beighton PH Horan F. Orthopedic aspects of the Ehlers-Danlos syndrome. J Bone Joint Surg [Br]. 1969; 51: 444-453.

ulnar translocation

2012-05-30T09:55:00.000-07:00

http://www.laboratoriosilesia.com/upfiles/sibi/T1107897.pdf

http://download.journals.elsevierhealth.com/pdfs/journals/0363-5023/PIIS0363502311600439.pdf

PAPER 43

Traumatic Ulnar Translocation
of the Carpus: Diagnosis and
Treatment Strategies
Level 4 Evidence
􀁶 John C. Berschback, MD
􀁍 David M. Kalainov, MD
Sohail N. Husain, MD
􀁍 Thomas A. Wiedrich, MD
Mark S. Cohen, MD
􀁍 Daniel J. Nagle, MD
􀀩􀀺􀀱􀀰􀀵􀀩􀀦􀀴􀀪􀀴
Repair of injured structures in traumatic ulnar translocation of the
carpus does not ensure maintenance of normal radiocarpal alignment.
􀀮􀀦􀀵􀀩􀀰􀀥􀀴
Twelve patients, 13 cases, with traumatic ulnar translocation of
the carpus were identified: 8 cases were ligamentous injuries and
5 cases were ligamentous injuries in association with fractures.
Static x-rays revealed ulnocarpal translocation in 11 cases,
whereas stress views showed the instability pattern in 2 cases.
Treatment was initiated within 3.5 months of injury and included
wrist immobilization (2 cases), volar radiocarpal ligament repair
(5 cases), volar and dorsal radiocarpal ligament repair (1 case),
fracture fixation alone or in combination with volar radiocarpal
ligament repair (4 cases), and radioscapholunate fusion (1
case). Seven patients, 8 cases, were examined specifically for
the purpose of this study at a mean of 4.9 years after injury.
Information in 5 cases was obtained from medical records at a
mean of 10 months following injury. Radiocarpal and intercarpal
radiographic measurements were made using established
methods. Interobserver reliabilities of ulnocarpal translocation
measurements were calculated using Kendall's tau test.
􀀳􀀦􀀴􀀶􀀭􀀵􀀴
At final evaluation, 9 patients described intermittent wrist pain, and
3 patients reported no wrist pain. Each patient demonstrated loss
of normal wrist flexion and/or extension. A variable amount of ulnar
translocation was detected with static and/or dynamic radiographs
in 10 of 11 wrists with follow-up images. Degenerative arthritis
involving the radioscaphoid articulation developed in 5 of these
cases. There was good to excellent interobserver agreement for
measurements of ulnocarpal translocation.
􀀴􀀶􀀮􀀮􀀢􀀳􀀺􀀁􀀱􀀰􀀪􀀯􀀵􀀴
∙ Post-traumatic ulnar translocation of the carpus can result
from ligamentous injury alone or in association with fracture.
∙ Stress radiographs may be necessary for diagnosis.
∙ Restricted wrist motion is expected and intermittent wrist pain
may persist following surgical intervention.
∙ Early repair of radiocarpal ligaments does not ensure maintenance
of radiocarpal stability or preclude the development of arthrosis.

some
references
1. Dumontier C, Meyer zu Reckendorf G, Sautet A, Lenoble E, Saffar
P, Allieu Y. Radiocarpal dislocations: classification and proposal for
treatment. A review of twenty-seven cases. J Bone Joint Surg Am.
2001;83:212-8.
2. Rayhack JM, Linscheid RL, Dobyns JH, Smith JH. Posttraumatic
ulnar translation of the carpus. J Hand Surg Am. 1987;12:180-9.
3. St bler A, Baumeister RG, Szeimies U, Fink U, Berger H. Rotatory
palmar subluxation of the lunate in post-traumatic ulnar carpal
translocation. Skeletal Radiol. 1994;23:103-6.
4. McMurtry RY, Youm Y, Flatt AE, Gillespie TE. Kinematics of the wrist
II. Clinical applications. J Bone Joint Surg Am. 1978:60:955-61.
5. DiBenedetto MR, Lubbers LM, Coleman CR. A standardized
measurement of ulnar carpal translocation. J Hand Surg Am.
1990;15:1009-10.
6. Wollstein R, Wei C, Bilonick RA, Gilula LA. The radiographic
measurement of ulnar translation. J Hand Surg Eur. 2009;34:384-7.
7. Viegas SF, Patterson RM, Ward K. Extrinsic wrist ligaments in the
pathomechanics of ulnar translation instability. J Hand Surg Am.
1995;20:312-8.
8. Yang Z, Mann FA, Gilula LA, Haerr C, Larsen CF.
Scaphopisocapitate alignment: criterion to establish a neutral
lateral view of the wrist. Radiology. 1997;205:865-9.
9. Larsen CF, Mathiesen FK, Lindequist S. Measurements of carpal
bone angles on lateral wrist radiographs. J Hand Surg Am.
1991;16:888-93.
10. Linscheid RL. Kinematic considerations of the wrist. Clin Orthop
Relat Res. 1986;202:27-39.

anatomy of the 1,2 intercompartmental supraretinacular artery

2012-05-30T06:58:00.000-07:00

http://www.ncbi.nlm.nih.gov/pubmed/18294536

The detailed anatomy of the 1,2 intercompartmental supraretinacular artery for vascularized bone grafting of scaphoid nonunions.

Waitayawinyu T, Robertson C, Chin SH, Schlenker JD, Pettrone S, Trumble TE.

Source

Department of Orthopaedics and Sports Medicine, University of Washington, Seattle, WA 98195, USA.

Abstract

PURPOSE:

To describe the configuration of the 1,2 intercompartmental supraretinacular artery (1,2 ICSRA), including the location of the perforators, and to discuss the clinical use of the 1,2 ICSRA for vascularized bone grafting of scaphoid nonunions.

METHODS:

Thirteen fresh-frozen cadaveric forearms were used to evaluate the variations in the anatomy of the 1,2 ICSRA. After injection of red latex, the 1,2 ICSRA and its perforators were characterized and measured. Pedicle length and distal reach of the transposed 1,2 ICSRA pedicle was evaluated. We noted the relationship of the 1,2 ICSRA to the dorsal scaphoid branch of the radial artery. Another 10 specimens were injected, frozen, and sectioned to evaluate vascular penetration into the dorsal distal radius.

RESULTS:

The 1,2 ICSRA branched from the radial artery 1.9 mm proximal to the tip of the radial styloid (range -6.3-3.2 mm), on average. The average pedicle length was 22.5 mm (range 15-31 mm), which permits its application for both dorsal and volar scaphoid. The relationship between the origin of the 1,2 ICSRA and the dorsal scaphoid branch was categorized into 3 types, including--separate, combined, and shared. The average number of perforating vessels arising from the pedicle was 5.5 (range 3-7), with an average of 2.75 (range 1-7) perforators overlying a 1 by 0.5 cm block of the distal radius bone graft. A graft located between 8-18 mm proximal to the articular surface of distal radius would incorporate the greatest numbers of perforators. The most notable vascular penetration of the distal radius was demonstrated at 10.0 mm proximal to the radial styloid.

CONCLUSIONS:

The detailed anatomy of the 1,2 ICSRA presented in this study may guide in planning and dissection to maximize the vascularity of a pedicled bone graft based on this vessel for the management of scaphoid nonunions.

pip fracture

2012-05-30T06:45:00.000-07:00

Considerations

source AO FOUNDATION

Avulsion fractures of the volar plate are very common injuries, often resulting from sporting injuries and usually involving the middle and ring fingers. Several classification systems for them have been proposed for them. The Eaton classification is useful and practical. Its premise is that successful treatment must be based on the stability of the fracture, which in turn depends on:

size of the fragment
degree of impaction
ruptures of one or both collateral ligaments
direction of the dislocation (palmar, lateral, or dorsal)

Eaton type I (hyperextension)
These are hyperextension injuries, with an avulsion of the volar plate and a longitudinal split in the collateral ligaments.

Eaton type II (dorsal dislocation)
Complete dorsal dislocation of the PIP joint and avulsion of the volar plate. The base of the middle phalanx rests dorsally on the condyles of the proximal phalanx, with no contact between the articular surfaces.

Eaton type III (fracture dislocation)
A fracture dislocation with an avulsed small fragment.

Stability of fracture dislocations (Eaton type III)
Stability of the reduction depends on the size of the avulsed fragment and the amount of ligament remaining attached to the middle phalanx.
If less than 40% of the articular segment is avulsed, the fracture is displaced dorsally, with the dorsal portion of the collateral ligament remaining attached to the middle phalanx. This helps to keep the reduction stable.
However, if more than 40% of the articular segment has avulsed, only very little or no ligament will remain attached to the base of the middle phalanx, rendering the reduction unstable.

Mechanism of the injury
These injuries are commonly caused by hyperextension of the finger causing an avulsion fracture of the volar plate.
Often, in addition to hyperextension, axial pressure applied to the fingertip, causes longitudinal compression forces on the middle phalanx towards the proximal phalanx; this can lead to an additional impaction fracture.

Deforming forces
The flexor digitorum superficialis (FDS) exerts a palmar pull on the middle phalanx around a pivotal point determined by the junction of intact cartilage and the fracture; this leads to subluxation and dorsal tilting, depending on the degree of the impaction.

Recognizing subluxation
Diagnosis is based on:

the clinical history of the trauma and mechanism of the injury
the clinical examination of the patient
the x-rays

AP and lateral x-rays are necessary for diagnosis. Be careful to avoid overlap of other fingers in the x-rays.
An AP view will help to recognize impaction fractures.
Often, a subluxation is not immediately apparent on the lateral view. Look for the characteristic “V” sign of diverging joint surfaces, which indicates this injury.

In the lateral view, the dorsal cortical profiles of the proximal and middle phalanges should be collinear. Any axial malalignment is a clear indication of subluxation.

Indication for nonoperative treatment
Ask the patient to flex the finger under image intensification.
If reduction of the avulsion fracture is achieved with less than a 30 degree bend, nonoperative treatment may be a good choice.
However, if it takes more than 30 degrees of flexion to reduce the fragment, operative treatment is indicated.
Reduction will not be achieved if soft tissues are interposed between the fracture fragments. This is also an indication for surgical treatment.
Passive lateral movement of the finger under image intensification will help to assess lateral stability.

Small-fragment avulsion fracture
When the avulsed fragment is very small (<30% of the articular segment), nonoperative treatment is usually a good choice.

Irreducible fracture – operative treatment
When the avulsed fragment is very small (<30% of the articular segment), nonoperative treatment is usually a good choice. In some cases, the fracture can not be reduced due to interposed tissues, or blood clot.
In these cases, internal fixation is indicated.
As the use of a lag screw could easily shatter such a small fragment, internal fixation with sutures is often chosen.

Management of proximal interphalangeal joint injuries

2012-05-30T06:15:00.000-07:00

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696003/

Can J Plast Surg. 2007 Winter; 15(4): 199–203.

PMCID: PMC2696003

Management of proximal interphalangeal joint injuries

Arnis Freiberg, MD FRCSC FACS

Author information ► Copyright and License information ►

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Abstract

Injuries to the proximal interphalangeal joint are common but frequently missed. They are often overtreated by prolonged immobilization, resulting in stiffness, which may be permanent. The purpose of the present article is to briefly review the relevant anatomy and biomechanics, present an approach to physical examination and diagnosis, and propose a practical clinical classification. The treatment of the most severe injury – the intra-articular fracture dislocation – is controversial. The various treatment options are discussed, based on personal experience and a review of the literature. A list of relevant references is presented.

Keywords: Management, Proximal interphalangeal joint injuries, Review of literature

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Résumé

Les lésions des articulations interphalangiennes proximales sont courantes, mais passent souvent inaperçues. Par ailleurs, elles sont souvent trop traitées par une immobilisation prolongée, ce qui provoque une raideur qui risque de devenir permanente. Le présent article vise à analyser brièvement l’anatomie et la biomécanique pertinentes, à présenter un mode d’examen physique et de diagnostic et à effectuer une classification clinique pratique. Le traitement de la lésion la plus grave, la fracture-luxation intra-articulaire, est controversé. On expose les diverses possibilités de traitement, d’après l’expérience personnelle et une analyse bibliographique. On présente également une liste de références pertinentes.

Proximal interphalangeal (PIP) joint injuries are commonly seen in athletes, both amateurs and professionals. There are two commonly seen pitfalls. The injury is initially considered to be ‘minor’ by either the patient, coach or emergency physician, or treated by unnecessarily long immobilization or surgery, both of which may lead to permanent stiffness or deformity.

In general, when dealing with finger fractures and dislocations, one must always remember that for every case of delayed or nonhealing fracture, there are at least 100 permanently stiff fingers.

For this reason, it is of utmost importance to make an early, correct diagnosis, and to outline a treatment program involving the patient, hand therapist and surgeon.

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ANATOMY AND BIOMECHANICS

The PIP joint is a hinge joint that is normally kept in alignment by a soft tissue envelope consisting of joint capsule, the volar plate, collateral ligaments and the central slip. These structures form a tight-fitting ‘box’ with a very narrow joint space. Injuries to this soft tissue envelope can be either partial or complete.

As long as this envelope is not severely disrupted, early motion aligns the damaged tissues and intra-articular fracture fragments – the basis for the rationale of early motion. A complete dislocation indicates that at least two of the above structures must have been completely disrupted. The collateral ligaments are usually avulsed at the insertion, as is the volar plate, with or without a bony fragment. Most PIP joint injuries are caused by high velocity, such as in sports injuries. The low-velocity injuries are less common and are usually caused by twisting; this often causes disruption of the thin and filmy volar plate origin.

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CLINICAL EXAMINATION AND DIAGNOSIS

At the time of the injury

A complete and thorough examination is quite often not possible because of swelling and pain, as seen in the more severe injuries. In less severe injuries, point tenderness and localized swelling quite accurately indicates the site of injury. Testing for joint stability at this point in time is not very important and can be deferred until the next early postinjury visit. Plain x-rays are valuable for two reasons:

to diagnose a complete dislocation or extent of subluxation; and
to look for avulsion fractures. Unless the fragment is large, the fracture itself is not important, but it will indicate the site of the ligamentous injury.

Late (one week or more after the time of injury)

Test joint stability gently to prevent further damage to the partially torn ligaments. Next, look for areas of point tenderness at the following six sites:

insertion and origin of the ulnar and radial collateral ligaments;
insertion and origin of the volar plate; and
insertion of the central slip.

The ideal time for this examination is approximately seven to 10 days following the injury.

Later, once the soft tissues have partially healed, the exact diagnosis may be more difficult. A correct and precise diagnosis is important in choosing the most appropriate treatment (eg, for injuries such as avulsion of the central slip insertion, splinting as opposed to early motion is performed to prevent a late boutonniere deformity). Similarly, it is important to identify the site of the collateral ligament injury to choose the correct digit for buddy-taping.

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IMAGING

Plain radiographs are sufficient in supporting the clinical diagnosis. It is important to order not only the standard anteroposterior and lateral views, but also two oblique views to properly identify small avulsion fractures. Although small avulsion fractures themselves are not important, they will identify the sites of the ligament injuries.

For larger bony fragments, it is important to assess not only the size of the avulsed fragment, but also the degree of displacement or rotation. A good lateral view is essential in identifying the degree of subluxation or dislocation.

It is also important to order postreduction films for two reasons:

to prove and document a successful reduction; and
for medicolegal reasons.

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CLASSIFICATION

Although there are several classifications described in the literature, I prefer a rather simple classification:

dislocations – volar, dorsal;
subluxations – volar, dorsal, ulnar, radial;
avulsion or ‘chip’ fractures associated with ligamentous injuries; and
intra-articular fractures or fracture dislocations:
- – unipolar – proximal phalanx: one condyle, two condyles or comminuted; middle phalanx: comminuted;
- – bipolar: complete joint destruction.

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DISLOCATIONS AND SUBLUXATIONS

Most dislocations are closed and are easily reduced when closed. Compound or open dislocations are usually volar and often irreducible closed, requiring open reduction.

Volar dislocations

Volar dislocations are the least common, are often most difficult to reduce and carry a poorer prognosis. Compound dislocations may require open reduction, because either one or both condyles can be caught between the flexor tendons and the flexor tendon sheath. The reduction is usually carried out under digital block anesthesia.

Following reduction, buddy-taping and early motion is usual. An extension block splint may be necessary in unstable cases.

Dorsal dislocations

Dorsal dislocations are the most common, are usually closed and easily reduced closed. Open reduction may be required in cases of volar plate entrapment. The postreduction routine is the same as in volar dislocations.

Subluxations

Depending on the degree, reduction may not be necessary. In most cases, buddy-taping is the only postinjury care needed; the appropriate digit depends on the site of injury (ulnar or radial). Poorest end results are seen in injuries to the little finger because of the length discrepancy between the little and ring fingers.

Splinting of the PIP joint at various angles is usually performed by emergency physicians and, if not seen early on, may lead to permanent stiffness. It is therefore important to see these patients as soon after the injury as possible. This requires educating the emergency physicians and screening of referrals to the hand clinics.

It is my firm belief that even a healthy, young, uninjured PIP joint can only be safely totally immobilized for two weeks. If one adds age, injury and type of finger to this equation, the safe immobilization time is even shorter.

Early protected motion is therefore the key to a reasonably successful outcome. It is also very important to warn the patient at the time of the initial visit that, in general terms, injuries to the PIP joint are serious and the final outcome will most likely result in a less-than-normal-looking and -functioning digit. It is the patient’s – often erroneous – perception that a simple ‘jammed’ digit, often reduced at the time of injury, may lead to serious consequences. It is also important to explain to the patient that there is a lot of hard work ahead as far as rehabilitation and hand therapy are concerned. The patient must be warned that the therapy will be painful and reminded of the old slogan seen in hand therapy departments: ‘no pain, no gain’. A prescription for an analgesic to be taken before the therapy will be appreciated by the patient.

It is interesting to note that one rarely sees unstable PIP joints, with the exception of individuals with congenitally hyperextensile joints. I believe that for any one unstable joint, there are at least 100 permanently stiff PIP joints!

Therefore, early motion is the key to a successful outcome. To accomplish this, I prefer to see these patients as soon as possible postinjury and follow them at weekly intervals.

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INTRA-ARTICULAR FRACTURE DISLOCATIONS

Treatment options

Because there are a number of well-recognized treatment options, it is obvious that there is not one method superior to another. Unfortunately, there are no prospective or controlled studies available, and as far as I can see, there will not be any in the foreseeable future. Because of the diversity of the various types of injury and digits involved, one would need a large number of cases to satisfy statistical requirements.

Long-term follow-up may also be difficult, because these injuries are more common in the young, mobile population. Each digit presents with specific problems – especially the little finger. Last but not least, the patient’s occupation and degree of motivation have to be taken into account, as well as the availability and skill of the hand therapist, who is of utmost importance for postinjury care.

Finally, there is the problem of a universally accepted classification of these injuries. A rather comprehensive and practical classification was presented by Schenck in 1994 (); however, a review of several articles dealing with various treatment method preferences found their authors preferred to use their own classifications, making outcome comparisons almost impossible.

During the past 20 years (or longer), I have used a simple and practical clinical classification for intra-articular fractures:

unipolar;
bipolar; and
complete joint destruction or comminuted bipolar fractures (the following subclassification deals with the size of the fracture fragment):
- – large – one that is large enough for fixation either by a pin or a lag screw, usually at the base of the proximal phalanx, or one or two condyles; and
- – small – not suitable for fixation, usually involving the head of the middle phalanx or both of the above (complete joint destruction).

The large fragment may be displaced, undisplaced or rotated.

Early motion and buddy-taping: My preferred treatment method of management is early motion and buddy-taping, with or without extension block splinting.

The rationale for this method is that all fractures eventually heal, but most, if not moved early, become stiff, some permanently.

In addition, the PIP joint has very limited space, and as long as the enclosing soft tissue ‘envelope’ has not been severely disrupted, early motion realigns the small fracture fragments in a nearly normal anatomical position.

The basic principles are twofold:

maintain concentric reduction of the joint; and
institute early motion to minimize or prevent stiffness.

Buddy taping is most successful in digits 2 to 4. Although the little finger is one the more commonly injured digits, because of length discrepancy between digit 4 and digit 5, the final results are inferior compared with the other digits.

If the fracture requires reduction and fixation, these are carried out at the time of the injury, and buddy taping started immediately after.

Indications for reduction: There are very very few indications for open reduction. They include:

unstable or rotated condylar fractures;
irreducible, usually volar, fracture dislocations; and
volar plate entrapment.

Contrary to some surgeons’ opinions, collateral ligaments do not need to be surgically repaired. My preference for operative exposure is a dorsal, longitudinal, midline incision that can be extended, if necessary, from the distal interphalangeal joint to the metacarpophalangeal joint.

Crossing a joint at right angles is only contraindicated on the volar surface. I have not encountered any problems using this incision on the dorsal surface. Furthermore, a midline incision avoids injury to the dorsal sensory branches.

Indications for extension block splinting: After reduction or fixation, the joint is tested in flexion and extension. We know that approximately 90% of finger fractures are stable in flexion; therefore, one must note the degree of extension at which the reduction becomes unstable. The splint is then designed to block at this angle. If there is no loss of fixation at maximum extension, the splint is not necessary. Weekly follow-up is necessary to make sure that the patient is following instructions and has not lost the reduction. Referral to a hand therapist is only needed if the patient has problems with the splint, needs assistance in buddy taping or shows lack of motivation.

Personal experience and comments

With a few exceptions, I have been using this approach for most intra-articular fractures over the past 20 years. Although I do not have a large number of cases with long-term follow-up, I have been generally quite satisfied with the results.

It is interesting to note the similarity of the radiological appearance over one year following injury, especially in cases involving the base of the middle phalanx.

The base of the middle phalanx remodels to a shape similar to an inverted umbrella. In general terms, very few patients complain of pain or instability. It is also interesting to note that post-traumatic arthritis is very rare in fractures confined to the base of the middle phalanx. The range of motion is also usually functionally quite satisfactory. We have always stressed the importance of flexion over extension in digits 4 and 5 and extension over flexion in digits 2 and 3. In general terms, final results are better in digits 2 and 3 than in digits 4 and 5 because of the length discrepancy between digits 4 and 5 during buddy-taping.

Advantages and disadvantages of early motion and buddy-taping

Advantages:

simplicity;
limited need for an experienced hand therapist;
absence of bulky splints; and
more suitable for cold climates – with the exception of extension block splints, the patient is able to wear mitts during cold weather.

Disadvantages:

Because of the absence of traction, foreshortening of the digit is not prevented. However, because the most commonly injured digit is the little finger, slight foreshortening is functionally not disabling. Patient compliance and motivation, or lack thereof, are most likely no different than with other treatment methods. Pain and discomfort during rehabilitation may be less when using distraction methods.

Again, it must be pointed out that it is almost impossible to compare this method with the others.

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ALTERNATIVE METHODS OF TREATMENT

The dynamic traction method

This method combines movement and traction, thus preventing foreshortening while maintaining mobility. The motion can be either active or passive, and there are several modifications described in the literature. The procedure was first described by Schenck in 1986 (). A comprehensive review was presented by Schenck in 1994 (). Various splinting techniques have been nicely presented by hand therapists Kearney and Brown ().

Because I decided early on in my practice to treat all PIP joint fracture dislocations by buddy-taping and early motion, I have no experience with this method. On reviewing the literature, it appears to be a popular and well-accepted treatment method.

Advantages:

combination of traction and motion;
choice between active and passive motion;
choice between continuous and intermittent motion;
reduction and realignment of articular fragments; and
distal distraction force, which prevents or minimizes contractures of ligaments and periarticular structures.

Disadvantages:

requires the services of a trained hand therapist;
the splint is bulky – not suitable for use in cold environments;
cost; and
patient understanding of the therapy protocol may be poor.

Closed reduction and percutaneous K-wire fixation

Indications:

relatively large fracture fragments; and
lack of comminution of fracture fragments.

Advantages:

reduced scarring and subsequent stiffness;
semi-rigid fixation; and
avoidance of added injury to the soft tissue ‘envelope’.

Disadvantages:

need for an image intensifier;
possible pin tract infection; and
possible need for a second procedure for K-wire removal.

Open reduction and internal fixation

Indications:

inability to obtain adequate reduction or fixation by percutaneous K-wire fixation;
relatively large fracture fragments;
absence of comminution; and
rotated condylar fractures.

Advantages:

ability to obtain anatomical reduction; and
stable fixation.

Disadvantages:

increased soft tissue scarring predisposing to stiffness; and
technically demanding.

Volar plate arthroplasty

First described and popularized by Eaton (), volar plate arthroplasty is indicated for reconstruction of a unipolar, comminuted fracture, usually at the base of the middle phalanx.

Advantages:

uses autogenous material;
maintains length;
may be used as a primary or secondary procedure; and
resurfaces the damaged articular surface.

Disadvantages:

technically demanding;
requires relatively extensive soft tissue dissection, hence potentially more scarring;
potential instability;
may produce an angular deformity;
precludes early motion;
may require removal of the K-wire or pull-out wire; and
potential K-wire infections.

Interpositional arthroplasty – silicone

This technique was first described and popularized by Swanson and de Groot Swanson ().

Advantages:

most suitable as a salvage procedure for secondary reconstruction;
maintains some movement;
eliminates or minimizes pain; and
maintains length.

Disadvantages:

requires extensive soft tissue dissection, therefore predisposing to postoperative stiffness;
technically demanding;
more expensive than other methods;
precludes the use of possible late arthrodesis;
not indicated for the index finger – not strong enough for power pinch; and
possible implant breakage and subsequent silicone synovitis.

Arthrodesis

Arthrodesis is most commonly used as a salvage procedure.

Advantages:

stability – especially indicated in the index finger; and
eliminates pain.

Disadvantages:

loss of movement;
some loss of length;
poor choice for little and ring fingers, where flexion is important; and
difficulty in determining the ideal angle of fusion, especially digits 4 and 5.

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SUMMARY AND CONCLUSIONS

Injuries to the PIP joint are serious and must be treated with respect. In addition, expectations and outcomes must be discussed with the patient. Emergency physicians must be made aware of the possible sequelae and educated in making an accurate diagnosis as well as the need for an early referral to a hand surgeon, to hopefully avoid potential complications. Surgeons must realize that the main problem in treating these injuries is to avoid permanent deformity and stiffness. Correct initial diagnosis is of utmost importance in choosing the most successful treatment plan. It must be remembered that most of the errors are committed by overtreatment rather than undertreatment! Open reduction and internal fixation predisposes to stiffness and should be avoided, if possible. There is no need for repair of collateral ligaments. Because there are many treatment choices available for treating severe intra-articular fracture dislocations and no reliable, scientifically proven studies, the surgeon must use the method with which he or she is most familiar and comfortable.

Unfortunately, well-controlled, outcome-based studies will not be forthcoming in the near future because of the relatively small number of cases available, the diversity of digits involved, injury patterns, lack of a universally accepted classification and outcome results. A multicentre project may provide the answer.

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REFERENCES AND SELECTED BIBLIOGRAPHY

1. Leibovic SJ, Bowers WH. Anatomy of the proximal interphalangeal joint. Hand Clin. 1994;10:169–78.[PubMed]

2. Salter RB. The physiologic basis of continuous passive motion for articular cartilage healing and regeneration. Hand Clin. 1994;10:211–9. [PubMed]

3. Schenck RR. Classification of fractures and dislocations of the proximal interphalangeal joint. Hand Clin. 1994;10:179–85. [PubMed]

4. Kearney LM, Brown KK. The therapist’s management of intra-articular fractures. Hand Clin.1994;10:199–209. [PubMed]

5. McPhee SD. Extension block splinting for the proximal interphalangeal joint. Am J Occup Ther.1987;41:389–90. [PubMed]

6. Freiberg A, Pollard BA, Macdonald MR, Duncan MJ. Management of proximal interphalangeal joint injuries. J Trauma. 1999;46:523–8. [PubMed]

7. Chinchalkar SJ, Gan BS. Management of proximal interphalangeal joint fractures and dislocations. J Hand Ther. 2003;16:117–28. [PubMed]

8. Lubahn JD. Dorsal fracture dislocations of the proximal interphalangeal joint. Hand Clin. 1988;4:15–24. [PubMed]

9. Majumder S, Peck F, Watson JS, Lees VC. Lessons learned from the management of complex intra-articular fractures at the base of the middle phalanges of fingers. J Hand Surg (Br) 2003;28:559–65.[PubMed]

10. Kang R, Stern PJ. Fracture dislocations of the proximal interphalangeal joint. J Am Soc Surg Hand.2002;2:47–59.

11. Dobyns JH, McElfresh EC. Extension block splinting. Hand Clin. 1994;10:229–37. [PubMed]

12. Lopez MS, Hanley KF. Dynamic extension block splinting for proximal interphalangeal joint injuries.Mil Med. 1985;150:423–6. [PubMed]

13. Newington DP, Davis TR, Barton NJ. The treatment of dorsal fracture-dislocation of the proximal interphalangeal joint by closed reduction and Kirschner wire fixation: A 16-year follow up. J Hand Surg (Br) 2001;26:537–40. [PubMed]

14. Aladin A, Davis TR. Dorsal fracture-dislocation of the proximal interphalangeal joint: a comparative study of percutaneous Kirschner wire fixation versus open reduction and internal fixation. J Hand Surg (Br) 2005;30:120–8. [PubMed]

15. Schenck RR. Dynamic traction and early passive movement for fractures of the proximal interphalangeal joint. J Hand Surg (Am) 1986;11:850–8. [PubMed]

16. Schenck RR. The dynamic traction method. Combining movement and traction for intra-articular fractures of the phalanges. Hand Clin. 1994;10:187–98. [PubMed]

17. Badia A, Riano F, Ravikoff J, Khouri R, Gonzalez-Hernandez E, Orbay JL. Dynamic intradigital external fixation for proximal interphalangeal joint fracture dislocations. J Hand Surg (Am)2005;30:154–60. [PubMed]

18. Freeland AE, Benoist LA. Open reduction and internal fixation method for fractures at the proximal interphalangeal joint. Hand Clin. 1994;10:239–50. [PubMed]

19. Kobayashi Ky, Torrono AL. Proximal interphalangeal joint arthroplasty of the hand. J Am Soc Surg Hand. 2003;3:219–26.

20. Swanson AB, de Groot Swanson G. Flexible implant resection arthroplasty of the proximal interphalangeal joint. Hand Clin. 1994;10:261–6. [PubMed]

21. Malerich MM, Eaton RG. The volar plate reconstruction for fracture-dislocation of the proximal interphalangeal joint. Hand Clin. 1994;10:251–60. [PubMed]

22. Jones BF, Stern P. Interphalangeal joint arthrodesis. Hand Clin. 1994;10:267–75. [PubMed]

Articles from The Canadian Journal of Plastic Surgery are provided here courtesy of Pulsus Group

collagen

2012-05-30T06:09:00.001-07:00

http://www.ncbi.nlm.nih.gov/books/NBK21582/

Section 22.3Collagen: The Fibrous Proteins of the Matrix

Collagen is the major insoluble fibrous protein in the extracellular matrix and in connective tissue. In fact, it is the single most abundant protein in the animal kingdom. There are at least 16 types of collagen, but 80 – 90 percent of the collagen in the body consists of types I, II, and III (Table 22-3). These collagen molecules pack together to form long thin fibrils of similar structure (seeFigure 5-20). Type IV, in contrast, forms a two-dimensional reticulum; several other types associate with fibril-type collagens, linking them to each other or to other matrix components. At one time it was thought that all collagens were secreted by fibroblasts in connective tissue, but we now know that numerous epithelial cells make certain types of collagens. The various collagens and the structures they form all serve the same purpose, to help tissues withstand stretching.

Table 22-3

Major Collagen Molecules.

The Basic Structural Unit of Collagen Is a Triple Helix

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Because its abundance in tendon-rich tissue such as rat tail makes the fibrous type I collagen easy to isolate, it was the first to be characterized. Its fundamental structural unit is a long (300-nm), thin (1.5-nm-diameter) protein that consists of three coiled subunits: two α1(I) chains and one α2(I).^* Each chain contains precisely 1050 amino acids wound around one another in a characteristic right-handed triple helix (Figure 22-11a). All collagens were eventually shown to contain three-stranded helical segments of similar structure; the unique properties of each type of collagen are due mainly to segments that interrupt the triple helix and that fold into other kinds of three-dimensional structures.

Figure 22-11

The structure of collagen. (a) The basic structural unit is a triple-stranded helical molecule. Each triple-stranded collagen molecule is 300 nm long. (b) In fibrous collagen, collagen molecules (more...)

The triple-helical structure of collagen arises from an unusual abundance of three amino acids: glycine, proline, and hydroxyproline. These amino acids make up the characteristic repeating motif Gly-Pro-X, where X can be any amino acid. Each amino acid has a precise function. The side chain of glycine, an H atom, is the only one that can fit into the crowded center of a three-stranded helix. Hydrogen bonds linking the peptide bond NH of a glycine residue with a peptide carbonyl (C═O) group in an adjacent polypeptidehelp hold the three chains together. The fixed angle of the C – N peptidyl-proline or peptidyl-hydroxyproline bond enables each polypeptide chain to fold into a helix with a geometry such that three polypeptide chains can twist together to form a three-stranded helix. Interestingly, although the rigid peptidyl- proline linkages disrupt the packing of amino acids in an α helix, they stabilize the rigid three-stranded collagen helix.

Collagen Fibrils Form by Lateral Interactions of Triple Helices

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Many three-stranded type I collagen molecules pack together side-by-side, forming fibrils with a diameter of 50 – 200 nm. In fibrils, adjacent collagen molecules are displaced from one another by 67 nm, about one-quarter of their length (Figure 22-11b). This staggered array produces a striated effect that can be seen in electron micrographs of stained collagen fibrils; the characteristic pattern of bands is repeated about every 67 nm (Figure 22-11c). The unique properties of the fibrous collagens — types I, II, III, and V — are due to the ability of the rodlike triple helices to form such side-by-side interactions.

Short segments at either end of the collagen chains are of particular importance in the formation of collagen fibrils (see Figure 22-11). These segments do not assume the triple-helical conformation and contain the unusual amino acid hydroxylysine (see Figure 3-16). Covalent aldol cross-links form between two lysine or hydroxylysine residues at the C-terminus of one collagen molecule with two similar residues at the N-terminus of an adjacent molecule (Figure 22-12). These cross-links stabilize the side-by-side packing of collagen molecules and generate a strong fibril.

Figure 22-12

The side-by-side interactions of collagen helices are stabilized by an aldol cross-link between two lysine (or hydroxylysine) side chains. The extracellular enzyme lysyl oxidase catalyzes (more...)

Type I collagen fibrils have enormous tensile strength; that is, such collagen can be stretched without being broken. These fibrils, roughly 50 nm in diameter and several micrometers long, are packed side-by-side in parallel bundles, called collagen fibers, in tendons, where they connect muscles with bones and must withstand enormous forces (Figure 22-13). Gram for gram, type I collagen is stronger than steel.

Figure 22-13

Electron micrograph of the dense connective tissue of a chick tendon. Most of the tissue is occupied by parallel type I collagen fibrils, about 50 nm in diameter, seen here in cross section. (more...)

Assembly of Collagen Fibers Begins in the ER and Is Completed outside the Cell

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Collagen biosynthesis and assembly follows the normal pathway for a secreted protein (see Figure 17-13). The collagen chains are synthesized as longer precursors called procollagens; the growing peptide chains are co-translationally transported into the lumen of the rough endoplasmic reticulum (ER). In the ER, the procollagen chain undergoes a series of processing reactions (Figure 22-14). First, as with other secreted proteins, glycosylation of procollagen occurs in the rough ER and Golgi complex. Galactose andglucose residues are added to hydroxylysine residues, and long oligosaccharides are added to certain asparagine residues in the C-terminal propeptide, a segment at the C-terminus of a procollagen molecule that is absent from mature collagen. (The N-terminal end also has a propeptide.) In addition, specific proline and lysine residues in the middle of the chains are hydroxylated by membrane-bound hydroxylases. Lastly, intrachain disulfide bonds between the N- and C-terminal propeptide sequences align the three chains before the triple helix forms in the ER. The central portions of the chains zipper from C- to N-terminus to form the triple helix.

Figure 22-14

Major events in the biosynthesis of fibrous collagens. Modifications of the procollagen polypeptide in the endoplasmic reticulum include hydroxylation, glycosylation, and disulfide-bond formation. (more...)

After processing and assembly of type I procollagen is completed, it is secreted into the extracellular space. During or followingexocytosis, extracellular enzymes, the procollagen peptidases, remove the N-terminal and C-terminal propeptides. The resultingprotein, often called tropocollagen (or simply collagen), consists almost entirely of a triple-stranded helix. Excision of both propeptides allows the collagen molecules to polymerize into normal fibrils in the extracellular space (see Figure 22-14). The potentially catastrophic assembly of fibrils within the cell does not occur both because the propeptides inhibit fibril formation and because lysyl oxidase, which catalyzes formation of reactive aldehydes, is an extracellular enzyme (see Figure 22-12). As noted above, these aldehydes spontaneously form specific covalent cross-links between two triple-helical molecules, which stabilizes the staggered array characteristic of collagen molecules and contributes to fibril strength.

Post-translational modification of procollagen is crucial for the formation of mature collagen molecules and their assembly into fibrils. Defects in this process have serious consequences, as ancient mariners frequently experienced. For example, the activity of both prolyl hydroxylases requires an essential cofactor, ascorbic acid (vitamin C). In cells deprived of ascorbate, as in the disease scurvy, the procollagen chains are not hydroxylated sufficiently to form stable triple helices at normal body temperature (Figure 22-15), nor can they form normal fibrils. Consequently, nonhydroxylated procollagen chains are degraded within the cell. Without the structural support of collagen, blood vessels, tendons, and skin become fragile. A supply of fresh fruit provides sufficient vitamin C to process procollagen properly.

Figure 22-15

Denaturation of collagen containing a normal content of hydroxyproline and of abnormal collagen containing no hydroxyproline. Without hydrogen bonds between hydroxyproline residues, the collagen (more...)

Mutations in Collagen Reveal Aspects of Its Structure and Biosynthesis

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Type I collagen fibrils are used as the reinforcing rods in construction of bone. Certain mutations in the α₁(I) or α₂(I) genes lead to osteogenesis imperfecta, or brittle-bone disease. The most severe type is an autosomal dominant, lethal disease resulting in death in utero or shortly after birth. Milder forms generate a severe crippling disease. As might be expected, many cases of osteogenesis imperfecta are due to deletions of all or part of the very long α₁(I) gene. However, a single amino acidchange is sufficient to cause certain forms of this disease. As we have seen, a glycine must be at every third position for the collagen triple helix to form; mutations of glycine to almost any other amino acid are deleterious, producing poorly formed and unstable helices. Since the triple helix forms from the C- to the N-terminus, mutations of glycine near the C-terminus of the α₁(I) chain are usually more deleterious than those near the N-terminus; the latter permit substantial regions of triple helix to form. Mutant unfolded collagen chains do not leave the rough ER of fibroblasts (the cells that make most of type I collagen), or they leave it slowly. As the ER becomes dilated and expanded, the secretion of other proteins (e.g., type III collagen) by these cells also is slowed down.

Because each type I collagen molecule contains two α₁(I) and one α₂(I) chains, mutations in the α₂(I) chains are much less damaging. To understand this point, consider that in a heterozygote expressing one wild-type and one mutant α₂(I) protein, 50 percent of the collagen molecules will have the abnormal α₂(I) chain. In contrast, if the mutation is in the α₁(I) chain, 75 percent of the collagen molecules will have one or two mutant α₁(I) chains. In fact, even low expression of a mutant α₁(I) gene can be deleterious, because the mutant chains can disrupt the function of wild-type α₁(I) chains when combined with them. To study such mutations, experimenters constructed a mutant α₁(I) collagen gene with a glycine-to-cysteine substitution near the C-terminus. This mutant gene was used to create lines of transgenic mice with otherwise normal collagen genes. High-level expression of the mutanttransgene was lethal, and expression at a rate 10 percent that of the normal α₁(I) genes caused severe growth abnormalities.

Collagens Form Diverse Structures

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Collagens differ in their ability to form fibers and to organize the fibers into networks. For example, type II is the major collagen in cartilage. Its fibrils are smaller in diameter than type I and are oriented randomly in the viscous proteoglycan matrix. Such rigid macromolecules impart a strength and compressibility to the matrix and allow it to resist large deformations in shape. This property allows joints to absorb shocks.

Type II fibrils are cross-linked to proteoglycans in the matrix by type IX, a collagen of a different structure (Figure 22-16a). Type IX collagen consists of two long triple helices connected by a flexible kink. The globular N-terminal domain extends from the composite fibrils, as does a heparan sulfate molecule, a type of large, highly charged polysaccharide (discussed later) that is linked to the α₂(IX) chain at the flexible kink. These protruding nonhelical domains are thought to anchor the fibril to proteoglycans and other components of the matrix. The interrupted triple-helical structure of type IX collagen prevents it from assembling into fibrils; instead, these three collagens associate with fibrils formed from other collagen types and thus are called fibril-associated collagens (see Table 22-3).

Figure 22-16

Interactions of fibrous and nonfibrous collagens. (a) Association of types II and IX collagen in a cartilage matrix. Type II forms fibrils similar in structure to type I, with a similar 67-nm(more...)

In many connective tissues, type VI collagen is bound to the sides of type I fibrils and may bind them together to form thicker collagen fibers (Figure 22-16b). Type VI collagen is unusual in that the molecule consists of relatively short triple-helical regions about 60 nm long separated by globular domains about 40 nm long. Fibrils of pure type VI collagen thus give the impression of beads on a string.

In some places, several ECM components are organized into a basal lamina, a thin sheetlike structure. Type IV collagen forms the basic fibrous two-dimensional network of all basal laminae. Three type IV collagen chains form a 400-nm-long triple helix with large globular domains at the C-termini and smaller ones of unknown structure at the N-termini. The helical segment is unusual in that the Gly-X-Y sequences are interrupted about 24 times with segments that cannot form a triple helix; these nonhelical regions introduce flexibility into the molecule (Figure 22-17a). Lateral association of the N-terminal regions of four type IV molecules yields a characteristic tetrameric unit that can be observed in the electron microscope (Figure 22-17b). Triple-helical regions from several molecules then associate laterally, in a manner similar to fibril formation among fibrous collagens, to form branching strands of variable but thin diameters. These interactions, together with those between the C-terminal globular domains and the triple helices in adjacent type IV molecules, generate an irregular two-dimensional fibrous network (Figure 22-17b). We will discuss the other components of the basal lamina and the functions of this specialized matrix structure in the next section.

Figure 22-17

Structure and assembly of type IV collagen. (a) Schematic diagram of 400-nm-long triple-helical molecule of type IV collagen. This molecule has a noncollagen domain at the N-terminus and (more...)

SUMMARY

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All 16 types of collagen contain a repeating Gly-Pro-X sequence and fold into a characteristic triple-helical structure.
The various collagens are distinguished by the ability of their helical and nonhelical regions to associate into fibrils, to form sheets, or to cross-link different collagen types.
Most collagen is fibrillar and composed of type I molecules. A two-dimensional network of type IV collagen is unique to thebasal lamina.
Fibrous type collagen molecules (e.g., types I, II, and III) assemble into fibrils that are stabilized by covalent aldol cross-links (see Figure 22-11).
Procollagen chains are modified and assembled into a triple helix in the ER (see Figure 22-14). Helix formation is aided by disulfide bonds between N- and C-terminal propeptides, which align the polypeptide chains in register. Generally, the propeptides are removed after secretion, and then collagen fibrils form in the extracellular space.
Fibrous collagen has specific structural requirements and is very susceptible to mutation, especially in glycine residues. Because mutant collagen chains can affect the function of wild-type ones, such mutations have a dominant phenotype.

Footnotes

*: In collagen nomenclature, the collagen type is in roman numerals and is enclosed in parentheses.

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The emerging role of Clostridium histolyticum collagenase in the treatment of Dupuytren disease

2012-05-30T06:02:00.002-07:00

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988615/

The emerging role of Clostridium histolyticum collagenase in the treatment of Dupuytren disease

Alexis Thomas¹ and Ardeshir Bayat^1,²

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This article has been cited by other articles in PMC.

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Abstract

Dupuytren disease (DD) is a common fibroproliferative disease of unknown etiopathogenesis affecting the palmar aponeurosis, causing reduced hand function and resulting in fixed flexion contractures of the digits. Current gold standard treatment for the management of DD is surgical excision involving removal of the affected palmar fascial tissue. However, there are potential complications associated with surgery as it is costly and a positive surgical outcome is often short-lived because the disease tends to recur. Therefore, there is growing interest in nonsurgical, outpatient-based treatments that could be quicker, cheaper, reduce morbidity, show a decreased rate of recurrence, and give DD patients an improved quality of life when compared with traditional surgical management. Of the available nonsurgical options, injectable Clostridium histolyticum collagenase (CHC) has received recent clinical interest. In this article, a brief overview of DD surgical and nonsurgical treatments utilized is given, followed by a detailed examination of the nine papers published to date on the use of CHC in DD (and similar fibrotic disorders). These papers have investigated safe and efficacious doses for the injection of CHC to treat palpable DD cords in adult patients and have shown significant short- to mid-term results for correction to near-full digital extension (≤5° extension) following CHC injection of DD cords. CHC has been shown to target the collagen-based DD cords while sparing surrounding neurovasculature, with a complication profile that appears comparable to that of the surgical methods currently utilized. In conclusion, clostridial collagenase is a novel nonsurgical treatment option of considerable potential in the management of DD when administered by specialist hand surgeons with detailed knowledge of the disease and the relevant anatomy. Nonetheless, there is a need for further data on long-term results, complications, and rate of recurrence with the use of this emerging treatment option.

Keywords: Dupuytren contracture, enzymatic injection, fibrosis, nonsurgical treatment

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Introduction

Dupuytren disease (DD) is a common, fibroproliferative disease affecting the hands and resulting in fixed flexion contractures that are progressive and irreversible. This deformity results in considerable disability and can limit patient activities of daily living, manual activities, and sporting hobbies, markedly reducing patients’ quality of life.2 There are a variety of treatments that have been investigated, with the ongoing mainstay being surgical correction involving either release or excision of the affected palmar fascia. However, there has been an increasing interest in the use of and clinical success with the utilization of injectable Clostridium histolyticum collagenase (CHC) for the nonoperative treatment of DD.–10 Recent clinical trials,,,–18 have shown encouraging results, to the extent that this novel technique will likely be used frequently in future clinical practice – hence, it is important to explore the efficacy and safety profile of such a technique.

The aims of this review are to give an overview of DD and its current treatment options, with particular focus on the nonsurgical methods trialed historically; to give a synopsis of the history and uses of CHCs to date; to summarize the uses of such CHCs within the field of DD (and associated fibrotic conditions); and, to highlight the growing utility of such collagenases within the treatment options available for DD.

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Methods

Searches were undertaken using Medline, PubMed, and Scopus to identify seminal studies and reviews using all keywords relating to DD and CHC. To ensure no studies were missed, the references of each selected study or review were also searched and any relevant articles were included. All relevant European and US patents were reviewed, plus all US Food and Drugs Administration (FDA) documentation relating to the Xiaflex^® (Auxilium Pharmaceuticals Inc., Malvern, PA) application for approval (granted in February 2010). Finally, the product specification sheets for the commercially available clostridial collagenases were reviewed.

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DD – an overview

DD is a benign yet progressive, fibroproliferative disorder of unknown origin affecting the palmar fascia and extending into the digits of the hands. It is commonly bilateral, with a pathological transformation of the fascial tissues into thickened fibrous nodules and cords which, on progression to the advanced stage of the disease, result in irreversible flexion contractures of the involved digits. DD can be associated with extra-palmar ectopic fibrosis over the knuckle pads, known as Garrod nodes; in the sole of the foot, known as Lederhose disease or plantar fibromatosis;21 formation of fibrotic plaques within the corpora cavernosal tunica albuginea, resulting in penile bending during erections, known as Peyronie disease (PD); and, uncommonly, with involvement of the wrist or with nodular fasciitis in the popliteal space.

DD was first described in the medical literature in 1831 by the eponymous Baron Guillaume Dupuytren,23 although Dupuytren was not the first to describe this disease. Henry Cline, in 1777, initially described DD as a palmar fascial disorder through his study of cadaveric specimens: he first noted the contribution of the palmar fascia to the disorder, then, 10 years later, suggested its treatment via palmar fasciotomy.23,24 In addition, Cline’s student, Sir Astley Cooper wrote in 1822 on this disease and demonstrated a procedure similar to needle fasciotomy. Dupuytren visited Cooper in 1826 but did not perform his first surgery (on his coach man) until 1831 – this was the operation he later described and published in Lancet.26

The prevalence of DD is thought to be affected by gender, age, ethnicity, and geographical origin.27 The male to female incidence ratio ranges between 5:1 and 15:1, although the frequency in women increases substantially with age, catching up to that seen in men in later life. Rarely, children as young as 9 years have been diagnosed with the condition. More commonly, men tend to present in the fifth decade, whereas women require treatment later23 – irrespectively, the incidence in both sexes increases with age, with the reported prevalence in northern Europe for men older than 65 years being between 18% and 30%. DD is primarily a disease of northern European caucasians, with only sporadic case reports of it affecting nonwhite individuals. Where nonwhite-skinned populations are affected, eg, the Japanese (where the prevalence is similar to that seen in northern Europe) and, rarely, African Americans, authors have postulated a prior interracial mixing in the genetic lineage of the affected individuals.23 Geographically, DD is commonest in the United Kingdom, Scandinavia, North America, Australasia, and Japan, with a markedly decreased prevalence in the more southerly Mediterranean regions and South America. DD is considered to be rare in Africa and China.27,

The etiology of DD remains controversial, with associations of varying significance having been found with heredity,27,,34 alcohol consumption, smoking, diabetes mellitus,37, epilepsy (or antiepileptic medications),, raised serum lipids, local injury (leading to algodystrophy and disuse of the affected hand), and occupations involving vibration exposure. Of these, genetic heritability undoubtedly has a significant etiological contribution, with some authors suggesting a Mendelian autosomal dominant transmission with variable penetrance and others suggesting DD to be a complex trait (like diabetes, hypertension, or cancer). The associations with smoking, diabetes, raised serum lipids, and alcohol consumption have been suggested to be related to the microangiopathic ischemia that underlies these conditions – this results in increased free radical production, which stimulates fibroblast proliferation and cytokine release, potentially leading to the development of DD.

The pathophysiology of DD is complex and multifactorial, to date eluding the establishment of an overarching pathophysiological model despite substantial investigative efforts. The disease affects the palmar fascial tissues, causing abnormalities in fibroblast proliferation, myofibroblast production, and collagen deposition that result in the development of the structurally distinct nodule and cord disease components. Three distinct histological phases have been described.23 The proliferative stage, the most biologically active phase of the disease, is characterized by local fascial fibroplasia and myofibroblast proliferation resulting in nodule formation. Next follows the involutional stage in which the myofibroblasts become aligned along lines of tissue mechanical stress, demonstrating progressive contractile behavior triggered by the effect of a variety of cytokines on the intracellular actin microfilaments – this results in the formation of the progressively shortening fascial cords. In the final disease stage, termed the residual phase, nodules regress leaving the tendon-like, inelastic, relatively acellular cords that cause the clinically apparent fixed flexion contractures.23 Normal palmar fascial tissue is primarily composed of type I collagen – in DD, the increased density and decreased apoptosis of fibroblasts, plus an imbalance in matrix metalloproteinase activity, result in excessive type III collagen production.

Irrespective of the underlying etiological factors, what primarily concerns patients is the degree of manual functional disability that DD imposes. Studies that objectively attempt to link severity of DD contractures and manual disability have shown little to no correlation between the severity of contracture and the degree of manual disability (as assessed by the disability of the arm, shoulder and hand [DASH] questionnaire). This may be unsurprising because the DASH is neither DD-specific nor hand-specific, with an emphasis on pain (not a cardinal feature of DD) – a DD-specific hand function questionnaire has yet to be validated. Also, there are no objective papers to date examining the impact of DD on patients’ quality of life. Nevertheless, the authors’ experience is that patients commonly complain of problems with shaking hands, putting on gloves, typing, performing recreational activities (eg, golf and gardening), and performing basic personal care activities (eg, washing their face). Despite a lack of formal documentation of the impact of such problems, it is obvious that such activity impairment must affect patients’ quality of life and thus stimulate the drive to seek correction of the imposed deformities.

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Management issues in DD

DD classically progresses in two distinct manners. In the less-common disease form associated with the term diathesis and usually found in patients with a strong familial predisposition to the disease, the progression tends to be more aggressive with contractures developing over a few months to years and with rapid disease recurrence after surgical interventions. 49 The more common disease form not associated with diathesis, where there is no obvious familial preponderance, usually progresses more slowly, often allowing the patient to maintain sufficient hand function to live with the disease for years prior to seeking treatment, following which there is a lower risk of disease recurrence.49 To date, there is no known cure for either form of the disease, but its impact has been commonly managed with appropriate surgical intervention.

In view of the variability in the rate of disease progression and the extent of disability caused to patients’ hand function, initial treatment of DD usually involves watchful waiting to observe the rate of progression of the disease until the contractures are significantly affecting a patient’s hand function or their activities of daily living. Currently, the gold standard treatment in DD is surgical, with a choice of selective, segmental, limited, or modified fasciectomy; radical or total aponeurectomy; or dermofasciectomy to excise the affected fascial tissue and restore digital extension (the operation is chosen at the surgeon’s discretion and depending on the extent of the disease – dermofasciectomy is most commonly used in recurrent cases, particularly those involving the proximal interphalangeal joint [PIPJ]). Other less-invasive surgical treatment options include closed fasciotomy and needle aponeurotomy, both of which incise the fascial bands, causing rupture of the cord.50– These methods are much less invasive and can achieve digital extension, but they have been associated with higher rates of recurrence, generally being reserved for elderly or infirm patients in whom the risks of more extensive surgery outweigh the improved recurrence rate benefit. Overall, the development of a nonsurgical treatment option for this disease may improve morbidity and recovery time and enhance patients’ quality of life.

To date, a variety of nonsurgical treatments have been investigated with variable success. These have included the administration of steroids,, dimethyl sulfoxide, vitamin E (tocopherol),radiotherapy,– ultrasonic therapy,61 physical therapy, methylhydrazine, allopurinol,enzymatic fasciotomy (using a combination of trypsin, hyaluronidase, and lidocaine), and collagenase,,,–18 (see Table 1). Steroid injection of the nodules has shown some clinical promise in modifying the disease progression (97% of nodules injected showed some softening or flattening; however, 50% of these patients exhibited recurrence within less than 3 years) and merits further investigation. However, to date, the most clinically promising of these treatments has been the use of injectable CHC to locally degrade the collagen structures, allowing rupture of the fibrous cords and restoration of complete or near-complete digital extension (see CHCs and fibrotic disease).

Table 1

All papers retrieved relating to CHC use in the management of fibrotic disorders, in their chronological order of publication

In view of the emergence of, and potential for, increasing clinical use of CHCs, this review gives an overview of the development, mode of action, pharmacokinetics, and current uses of the commercially available collagenases and details the issues related to its application in the nonsurgical treatment of DD.

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Collagenase C. histolyticum

The history of the proteolytic enzymes derived from Clostridium bacterial species dates back to the early 20th century when it was observed that culture filtrates from Clostridium perfringens had the ability to digest healthy muscle tissue. However, it was not until the 1940s when the ability of such culture filtrates to break down the collagen framework of healthy Achilles tendon was observed, that this novel enzyme was named collagenase. Since then, an increasing number of bacterial species, often those that are pathogenic in humans, have been shown to produce collagenases, which contribute to their pathogenicity. Collagen, which comprises nearly 30% of all proteins within mammalian bodies, is an insoluble structural matrix protein composed of three helically wound polypeptide fibrils – it is resistant to degradation by the majority of proteases due to its triple helical structure which requires unwinding before proteolytic degradation can occur.,

Degradation is key to a variety of both physiological (eg, embryological bone development and wound repair) and pathological conditions (eg, tumor invasiveness and soft tissue bacterial infection), so the human body also produces its own endogenous collagenase as part of the family of zinc-dependent matrix metalloproteineases.

To date, CHCs have been investigated for clinical use in the treatment of herniated intervertebral discs,– retained placenta,72 frozen shoulder adhesive capsulitis,73 DD (see section “CHC and fibrotic disease”), PD,,17, wound healing, 75–77 in the debridement of burns,,77 and in the preparation of pancreatic islet cells for transplantation., It has also been suggested that CHC could be used in the treatment of keloid scars, for recannalization of chronically occluded arterial vessels or stents within peripheral arterial angioplasty procedures79 and in the amelioration of plantar fasciitis,7lateral epicondylitis,7 and cellulite removal.10 This review focuses on the uses of clostridial collagenases in the treatment of fibrotic disorders, with the primary focus on its use in the nonsurgical management of DD.

Pharmacology

Seven collagenases have been isolated from the culture filtrate of the bacteria C. histolyticum, namely α, β, γ, δ, ɛ, ξ, and η collagenases. They are all zinc-dependent matrix metalloproteinases whose unique specificity is in the hydrolysis of collagen molecules via the peptide bond between the Gly-Pro and residue X of the tri-peptide repeat unit (where residue X is often proline or hydroxyproline). The seven collagenases can be divided into two classes, I and II, which are classified based on their bacterial gene of origin (colG and ColH, respectively) and on their point of hydrolytic attack on the collagen molecule – class I enzymes act at loci near the ends of the collagen triple-helical domains, whereas class II enzymes make internal initial cleavages– (see Figure 1) – their combined action at many sites along the peptide chain results in the sequential cleavage of short segments. Both classes have specific binding domains that enable them to recognize and bind to triple helical collagen., The biochemical properties of CHCs mark them out as potentially useful targets for in vivo clinical applications: these include their ability to remain active over a wide pH range (the optimum being pH 7.4); a high degree of substrate specificity, with degradation of only the collagen components of connective tissue structures; a good enzymatic activity at body temperature (37°C); a lack of autodigestion; and, that they can be lyophilized safely and then reconstituted directly prior to use allowing for easy storage and a good stability profile. With regard to inhibitors of CHC activity, CHCs are dependent on the presence of Ca²⁺ ions and, thus, must be diluted in buffer solution containing Ca²⁺ prior to their utilization – interestingly, a dose-dependent, predominantly noncompetitive inhibition of CHC activity has been noted with the aloin compounds contained within the mucilaginous sap of the Aloe barbadensis plant, commonly referred to as Aloe vera gel (however, this is via direct interaction with the collagenase molecule and not via its catalytic domain).

Figure 1

Illustration of classes of Clostridium histolyticum collagenase (CHC) based on their hydrolytic point of attack on collagen molecule: class I CHCs act at loci near the N and C terminals of the collagen domain; class II CHCs cleave within the central collagen(more ...)

CHCs are manufactured via bacterial fermentation, following which the different collagenases can be separated off chromatographically – the majority of commercially available CHCs are produced in this manner. However, a drawback of this method is that the ratio and activity of class I and class II CHCs yielded is unreliable, so each CHC batch can have differing biological effects.7 There are a large variety of commercially available CHC preparations, each with differing selectivity of included CHCs, and this allows for the different uses to which CHCs are put in the laboratory setting. For in vivo human clinical trials, the investigators have been careful to select highly purified preparations in order to maintain maximal reproducibility. However, more recent work has utilized a novel CHC, designed specifically for medical therapeutic applications and marketed as Xiaflex ^®, which gained US FDA approval on February 2, 2010 and is expected to achieve European approval in January 2011. This bypasses the issues of unreliable interbatch reproducibility by highly purifying the initial culture filtrate to select a 1:1 mass ratio of class I to class II CHCs, thereby guaranteeing a reproducible collagenolytic effect.7

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CHCs and fibrotic disease

A timeline of key events in the development of CHC use in DD is illustrated in Figure 2. Literature searches retrieved all papers relating to CHC use in the management of fibrotic disease (ie, DD, PD, and keloid scarring), and these are listed for ease of reference in Table 1 and discussed in chronological order of publication hereafter.

Figure 2

Timeline of key milestones in the history of Clostridium histolyticum collagenases (CHCs) and their use in Dupuytren disease (DD).

The initial pilot study in the examined series was a multifaceted pilot by Gelbard et al who looked at the in vitro collagenolytic effect of commercially available CHC on human PD tissue, healthy tunica albuginea, pericardium, and corpora cavernosal sections, plus the in vivo effect of CHC on the femoral neurovascular bundle of an anesthetized rat. First, they compared CHC activity (via measurement of desiccated tissue weight and release of free α-amino acid groups) on PD plaque tissue and healthy tunica albuginea tissue, with tissue derived from three patients for each tissue type. They showed there was no significant difference in the degree of collagen degradation between the diseased and healthy tissues, ie, CHC did not selectively degrade PD plaque collagen but would affect surrounding healthy tissues. To look into the effect of local injection of CHC and dispersion into surrounding tissues they investigated injecting CHC at a variety of unit strengths into human pericardium and demonstrated that when CHC was injected locally into tissue, there was a dose-related response, but this was always limited to the injection site – with a dose of 400 U, there was visible tissue clearing within the injection zone but not outside the radius of the zone. They suggested this confinement of digestion to be related to the mucopolysaccharide “ground substance” in which the collagen is embedded and which does not undergo digestion itself. Next, they injected 400 U into sections of PD-affected and healthy corpora cavernosa – this caused collagenolysis (varying on histological examination from decreased stain uptake to total disappearance of collagen bundles) but with preservation of elastin and with no evidence of injury to the local neurovasculature. Finally, they injected 600 U of CHC into the adventitia surrounding the left femoral neurovascular bundle of an anesthetized rat – 24 hours later, the rat was sacrificed, and the treated and untreated femoral neurovascular bundles were compared. Macroscopically, a moderate hematoma was noted with no signs of active bleeding. Microscopically, venules and the fibrous perineurium underwent degradation, but there was no effect on arterioles or the nerve fibers themselves – this was postulated to be due to the smooth muscle in the arteriolar walls and the myelin sheaths enveloping and thus protecting the nerves. Based on Garvin’s experiments on the cytotoxicity of intravenous CHC in rats (see Discussion for greater detail), the authors extrapolated that the cytotoxic dose in a 70 kg human might be around 89,040 U, which was 356 times more potent than the doses they had found to be required for adequate collagenolysis at a local injection level.

In the first of a number of papers submitted by the same US-based group of investigators, Starkweather et al analyzed the effect of injected CHC on the tensile strength of DD cords obtained from patients who had undergone fasciectomy. All cords were subjected to controlled stretching within a mechanical testing device that recorded stress and strain effects within the cords, following which they underwent histological examination. In the first phase of the study, the authors compared the effect of 3,600 U CHC injections in 10 DD cord samples against 10 cords injected with a control buffer solution. Cords injected with CHC showed a statistically significant 93% decrease in tensile modulus when compared with the control buffer-injected cords. In the second phase of the study, 20 DD cord samples were randomly allocated into groups and subjected to an injection of 150, 300, or 600 U of CHC or a control buffer solution. Each cord was stressed to failure, ie, until cord rupture was achieved, with a curvilinear trend being demonstrated between increasing CHC dose and decreasing stress required to achieve cord rupture – 89% of the trend was directly attributable (following regression analysis) to the CHC dose administered. The stress to failure values were then compared with the average stress normally generated by the active extension of each of the fingers in a healthy hand. This allowed extrapolation that a CHC injection of 300 U was the minimum potential dose for in vivo clinical use that would result in DD cord rupture (and hence correction of the fixed flexion deformity) following normal active digital extension. One point to note was that the authors believed that it was important to inject CHC into DD cords (these being in the residual disease stage and relatively acellular when compared with the more active nodular areas of disease) as it was suggested this might minimize early recurrence or the risk of worsening the flexion contractures.

Investigation of the utility of CHC in the treatment of DD was next progressed by Badalamente and Hurst who assessed the in vivo efficacy and, importantly, safety of CHC injection within a 32-patient Phase II open-label trial. The study end point was correction of metacarpophalangeal joint (MCPJ) or PIPJ fixed flexion contractures to full extension (0°–5°) and assessment of any related adverse reactions (see Figure 3 for an illustration of the anatomical landmarks associated with CHC in vivo injections). The immunological effect of CHC injection was also assessed via serial serum immunoglobulin E (IgE) assays at days 1 and 14 postinjection. Follow-up was maintained between 2 and 5 years postprocedure to assess disease recurrence. Based on the prior in vitro determination of 300 U being a safe and effective CHC dose for cord rupture, the first patient was given an injection of 300 U – this failed to achieve cord rupture. The dose was then escalated, with trials of 600, 1,200, 4,800, and 9,600 U each in a single patient – again cord rupture was not achieved. The remaining 29 patients (ie, 34 MCPJ, 9 PIPJ, and 1 thumb joint contractures) had 10,000 U CHC injected into each contracture-contributing DD cord with passive digital extension 24 hours later to effect cord rupture. Following rupture, participants were asked to undertake patient-guided extension exercises and application of night extension splints for 4 months following the procedure to maintain maximal digital extension. Within 2 weeks of the procedures (some of which required repeat injections to achieve cord rupture), an 88% success rate was noted in the correction of MCPJ contractures and a 44% success rate in PIPJ contracture correction (to 0°–5° of extension). Two patients with MCPJ disease and 2 with PIPJ involvement failed to achieve cord rupture and digital extension so required surgical correction via fasciectomy. There were no major adverse reactions, but there were transient (1–2 week) minor reactions local to the injection site, including tenderness, palmar and/or dorsal edema, small local hematoma formation, forearm tenderness, and elbow/axilla lymphadenopathy. Three MCPJ contractures relapsed at 2-year postprocedure follow-up along with one PIPJ recurrence 3 months following treatment. Finally, IgE titers were seen to increase, especially in patients requiring repeat treatments; however, they were not associated with any adverse clinical effects and decreased with time postprocedure.

Figure 3

Diagram illustrating: A) hand with palpable “bow-stringed” Dupuytren disease (DD) cord. B) anatomical landmarks in DD-affected hand.

This work was followed in 2002 by another Phase II trial undertaken by the same group of authors, Badalamente et al. The first trial leg was a single-center, randomized, placebo-controlled, double-blinded trial comparing the effect of injection of 10,000 U of CHC against placebo in patients with MCPJ or PIPJ DD-related contractures. 36 MCPJ and 13 PIPJ contracture patients were recruited and split equally between the treatment and placebo groups. Again, the primary end point of the study was correction of MCPJ or PIPJ fixed flexion contractures to full extension (0°–5°), the secondary end point was the percentage change from the preinjection baseline of range of motion and grip strength, and the final goal was identification of any related adverse reactions. In patients with multidigit involvement, the injections were repeated as required up to a maximum of 50,000 U. In the MCPJ group, there was a statistically significant difference between the treatment and placebo groups with 14 of 18 treated patients achieving the primary end point within 2 weeks, compared with two of 18 placebo patients. Within the 4-year follow-up period, four treated patients had disease recurrence. In the PIPJ group, five of seven treated patients achieved the primary end point within 4 weeks, compared with none of six placebo patients. Within the 3.8-year follow-up period, four treated patients had disease recurrence. Range of motion and grip strength showed no significant decline from baseline in either group. Adverse effects of CHC injection were the same as detailed in the authors’ previous paper, remaining locally confined and well tolerated, with the addition of three superficial skin tears secondary to rapid stretching of the overlying skin during cord rupture. The next study leg was a dual-center, randomized, placebo-controlled, double-blinded trial investigating the optimum dose of CHC required and involving 80 patients, evenly randomized to placebo, 2,500, 5,000, or 10,000 U doses. The end points were identical to the first trial leg. The success rate in restoration of full extension at 1-month postprocedure was significantly dose related, with MCPJ joints injected with 10,000 U showing a 90% success rate and PIPJ joints 70% success. Flexion and grip strength showed no significant deviation from the baseline and adverse effects were similar to those shown in the first trial leg. One MCPJ and one PIPJ had a disease recurrence within the follow-up period of 2 years. Finally, there were two substudies undertaken. The first investigated CHC pharmacokinetics – four participants given the 10,000 U CHC treatment had serial blood and urine samples taken over an 180-minute period and 24-hours postinjection for analysis of their collagenase content. There was no collagenase detected within the serum (likely due to its slow release into the bloodstream); however, levels were detectable in the urine primarily in the first hour postinjection, with up to 28% of the administered dose recovered from the urine. The second substudy examined five patients receiving 10,000 U but who had lidocaine injected prior to the passive digital manipulation to cause cord rupture 24 hours postinjection. This was well tolerated and demonstrated no effect on the study end points. Overall, the authors concluded CHC injection to be safe, effective, and less-invasive treatment option for the management of DD contractures.

Following these impressive results, the use of CHC in the treatment of keloid and hypertrophic scarring was piloted by Kang et al. They injected CHC, triamcinolone, or a combination into the keloid or hypertrophic scars of seven patients, and the response was measured by scar volume studies, visual subjective evaluation of response, serial photographs, and diarized patient experiences. A 33% reduction in proportional keloid scar volume was noted in the first 6 months with collagenase, but this effect disappeared thereafter. CHC produced no alteration in volume in the injected hypertrophic scars. CHC injection was associated with moderate local pain, severe blistering, skin ulceration, bruising, and swelling – one participant had severe enough symptoms to necessitate hospital admission for antipyretics and supportive measures. Overall, the authors concluded that intralesional injection of collagenase is ineffective and, coupled with the possibility of serious adverse reactions, has little scope as a clinical treatment for keloid or hypertrophic scars. However, it must be noted that the study sample size was not large enough, nor the scar group selected of a sufficient homogeneity, to draw any strong conclusions for or against the technique.

Returning to the previously discussed US group, the next article by Badalamente and Hurst continues on from their earlier studies with a Phase III randomized, placebo-controlled, double-blinded trial followed by an open-label extension. A total of 55 DD-contracted digits requiring treatment were recruited for injection with 10,000 U of a novel, mixed subtype CHC preparation. Within the main trial, patients had up to three joints injected, with a maximum of three injections into the primary joint followed by up to two in any remaining joints. A further three injections were allowed in the extension study if required. The primary end point was overall clinical success ie, reduction in deformity to ≤5° within 30 days of primary joint injection(s) – again, adverse reactions were recorded. Within the blinded phase, 91% of CHC-treated joints (86% of MCPJ and 100% of PIPJ joints) vs 0% of placebo group achieved clinical success (with up to three injections given and a mean number of injections to success of 1.4). 35 joints were entered into the open phase, where all were treated with CHC – 77% achieved clinical success. Over the 2-year followup period, one MCPJ and four PIPJ joints exhibited a disease recurrence – of these, the four male patients had a family history of DD, but the single female patient had de novo disease. Adverse events were of the same nature as detailed in the earlier Badalamente et al studies, with no summative systemic enzymatic effect or change in event severity demonstrated with repeated injections. There were no adverse immune events.

Xiaflex^® was then utilized in a study by Del Carlo et al17 examining its in vitro effect when PD plaques and DD cords were injected with increasing concentrations of the CHC. Maximal enzymatic activity occurred within the first 4 hours, and near-complete digestion of the samples occurred following 12 hours of CHC exposure – small fibrils were preferentially degraded in the first 4 hours, following which the degradation of the larger fibrils proceeded. No cell death was observed at any concentration of CHC and all noncollagenous tissue structures remained histologically intact.

The two most recent CHC papers published originated from members of the same US-based group. The first, by Hurst et al (who make up the Collagenase Option for Reduction of Dupuytren’s [CORD] I study group) expands on the earlier Phase III study by Badalamente and Hurst. However, this 90-day Phase III prospective, randomized, placebo-controlled, double-blinded trial extended across 16 centers and had a substantially larger patient sample group (of 308 participants or 512 DD-affected joints) than previous studies. DD cords were injected with 0.58 mg of CHC (Xiaflex^®) – a diagrammatic overview of the precise injection methodology utilized can be seen in Figure 4. As with previous studies, following injection the cords were ruptured 24 hours later via passive digital extension and the participants were asked to wear a night splint for 4 months. Three treatment cycles per DD cord were allowed. The primary end point remained extension to ≤5° within 30 days of the final injection alongside recording of all adverse reactions. The diseased joints were split into two baseline-characteristic matched groups, with 204 receiving CHC and 104 receiving placebo injections. The primary end point was achieved in 64% of the CHC group compared with 6.8% of joints in the placebo group. CHC-treated joints also showed a greater improvement in range of movement when compared with placebo-injected joints and all of the successfully treated joints showed no evidence of recurrence at the 90-day assessment. Of those CHC joints that did not achieve the primary end point, more than half did not receive the maximum allowable number (3) of CHC injections, either because the cord was no longer palpable (and thus could not safely be injected) or the patient was happy with the result despite lacking restoration of complete digital extension. However, preinjection baseline severity of contracture affected the likelihood of achieving the primary end point: 88.9% of CHC-injected MCPJ joints with a baseline contracture of 50° or less met the primary end point compared with 57.7% of those joints with a contracture greater than 50°; this effect was also seen in PIPJ joints (80.9% in the smaller than 40° group when compared with 22.4% in the greater than 40° group). This would suggest that CHC treatment may be more applicable for use in less severely affected joints, whereas perhaps those that are more severely contracted might derive greater benefit from traditional surgical correction. 96.6% of all CHC-treated joints developed one or more treatment-related adverse event as compared with 21.2% of those receiving the placebo injections; however, most were rated as mild to moderate with resolution without any medical intervention within a median of 10 days. Twenty-two patients (20 receiving CHC and two receiving placebo) reported adverse reactions, which they rated to be severe in nature, all of which were deemed to be treatment related except the single reports of contact dermatitis, muscular spasms, myocardial infarction (each in a CHC-treated patient), acute cholecystitis, nasopharyngitis, and radius fracture (each of which occurred in a placebo-group patient). The reported treatment-related events were primarily localized to the injection sites (edema [2%], pain [2%], hemorrhage [1.5%], contusion [1%], tenderness [1%], ecchymosis [0.5%], cellulitis [0.5%], and skin laceration [0.5%]) or to the injected side of the body (upper limb pain [2%] and chest-wall pain [0.5%]). Two participants deemed their reaction to be too severe to continue with the CHC treatment: one due to local pain secondary to the first CHC injection and the other due to dizziness 28 days post-CHC treatment which the patient attributed to the treatment. However, the authors deemed that three participants who received CHC injections suffered serious adverse events directly related to the treatment: two cases of tendon rupture (requiring surgical reparation) and a case of complex regional pain syndrome. There were no clinically observed systemic allergic reactions, alterations in grip strength, nerve injuries, or deaths associated with the treatment. With regard to biochemical or immunological response to the CHC, baseline blood results were compared with samples from 30 and 90 days posttreatment: ≥85.8% of those receiving a single injection developed anti-CHC antibodies, with 100% of patients testing positive following three injections. There were no clinically relevant blood result changes.

Figure 4

Diagram illustrating indications, relative contraindications, injection technique with adjustments for metacarpophalangeal (MCP) vs proximal interphalangeal (PIP) joints and suggested aftercare following successful Dupuytren disease (DD) cord rupture (more ...)

The final paper published to date, by Watt et al reviewed participants from an earlier study undertaken 8 years previously (published by Badalamente and Hurst and discussed previously). Twenty-three patients from a single study arm were contacted 8 years after their initial treatment. Of these 23, only eight were alive, contactable at the same address, available within the study period and received a CHC injection and thus were eligible for reevaluation to assess the state of their DD since the study. Notably, seven of the eight subjects had a family history of DD making them more likely to have aggressive disease and be at higher risk of relapse. All patients had a single CHC injection, six into MCPJ and two into PIPJ; however, varying injection dosages were administered, and not all patients achieved the primary goal of extension to ≤5%. Of the MCPJ joints, two had no evidence of DD recurrence and four had recurrent disease, although the extent of contracture seen at the 8-year assessment was still less than that previously noted for pre-CHC injection in all four patients (60%–20%; 70%–40%; 52%–20%; and 55%–55%, respectively). In the two PIPJ patients, there was a 100% recurrence rate with the degree of contracture (which initially demonstrated a marked improvement at the 1-year assessment) being more extensive than prior to the treatment (35% pretreatment, 0% at 1 year, and 50% at 8 years; and 55% pretreatment, 25% at 1 year, and 70% at 8 years, respectively). Patients subjectively ranked the treatment as being 60% successful, and seven out of eight stated they would consider having the treatment again.

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Discussion

DD is a prevalent disease that causes considerable impairment to patients’ hand function. It has a complex, multifactorial etiology and pathophysiology, a complete understanding of which remains elusive. Despite explorative studies of a broad variety of alternative nonsurgical therapies, few of these have yet shown sufficient promise for them to be considered a valid alternative to the gold standard surgical methods that currently remain the mainstay of DD management. However, the developments discussed earlier in the use of CHC injection therapy indicate that this is likely to become a significant clinically applicable alternative method for the management of DD. Surgery is, however, likely to remain a valid treatment option, especially for recurrent cases following CHC injection, in patients with the aggressive form of the disease (strong diathesis), and in those patients with PIPJ involvement (which appears to not respond as favorably to the CHC-based technique when compared with simple MCPJ disease). Figure 5 presents a treatment algorithm, illustrating where CHC injection is likely to contribute for the management of DD.

Figure 5

Flowchart for managing patients with Dupuytren disease (DD) from initial presentation to treatment, demonstrating the role ofClostridium histolyticum collagenase (CHC) injection within the treatment algorithm of DD.

The CHC studies undertaken to date have clearly demonstrated that injection of CHC is a valid alternative to the traditional surgical options, despite neither treatment facilitating a definitive cure. CHC demonstrates an impressive degree of digital extension with low rates of disease recurrence – certainly the benefits it offers, such as reduced invasiveness and procedure time, rapidity of recovery of premorbid hand function and the likely reduction in cost of administration (being an office-based method rather than surgical theater-based technique) could be instrumental in its likely increase in popularity both with patients and surgeons over the coming years.

A precise comparison of procedure risk vs derived health benefit between the gold standard selective fasciectomy and CHC injection is difficult. Surgery, with its reported surgeon-dependent and technique-dependent complication rate of 17%–50%,24 still carries a significant morbidity. Some of the local complications are similar to those seen in CHC injection (local pain, tenderness, ecchymosis, edema, risk of infection, and hematoma are expected sequelae), but surgery is also associated, especially those more complex revision operations in which there is often considerable local scarring, with risk of flexor tendon or pulley injury, digital nerve damage, and reflex sympathetic dystrophy. CHC injection has also been noted to be associated with tendon rupture and complex regional pain syndrome (two of 204 and one of 204 patients, respectively, in Hurst et al’s most recent study), but the authors suggested that the risk of these serious complications might be minimized by careful adherence to the proposed injection technique, especially when injecting distal PIPJ contractures (see Figure 4). In view of this requirement for meticulous technique, it is clear that CHC injection will remain, based on the need for sound anatomical knowledge and manual dexterity, within the surgeons’ remit.

As with any novel therapy, the primary concerns that must be addressed prior to its use in the clinical environment are its efficacy – this has been illustrated in the previously mentioned studies – and whether the safety risks it imposes are outweighed by the health benefit it provides. As CHCs act via the degradation of collagen and 25%–33% of the total protein within humans is comprised of collagen, it is clear that it is essential to ensure CHCs act only on the diseased DD collagen against which they are therapeutically targeted.

The toxicity of intravenously injected CHC in mice was explored by Garvin Jr who showed a median lethal dose of 1,176 ± 208 U/kg – the main signs of toxicity were pulmonary hemorrhage and disseminated tissue digestion. The authors extrapolated this to an average 70 kg human, suggesting a lethal dose of 89,040 U (although this is with direct intravenous administration which is likely to be substantially more systemically damaging when compared with contained local tissue injection). However, the manufacturers of Xiaflex^® reported much higher estimated safety margins for the inadvertent intravenous administration of the drug, suggesting a minimum lethal dose of more than 43 times the recommended dosage. Rydevik et al– undertook a number of studies into the effect of CHC on neural, vascular, epidural, and intrathecal tissues in animal models (rabbit ears and hamster cheek pouches). They demonstrated a dose-related short-term and long-term response within the microvasculature of rabbit ears to local CHC injection. At low doses (120 U/mL), acutely, there was a slight reduction in blood flow and functional recruitment of capillaries with a localized hyperemic area persisting at 7 days postinjection and evidence of small vessel proliferation but not of revascularization. At high doses (3000 U/mL), an immediate transient hyperemia was seen, with stagnant flow in venules and capillaries at 60 minutes postinjection and evidence of microbleeding increasing over time. This progressed by day 3 to evidence of marked local hemorrhage extending beyond the injection site with a central area of necrosis observable – microangiograms displayed a central vessel-free zone with peripheral proliferation of wide, tortuous vessels typical of those seen in granulation tissue. In another study, they showed that CHC injected epidurally resulted in local dural thinning at higher concentrations, whereas even small concentrations of CHC injected intrathecally resulted in intrathecal hemorrhage and acute paraplegia. It might be assumed that such CHC-related neurological damage infers that a similar effect that might occur in digital nerves exposed to CHC, resulting in transient neuropraxia or persistent nerve damage. However, none of the clinical studies described in this review have noted any such clinical deficits. Perhaps this is due to the limited follow-up length and relatively small numbers treated to date or that, rather than directly damaging the neuronal fibers, the intrathecally injected CHC created a similar effect on the microvasculature as in the rabbit ear study, inducing a cord ischemia secondary to the local hyperemia, hemorrhage, and resultant edema. Interestingly, at a cellular level, Del Carlo et al17 noted no evidence of cell death or damage to nerve fibers at any of the CHC concentrations tested. Despite this lack of cellular sequelae, the manufacturers of the CHC Xiaflex^® advise that CHC injection has not been tested in pregnant, breast-feeding, or pediatric populations in whom its safety and efficacy have not yet been established.

The ability to localize the effect of injected CHC has been demonstrated by Badalamente and Hurst92who injected CHC in vivo into anesthetized rat tail tendons and demonstrated that no adverse extravasation of CHCs (at doses between 150–300 U) occurred into adjacent muscle, nerve, other tendons, vessels, bone, or skin. Gelbard et al in their study investigating the effect of CHC in vivo, also used an anesthetized rat. CHC was injected into the left femoral adventitial tissues surrounding the femoral neurovascular bundle: histological examination revealed that the collagenolytic effect was limited purely to the injection site – only small local venules were degraded with sparing of the nerves and smooth muscle–containing arterioles. Indeed, Mandl described the use of CHC to selectively remove connective tissue from the surrounding of nerves before histological studies of the intact nerves.

As CHC is a foreign protein, its injection would be presumed to evoke an immunological response. Indeed, Hamilton et al demonstrated such an immune response to injection of CHC for the treatment of PD plaques: pretreatment, anticollagenase IgG was detected in 34% of the healthy controls vs 58% of untreated PD patients. Following intralesional CHC injection of 3,000–12,650 U, an increase of twofold to 10-fold in IgG levels was seen at 1–2 months postinjection in 88% of patients. Only 0.5% showed detectable collagenase-specific IgE antibody. Braun described a contact dermatitis in two patients in whom a topical ointment composed of CHC and chloramphenicol (Iruxol™; Smith & Nephew) was applied – although a positive local response was observed, no specific allergen was detected. Finally, Hurst et al demonstrated that ≥85.8% of those receiving a single in vivo CHC injection into DD-affected cords developed anti-CHC antibodies, with 100% of patients testing positive following three injections. However, they showed no clinical evidence of systemic allergic response.

With respect to the systemic biochemical and hematological response to local tissue injection of CHCs, Sussmann and Mann,,, demonstrated no adverse changes in red blood cell, white blood cell, or platelet counts in rats receiving >100 times the effective dose required for intervertebral disc lysis. Hurst et al reported no clinically meaningful changes in hematological or biochemical variables following CHC injection in DD cords. Badalamente et al also reviewed the pharmacokinetics of locally injected CHC, showing that despite no evidence of CHC circulating within serum, an estimated 28% of the dose injected was concentrated and excreted in the urine with no evidence of damage to the renal function. They suggested the absence of CHC within serum to be due to the CHC not being released into the circulation as a bolus but rather via incremental leaching from the injection site – thus, the tiny volumes slowly released over the sampling period were below the 4 ng/mL test threshold. However, the manufacturers of Xiaflex^® later repeated the pharmacokinetic studies and detected no systemic levels of CHC following a single-dose Xiaflex^® injection. This lack of quantifiable systemic exposure negated the need for tissue distribution, metabolism, or excretion studies.99

Overall, it can be concluded that the efficacy, safety, and complication profiles of CHCs appear to compare favorably with the current surgical techniques in adult patients with a palpable DD cord. However, this is still a method relatively within its infancy and thus there is no evidence relating to the possible long-term sequelae of CHC injections, nor any indication as to its safety in pregnancy, in breast-feeding women or in pediatric patients – further studies will be required to elucidate any long-term issues with the technique.

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Conclusion

DD is a prevalent disease that has a marked effect on patients’ hand function and for which there is still no curative treatment. CHC is a novel nonsurgical treatment option of considerable potential in the management of DD when administered by specialist hand surgeons with detailed knowledge of the disease and its relevant anatomy. CHC injection has been shown to have a good efficacy and safety profile when compared with the current gold standard of surgery and appears likely to have a role in the therapeutic arsenal for the management of DD.

Nonetheless, there is a need for further data on long-term results, complications, and rate of recurrence with the use of this emerging treatment option.

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Acknowledgments

The authors would like to thank Helen Carruthers for professional illustration of Figures 3 and and4.4. The senior author is a recipient of NIHR (UK) funding.

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Footnotes

Disclosure

No authors have conflicting financial interests and no funds have been obtained for the completion of this work.

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References

1. Bayat A, McGrouther DA. Management of Dupuytren’s disease – clear advice for an elusive condition.Ann R Coll Surg Engl. 2006;88(1):3–8. [PMC free article] [PubMed]

2. Bayat A, Cunliffe EJ, McGrouther DA. Assessment of clinical severity in Dupuytren’s disease. Br J Hosp Med. 2007;68(11):604–609.

3. Watt AJ, Curtin CM, Hentz VR. Collagenase injection as nonsurgical treatment of Dupuytren’s disease: 8-year follow-up. J Hand Surg Am. 2010;35(4):534–539. [PubMed]

4. Barbir A, Michalek AJ, Abbott RD, Iatridis JC. Effects of enzymatic digestion on compressive properties of rat intervertebral discs. J Biomech. 2010;43(6):1067–1073. [PMC free article] [PubMed]

5. Hurst LC, Badalamente MA, Hentz VR, et al. Injectable collagenase clostridium histolyticum for Dupuytren’s contracture. N Engl J Med. 2009;361(10):968–979. [PubMed]

6. Badalamente MA, Wang E. Methods for treatment using collagenase. 20090010918. US patent. 2009 Jan 8;

7. Sabatino GL, Del Tito JRBJ, Bassett PJ, Tharia HA, Hitchcock AG. Compositions and methods for treating collagen-mediated diseases. 20070224183. US patent. 2007 Jan 29;

8. Badalemente MA, Dagum AB. Collagenase for treating cellulite. World intellectual property organisation patent. 2007100675 (A2) WO. 2007 Sep 7;

9. Badalamente MA, Hurst LC. Efficacy and safety of injectable mixed collagenase subtypes in the treatment of Dupuytren’s contracture. J Hand Surg Am. 2007;32(6):767–774. [PubMed]

10. Badalamente MA. Methods for treating cellulite. World intellectual property organisation patent. 2007100675 (A2) WO. 2007 Sep 7;

11. Gelbard MK, Walsh R, Kaufman JJ. Collagenase for Peyronie’s disease experimental studies. Urol Res. 1982;10(3):135–140. [PubMed]

12. Starkweather KD, Lattuga S, Hurst LC, et al. Collagenase in the treatment of Dupuytren’s disease: an in vitro study. J Hand Surg Am. 1996;21(3):490–495. [PubMed]

13. Badalamente MA, Hurst LC. Enzyme injection as nonsurgical treatment of Dupuytren’s disease. J Hand Surg Am. 2000;25(4):629–636. [PubMed]

14. Badalamente MA, Hurst LC, Hentz VR. Collagen as a clinical target: nonoperative treatment of Dupuytren’s disease. J Hand Surg Am. 2002;27(5):788–798. [PubMed]

15. Badalamente MA, Stern L, Hurst LC. The pathogenesis of Dupuytren’s contracture: contractile mechanisms of the myofibroblasts. J Hand Surg Am. 1983;8(3):235–243. [PubMed]

16. Kang N, Sivakumar B, Sanders R, Nduka C, Gault D. Intra-lesional injections of collagenase are ineffective in the treatment of keloid and hypertrophic scars. J Plast Reconstr Aesthet Surg.2006;59(7):693–699. [PubMed]

17. Del Carlo M, Cole AA, Hart SGE, Levine LA. Comparative analysis of collagen degradation in Peyronie’s disease plaque and Dupuytren’s contracture cord tissues injected with mixed collagenase subtypes. J Urol. 2009;181(4 Suppl 1):S279–279.

18. Hurst LC, Badalamente M, Smith T. Injectable collagenase clostridium histolyticum for Dupuytren’s contracture. The authors’ reply. N Engl J Med. 2009;361(26):2578–2580.

19. Rayan GM. Dupuytren’s disease: anatomy, pathology, presentation, and treatment. Instr Course Lect. 2007;56:101–111. [PubMed]

20. Sinha A. Dupuytren’s disease may extend beyond the wrist crease in continuity. J Bone Joint Surg Br. 1997;79(2):211–212. [PubMed]

21. Lee TH, Wapner KL, Hecht PJ. Plantar fibromatosis. J Bone Joint Surg A. 1993;75(7):1080–1084.

22. Sasso F, Gulino G, Falabella R, et al. Peyronie’s disease: lights and shadows. Urol Int. 2007;78(1):1–9. [PubMed]

23. Thurston AJ. Dupuytren’s disease. J Bone Joint Surg B. 2003;85(4):469–477.

24. Caufield RJ, Edwards SG. Dupuytren disease: an update on recent literature. Curr Orthop Pract.2008;19(5):499–502.

25. Elliot D. The early history of contracture of the palmar fascia. Part 1: the origin of the disease: the curse of the MacCrimmons: the hand of benediction: Cline’s contracture. J Hand Surg Br.1988;13(3):246–253. [PubMed]

26. Dupuytren G. Permanent retraction of the fingers, produced by an affection of the palmar fascia.Lancet. 1834;2:222–225.

27. Hindocha S, McGrouther DA, Bayat A. Epidemiological evaluation of Dupuytren’s disease incidence and prevalence rates in relation to etiology. Hand (NY) 2009;4(3):256–269.

28. Degreef I, Steeno P, de Smet L. A survey of clinical manifestations and risk factors in women with Dupuytren’s disease. Acta Orthop Belg. 2008;74(4):456–460. [PubMed]

29. Stahl S, Calif E. Dupuytren’s palmar contracture in women. Isr Med Assoc J. 2008;10(6):445–447.[PubMed]

30. Urban M, Feldberg L, Janssen A, Elliot D. Dupuytren’s disease in children. J Hand Surg Br.1996;21(1):112–116. [PubMed]

31. Burge P. Genetics of Dupuytren’s disease. Hand Clin. 1999;15(1):63–71. [PubMed]

32. Murrell GA, Hueston JT. Aetiology of Dupuytren’s contracture. Aust N Z J Surg. 1990;60(4):247–252. [PubMed]

33. Hindocha S, John S, Stanley JK, Watson SJ, Bayat A. The heritability of Dupuytren’s disease: familial aggregation and its clinical significance. J Hand Surg Am. 2006;31(2):204–210. [PubMed]

34. Bayat A, Watson JS, Stanley JK, et al. Genetic susceptibility in Dupuytren’s disease. J Bone Joint Surg B. 2002;84(2):211–215.

35. Attali P, Ink O, Pelletier G, et al. Dupuytren’s contracture, alcohol consumption, and chronic liver disease. Arch Intern Med. 1987;147(6):1065–1067. [PubMed]

36. An HS, Southworth SR, Jackson WT, Russ B. Cigarette smoking and Dupuytren’s contracture of the hand. J Hand Surg Am. 1988;13(6):872–874. [PubMed]

37. Gudmundsson KG, Arngrimsson R, Sigfusson N, Bjornsson A, Jonsson T. Epidemiology of Dupuytren’s disease: clinical, serological, and social assessment. The Reykjavik Study . J Clin Epidemiol.2000;53(3):291–296.

38. Arkkila PET, Kantola IM, Viikari JSA. Dupuytren’s disease: association with chronic diabetic complications. J Rheumatol. 1997;24(1):153–159. [PubMed]

39. Strzelczyk A, Vogt H, Hamer HM, Kramer G. Continuous phenobarbital treatment leads to recurrent plantar fibromatosis. Epilepsia. 2008;49(11):1965–1968. [PubMed]

40. Hart MG, Hooper G. Clinical associations of Dupuytren’s disease. Postgrad Med J.2005;81(957):425–428. [PMC free article] [PubMed]

41. Sanderson PL, Morris MA, Stanley JK, Fahmy NR. Lipids and Dupuytren’s disease. J Bone Joint Surg Br. 1992;74(6):923–927. [PubMed]

42. Livingstone JA, Field J. Algodystrophy and its association with Dupuytren’s disease. J Hand Surg Br.1999;24(2):199–202. [PubMed]

43. Bovenzi M. Hand-arm vibration syndrome and dose-response relation for vibration induced white finger among quarry drillers and stonecarvers. Occup Environ Med. 1994;51(9):603–611.[PMC free article] [PubMed]

44. Ling RSM, Edinburgh S. The genetic factor in Dupuytren’s disease. J Bone Joint Surg Br.1963;45(4):709–718. [PubMed]

45. Al-Qattan MM. Factors in the pathogenesis of Dupuytren’s contracture. J Hand Surg Am.2006;31(9):1527–1534. [PubMed]

46. Townley WA, Baker R, Sheppard N, Grobbelaar AO. Dupuytren’s contracture unfolded. Br Med J.2006;332(7538):397–400. [PMC free article] [PubMed]

47. Engstrand C, Boren L, Liedberg GM. Evaluation of activity limitation and digital extension in Dupuytren’s contracture three months after fasciectomy and hand therapy interventions. J Hand Ther.2009;22(1):21–27. [PubMed]

48. Degreef I, Vererfve PB, de Smet L. Effect of severity of Dupuytren contracture on disability. Scand J Plast Reconstr Surg Hand Surg. 2009;43(1):41–42. [PubMed]

49. Hindocha S, Stanley JK, Watson S, Bayat A. Dupuytren’s diathesis revisited: evaluation of prognostic indicators for risk of disease recurrence. J Hand Surg. 2006;31(10):1626–1634.

50. Cheng HS, Hung LK, Tse WL, Ho PC. Needle aponeurotomy for Dupuytren’s contracture. J Orthop Surg. 2008;16(1):88–90.

51. Foucher G, Medina J, Navarro R. Percutaneous needle aponeurotomy: complications and results. J Hand Surg Br. 2003;28(5):427–431. [PubMed]

52. van Rijssen AL, Werker PMN. Percutaneous needle fasciotomy in Dupuytren’s disease. J Hand Surg Br. 2006;31(5):498–501. [PubMed]

53. Rayan GM. Nonoperative treatment of Dupuytren’s disease. J Hand Surg Am. 2008;33(7):1208–1210. [PubMed]

54. Ketchum LD, Donahue TK. The injection of nodules of Dupuytren’s disease with triamcinolone acetonide. J Hand Surg Am. 2000;25(6):1157–1162. [PubMed]

55. Al-Qattan MM, Ketchum LD. The injection of nodules of Dupuytren’s disease with triamcinalone acetonide. J Hand Surg Am. 2001;26(3):560–561. [PubMed]

56. Vuopala U, Kaipainen WJ. DMOS in the treatment of Dupuytren’s contracture. A therapeutic experiment. Acta Rheumatol Scand. 1971;17(1):61–62. [PubMed]

57. Kirk JE, Chieffi M. Tocopherol administration to patients with Dupuytren’s contracture; effect on plasma tocopherol levels and degree of contracture. Proc Soc Exp Biol Med. 1952;80(4):565–568.[PubMed]

58. Keilholz L, Seegenschmiedt MH, Sauer R. Radiotherapy for prevention of disease progression in early-stage Dupuytren’s contracture: initial and long-term results. Int J Radiat Oncol Biol Phys.1996;36(4):891–897. [PubMed]

59. Seegenschmiedt MH, Olschewski T, Guntrum F. Radiotherapy optimization in early-stage Dupuytren’s contracture: first results of a randomized clinical study. Int J Radiat Oncol Biol Phys.2001;49(3):785–798. [PubMed]

60. Betz N, Ott OJ, Adamietz B, Sauer R, Fietkau R, Keilholz L. Radiotherapy in early-stage Dupuytren’s contracture. Long-term results after 13 years. Strahlenther Onkol. 2010;186(2):82–90.[PubMed]

61. Stiles PJ. Ultrasonic therapy in Dupuytren’s contracture. J Bone Joint Surg B. 1966;48(3):452–454.

62. Duperrat B, Colliard H. [Hypertrophic aponeurosis, peculiar variation of Dupuytren’s disease? Excellent therapeutic result with a cytostatic agent (methylhydrazine)]. Une aponévrosite hypertrophique, variante particulière de la maladie de Dupuytren? Excellent résultat thérapeutique d’un agent cytostatique (méthyl-hydrazine) Bull Soc Fr Dermatol Syphiligr. 1969;76(1):14–15. [PubMed]

63. Murrell GAC, Francis MJO, Bromley L. Free radicals and Dupuytren’s contracture. Br Med J.1987;295(6610):1373–1375. [PMC free article] [PubMed]

64. Hueston JT. Enzymic fasciotomy. Hand. 1971;3(1):38–40. [PubMed]

65. Maclennan JD, Mandl I, Howes EL. Bacterial digestion of collagen. J Clin Invest. 1953;32(12):1317–1322. [PMC free article] [PubMed]

66. Harrington DJ. Bacterial collagenases and collagen-degrading enzymes and their potential role in human disease. Infect Immun. 1996;64(6):1885–1891. [PMC free article] [PubMed]

67. Chung L, Dinakarpandian D, Yoshida N, et al. Collagenase unwinds triple-helical collagen prior to peptide bond hydrolysis. EMBO J. 2004;23:3020–3030. [PMC free article] [PubMed]

68. Watanabe K. Collagenolytic proteases from bacteria. Appl Microbiol Biotechnol. 2004;63(5):520–526. [PubMed]

69. Sussman BJ, Mann M. Experimental intervertebral discolysis with collagenase. J Neurosurg.1969;31(6):628–635. [PubMed]

70. Sussman BJ. Experimental intervertebral discolysis. A critique of collagenase and chymopapain applications. Clin Orthop Relat Res. 1971;80:181–190. [PubMed]

71. Bromley JW, Varma AO, Santoro AJ. Double-blind evaluation of collagenase injections for herniated lumbar discs. Spine. 1984;9(5):486–488. [PubMed]

72. Fecteau KA, Haffner JC, Eiler H. The potential of collagenase as a new therapy for separation of human retained placenta: hydrolytic potency on human, equine and bovine placentae. Placenta.1998;19:5–6. 379–383.

73. Badalamente M. Methods for treating adhesive capsulitis. World intellectual property organisation patent. 2006078870 (A2) WO. 2006 Jul 27;

74. Hamilton RG, Mintz GR, Gelbard MK. Humoral immune responses in Peyronie’s disease patients receiving clostridial collagenase therapy. J Urol. 1986;135(3):641–647. [PubMed]

75. Yavuzer R, Latifoglu O, Ayhan S, Edali N, Celik B, Atabay K. Enhanced wound healing using collagenase in guinea pig. Gazi Med J. 1997;8(3):110–113.

76. Klasen HJ. A review on the nonoperative removal of necrotic tissue from burn wounds. Burns.2000;26(3):207–222. [PubMed]

77. Vaccaro S, Gennari G, Callegaro L, Giannelli A, Caruso S. New pharmaceutical compositions containing hyaluronic acid and collagenase for the topical treatment of wounds, burns and ulcers. World intellectual property organisation patent. 2007006484 (A1) WO. 2007 Jan 18;

78. Johnson PRV, White SA, London NJM. Collagenase and human islet isolation. Cell Transplant.1996;5(4):437–452. [PubMed]

79. Strauss BH, Segev A. Use of collagenase to facilitate guide wire crossing in total arterial occlusions. World intellectual property organisation patent. 2005097177 (A1) WO. 2005 Oct 20;

80. Mookhtiar KA, van Wart HE. Clostridium histolyticum collagenases: a new look at some old enzymes. Matrix Suppl. 1992;1:116–126. [PubMed]

81. Mallya SK, Mookhtiar KA, van Wart HE. Kinetics of hydrolysis of type I, II, and III collagens by the class I and II Clostridium histolyticum collagenases. J Protein Chem. 1992;11(1):99–107. [PubMed]

82. French MF, Mookhtiar KA, van Wart HE. Limited proteolysis of type I collagen at hyperreactive sites by Class I and Class II Clostridium histolyticum collagenases: complementary digestion patterns.Biochemistry. 1987;26:681–687. [PubMed]

83. Matsushita O, Koide T, Kobayashi R, Nagata K, Okabe A, Itano T. Collagen-binding domain of a Clostridium histolyticum collagenase exhibits a broad substrate spectrum both in vitro and in vivo.Connect Tissue Res. 2001;42(4):281–290. [PubMed]

84. Toyoshima T, Matsushita O, Minami J, Nishi N, Okabe A, Itano T. Collagen-binding domain of a Clostridium histolyticum collagenase exhibits a broad substrate spectrum both in vitro and in vivo.Connect Tissue Res. 201;42(4):281–290. [PubMed]

85. Barrantes E, Guinea M. Inhibition of collagenase and metalloproteinases by aloins and aloe gel. Life Sci. 2003;72(7):843–850. [PubMed]

86. Garvin PJ., Jr Toxicity of collagenase: the relation to enzyme therapy of disk herniation. Clin Orthop Relat Res. 1974;(101):286–291. [PubMed]

87. Bulstrode NW, Jemec B, Smith PJ. The complications of Dupuytren’s contracture surgery. J Hand Surg Am. 2005;30(5):1021–1025. [PubMed]

88. Olmarker K, Rydevik B, Dahlin LB. Effects of epidural and intrathecal application of collagenase in the lumbar spine: an experimental study in rabbits. Spine. 1987;12(5):477–482. [PubMed]

89. Rydevik B, Brown MD, Ehira T, Nordborg C. Effects of collagenase on nerve tissue: an experimental study on acute and long-term effects in rabbits. Spine. 1985;10(6):562–566. [PubMed]

90. Rydevik B, Ehira T, Linder L, Olmarker K, Romanus M, Branemark PI. Microvascular response to locally injected collagenase. An experimental investigation in hamsters and rabbits. Scand J Plast Reconstr Surg Hand Surg. 1989;23(1):17–21. [PubMed]

91. Rydevik M, Bergström F, Mitts C, Danielsen N. Locally-applied collagenase and regeneration of transsected and repaired rat sciatic nerves. Scand JPlast Reconstr Surg Hand Surg. 2002;36(4):193–196.[PubMed]

92. Badalamente MA, Hurst LC. Enzyme injection as a nonoperative treatment for Dupuytren’s disease.Drug Delivery: Journal of Delivery and Targeting of Therapeutic Agents. 1996;3(1):35–40.

93. Mandl I. Collagenase. Science. 1970;169(951):1234–1238. [PubMed]

94. Braun WPH. Contact allergy to collagenase mixture (Iruxol) Contact Derm. 1975;1(4):241–242.[PubMed]

95. Sussman BJ. Intervertebral discolysis with collagenase. J Natl Med Assoc. 1968;60(3):184–187.[PMC free article] [PubMed]

96. Sussman BJ, Bromley JW, Gomez JC. Injection of collagenase in the treatment of herniated lumbar disk. Initial clinical report. JAMA. 1981;245(7):730–732. [PubMed]

97. Bassot J. Traitement de la maladie de Dupuytren par “exerese” pharmaco-dynamique isolee ou completee par un temps plastique uniquement cutane. 1965;20:38–44.

98. McCarthy DM. The long-term results of enzymic fasciotomy. J Hand Surg Br. 1992;17(3):356.[PubMed]

99. US Food and Drug Administration. Meeting of the Arthritis Drugs Advisory Committee; September 16, 2009; [Accessed 2010 Oct 3]. Briefing information. Available fromhttp://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/Drugs/ArthritisDrugsAdvisoryCommittee/ucm182012.htm.

HAND AND ORTHO ARTICLES

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ORIGINS

STRUCTURE AND FUNCTION

THE MUSCLES

RESTORATION

References

Articles from Proceedings (Baylor University. Medical Center) are provided here courtesy of Baylor Health Care System

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Purpose

Methods

Results

Conclusions

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Patients and methods

Treatment protocol

Results

Clinical findings

Family history

Prenatal history

General examination

Associated syndromes

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Operative findings

Abnormal pathological anatomy

Post operative complications

Results of treatment

Results of operative treatment

Results of non-operative treatment

Discussion

References

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FIGURE 1.

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Complications

FIGURE 2.

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