Algodystrophy following Colles' fracture

ALGODYSTROPHY

FOLLOWING

COLLES’

FRACTURE

R. M. ATKINS,T. DUCKWORTHandJ. A. KANIS From the Royal Hallamshire Hospital, Shefield

The prevalence of algodystrophy in the hand was determined at nine weeks and six months following Colles’ fracture. At nine weeks, 27 of 109 patients showed signs of algodystrophy, all of whom demonstrated more than one feature of the disorder. Thereafter, no unaffected patient developed the disorder. At six months, 62% of the previously affected patients showed some residual abnormalities. In 66% of these, there was evidence of continuing vasomotor instability or swelling, suggesting that the syndrome was still active. These observations suggest that algodystrophy of the hand is a more common complication of Colles’fracture than is generally realised. Journal of Hand Surgery (British Volume, 1989) 14B: 161-164 Algodystrophy (reflex sympathetic dystrophy syndrome or Sudeck’s atrophy) is a relatively ill-defined syndrome. Its features include pain and tenderness, vasomotor instability and loss ofjoint mobility due to swelling which occurs early in the condition (Doury et al., 1981; Lackford, 1982; Lankford and Thompson, 1977). Later in the disorder, atrophy of the skin and subcutaneous tissues become more prominent features, and loss of joint mobility occurs as a consequence of fixed contracture. Regional osteoporosis is also a later feature of the condition. The cause of algodystrophy is unknown but it is commonly triggered by injury (Doury et al., 1981). The incidence of algodystrophy after Colles’ fracture is controversial. It appears rare in most retrospective series, being observed in up to 2% of patients (Bacorn and Kurtzke, 1953; Green and Gay, 1956; Plewes, 1956; LidstrGm, 1959; Frykman, 1967; Pool, 1973). In one large prospective randomised trial of the efficacy of different forms of bracing for Colles’ fracture, no patient appeared to develop the condition when assessed three months or six months after the fracture (Stewart et al., 1985). In contrast, other studies suggest a much higher incidence. Aubert (1980) and Hoffman (1953) found an incidence of 19% and 29% soon after fracture, raising the possibility that the retrospective investigations may have missed a transient form of the disorder. For this reason, we decided to assess the incidence of the disorder prospectively in patients with Colles’ fractures and to determine whether it was associated with significant morbidity. Patients and methods We studied 109 unselected patients who attended the Casualty Department of the Royal Hallamshire Hospital following a Colles’ fracture. The patients remained under the care of the orthopaedic surgeon to whom they had been referred, but they were asked to attend a special review clinic four weeks after removal of plaster (generally nine weeks after injury) and again six months after the fracture. At these visits, the patients were reviewed by a single observer (R.M.A.). No change in VOL. 14-B No. 2 MAY 1989

the clinical management was caused by their participation in the study, which had the prior approval of the local Ethics Committee. The patients were questioned and examined clinically to determine the prevalence of ten pre-selected features of the disorder, grouped according to four aspects of the syndrome. Pain and tenderness were assessed by : 1. The complaint of pain in the hand or fingers (not the wrist) on direct questioning; 2. The complaint of pain in the shoulder of the fractured side on direct questioning; Vasomotor and sudomotor instability were assessed by: 3. Discolouration of the affected hand on clinical examination; 4. A history of vasomotor instability of the affected hand occurring since the fracture; 5. Excessive sweating of the affected hand on history or clinical examination; Swelling and dystrophy were assessed by : 6. Swelling of the hand either on history or clinical examination; 7. Thinning of the skin with shininess and dystrophy; Impairment ofjoint mobility was assessed by: 8. A history of finger stiffness; 9. Loss of finger movement assessed by a measurable pulp-to-palm distance on flexion or clinically obvious loss of finger joint extension; 10. Loss of shoulder movement. These ten features were selected because a review of the literature suggested that they were the ones most commonly associated with the syndrome. The severity of the pain in the hand was quantified using a 10 cm visual analogue scale (Huskisson, 1974), but no attempt was made to measure the severity of the other features, which were scored only as being present or absent. The interrelationships between the features sought were assessed using chi square analysis with Yates’ correction if appropriate. 161

R. M. ATKINS, T. DUCKWORTH AND .I. A. KANIS

Table l-Features

of algodystrophy found in 27 patients. Each horizontal line indicates the features present in one particular patient. Feature*

Hand pain

1 1 1

Shoulder pain

Discolouration

Vasomotor instability

1 1

1 _

0 _ _ 0 0 0 0 1 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0

Swelling

1 1 1 _

I 1 1 1 1 1 1 1 0 1 0 0 1 0 1 0 1

Excessive sweating

0 _ 1 1

_

1 1 1 1 1 1 _

0 0

1 1 1 1 0 1 1 0 0

0 1

1 1

1 _ 1 _ 1 _ _

1 0 0 1 0 1 1 1 1 0 1 0 0 1 0 1 0 1 0

Skin dystrophy

1 1 1 1 1 1 1 1 1 1 1 1 1 0 0 0 1 1 0 0 0 0 1 0 0 0 0

History of stifSness of hand

1 1 1 1 1 1 1 1 1 1 1 0 _ 1 1 0 0 _ 0 0 0

Finding of stl@zess of Hand 1 1 1 1 1 1 1 1 0 1 1 0 1 1 1 1 0 0 1 1 0 1 1 0 0 1 0

Stzflness of shoulder

1 0 0 0 0 0 0 0 0 0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 0 0

Score

100 100

89 88 80 80 75 71 70 70 67 67 67 61 63 60 56 50 50 50 44 44 40 33 30 30 22

*Fuller definitions of these features are given in the text

Results

The 109 patients studied had a mean age of 66 years ( + SD 15 years) and comprised 93 women and 16 men. First review, at nine weeks All attended for review at nine weeks. The majority (82) had no evidence whatsoever of algodystrophy, in that none of the features was present. The remaining 27 patients had some features of the disorder and in all of them more than one feature was identified (Table 1). Indeed, each feature sought was significantly associated with each of the other features (p ~0.01). If all these patients are considered to have algodystrophy, its prevalence at nine weeks after fracture was 24.8%. The extent of the disorder was assessed in a semiquantitative manner by adding the number of features present and expressing them as a percentage of the total number of features sought (normally ten). The scores ranged from 22x-100% of features (mean = 61.3 + SD 21.1). 162

When the results were analysed with respect to the four aspects of the disorder (pain, vasomotor and sudomotor instability, swelling and dystrophy and loss of joint mobility), 13 patients had abnormalities of all four aspects and eleven patients had three of the aspects. Four of these eleven patients had no pain; another four had full joint mobility, two lacked evidence of swelling and one patient had no evidence of vasomotor instability. In only two patients were two abnormalities present and in one, only evidence of vasomotor instability was present. Several difficulties were encountered in completing the history and examination, particularly in the assessment of pain, Thus, nine of the patients with other features of algodystrophy did not complain of pain in the fingers (Table l), but in five patients it was obvious that they were suffering some discomfort that they were unwilling to admit. Clinical examination of the fingers in these cases appeared to demonstrate increased sensitivity to pressure compared to the unfractured side. A further difficulty in assessing pain in the hand occurred in those patients who had residual pain at the THE JOURNAL OF HAND SURGERY

ALGODYSTROPHY FOLLOWING COLLES’FRACTURE

wrist due to ulnar impingement or malunion. Some of these patients found it difficult to understand that it was not the pain due to the fracture which was being assessed, but pain at a different site (which was sometimes less severe), This problem became more evident with the use of the pain analogue scale and it was not possible, therefore, to quantify pain in the hand accurately by this method. The nature of the pain was variable. Two patients complained of burning in the whole of the hand (originally described by Mitchell et al. (1864) as causalgic pain) and another described a dysaesthetic, unpleasant sensation throughout the hand. Two patients had trigger points which, when lightly touched, caused severe stabbing pain in the hand and arm; the trigger points were on the middle finger of the hand and the dorsum of the carpus respectively. One of these patients held the arm in a protective position so as to prevent it being touched. The remaining 13 patients who complained of pain described the pain as gnawing or like toothache. Two of the cases held the hand in a protective manner and all the patients agreed the pain was unpleasant in nature. In 11 patients, evidence of skin discoloration was equivocal and was not characterised. In eight patients, the finger-joint movements were normal to qualitative climcal examination. It was, however, apparent that in some patients there were minor fixed flexion contractures, particularly of the P.I.P. joints. Since these were not certain on simple clinical examination, they were not recorded but they suggest that goniometry might improve the sensitivity of the examination. Four patients with full finger-joint movements complained of stiffness of the fingers. Five patients were referred for hand physiotherapy before the review at nine weeks. When reviewed, four of these patients had a residual loss of finger flexion resulting in a measurable pulp-to-palm distance, while the other one had a full range of finger movement.

Second review, at six months Of the 82 patients without algodystrophy at nine weeks, 72 (88%) attended for review six months after the fracture. None of these patients had developed any features of algodystrophy. Eight of the 27 affected patients failed to attend for review at six months, but of the remaining 19 (70x), 12 (62%) still had discernible abnormalities. In 8 of these 12, there was evidence of continuing vasomotor instability or swelling, suggesting that the syndrome was still active. The remaining four patients had residual joint stiffness. There was no significant association between the number of features of algodystrophy present at nine weeks and the finding of residual abnormalities at six months (chi squared = 0.37, NS). VOL. 14-B No. 2 MAY 1989

Discussion This prospective study of Colles’ fracture suggests that this fracture is commonly associated with residual abnormalities at sites distant from the fracture itself. The features which we sought were all highly significantly associated with each other, and the vast majority (89%) had three or more of the four aspects commonly associated with algodystrophy. Thus, algodystrophy appears to occur more commonly following Colles’ fracture than has been hitherto thought. When these same patients were assessed at six months, 62% of affected patients had residual abnormalities, whereas none of the unaffected patients developed algodystrophy. This suggests that the features of algodystrophy were temporally associated with fracture, but also that it is a transient disorder in many patients. Our estimate of the prevalence of features of algodystrophy at nine weeks is likely to be an underestimate, mainly because of the difficulties encountered with the history and examination; more sensitive techniques might have revealed a greater number of affected patients. Similar considerations apply to our assessment at six months, but it is notable that a slightly smaller proportion (70%) of patients with algodystrophy attended for review than patients without features of the disorder (88%). This may have biased our estimate, since patients with continuing symptoms might have been more willing to be followed-up. If all patients with continuing algodystrophy attended for review, the true incidence at six months would be 11% rather than 17% and the incidence of active algodystrophy would be only 7%. The scoring of the extent of the condition by summing the number of feature found is not intended to imply severity of algodystrophy but to demonstrate the significant association of the features. It is not possible from this study to give an accurate indication of the morbidity caused by the condition (since no successful attempt was made to quantify the degree of abnormality) but only the number of abnormalities present. This is an important question to resolve and will require the application of quantitative techniques. The failure of all patients to show every feature of the syndrome raises the question of the minimal requirements for a diagnosis of algodystrophy of the hand. The features which we sought are not at all equally important for the diagnosis. Thus, for example, shoulder pain and stiffness are less essential than loss of finger movement and hand pain. Also the presence of vasomotor instability can be inferred from either finding skin discoloration on examination or a positive history. The finding of one of these without the other may depend more on the weather conditions and the patient’s mental powers than the syndrome itself. If, for the purposes of diagnosis, the patient should have evidence of all the aspects of the syndrome, then 163

R. M. ATKINS,

T. DUCKWORTH

only 13 cases at nine weeks fulfilled this criterion. However, the patients who had not noticed any pain may have simply been stoical. This suggestion is supported by the observation that five patients appeared to have discomfort in movement of the fingers but admitted to no pain. This limitation could be overcome by the use of a method for the quantification of pain and tenderness, such as the dolorimeter (McCarty et al., 1965) and in this respect it is interesting that those patients who did not complain of pain in the fingers nevertheless appeared clinically to have tenderness of them. Similarly, the failure to report vasomotor instability or swelling may relate to the patient’s powers of observation. Four patients had normal mobility of the finger-joints and no stiffness and this raises the question whether algodystrophy of the hand can be diagnosed in the presence of normal finger-joint movements. Early in the evolution of algodystrophy, loss of joint mobility is due to swelling and pain and therefore a full range of joint movement might be possible if the condition were mild and the patient determined. However, the failure of finger stiffness to resolve rapidly in four patients treated by physiotherapy suggests that, in these patients at least, the loss of joint mobility was due to more than simple immobilisation (Channon et al., 1979). It is of interest that the apparent prevalence of algodystrophy decreased with time from 25% at nine weeks to 17% by six months. It is possible, therefore, that the incidence shortly after the fracture could be even higher, but this can only be determined by examination of patients at these earlier times. The present study only gives an indication of the possible natural history of the disorder; it was notable that at the second examination, fewer features were present in affected patients. These considerations suggest that the disorder which we are describing is transient, at least in the majority of patients and so would not have been picked up in retrospective surveys. This may explain, at least in part, the widely differing estimates of the incidence of algodystrophy. The condition which we are describing differs from the classic “Sudeck’s atrophy” in several respects. It may be transient, milder and more common and a number of patients did not exhibit all the features classically described. Whether these differences are merely of degree, or whether the features of algodystrophy which we have described occur to a limited extent following every fracture, can only be established by the application

164

AND J. A. KANIS

of quantitative, sensitive techniques for the independent and objective assessment of each aspect of the condition. Such techniques are currently under development and will be the subject of further reports. Acknowledgements We are grateful to MI D. K. Evans, Mr R. H. Baker and Mr N. R. M. Kay for allowing us to study their patients. R.M.A. was supported by an Action Research Training Fellowship and the work was supported by an MRC programme grant.

References AUBERT, P. G. Etude sur le risque algodystrophique chez 500 hospitalises au milieu orthopaedique. These pour le doctorat en medecin diplome d’etat. Universite Paris Val de Marne, 1980. BACORN, R. W. and KURTZKE, J. F. (1953). Colles' fracture. A Study of Two Thousand Cases from the New York State Workmen’s Compensation Board. Journal of Bone and Joint Surgery, 35A: 3 : 643-658. CHANNON, G. M. and LLOYD, G. J. (1979). The investigation of hand stiffness using Doppler ultrasound, radionuclide scanning and thermography. JoumalofBone and Joint Surgery, 61B: 4: 519. DOURY, P., DIRHEIMER, Y. and PATTIN, S. Algodystrophy. Berlin, Springer Verlag, 198 1. FRYKMAN, G. (1967). Fracture of the distal radius including sequelaeshoulder-hand-finger syndrome, disturbance in the distal radio-ulnar joint and impairment of nerve function. A clinical and experimental study. Acta Orthopaedica Scandinavica, Supplement 108. GREEN, J. T. and GAY, F. H. (1956). Colles’ Fracture-Residual Disability. American Journal of Surgery, 91: 636-646. HOFFMAN, B. P. (1953). Fractures of the distal end of the radius in the adult and in the child. Bulletin of the Hospital for Joint Diseases, 14: 114-124. HUSKISSON, E. C. (1974). Measurement ofpain. Lancet 2: 1127-1131. LANKFORD, L. L. Reflex sympathetic dystrophy. In: Green, D. P. (Ed.) Operative Hand Surgery. New York. Churchill Livingstone, 1982: Vol 1: 539-563. LANKFORD, L. L. and THOMPSON, J. E. Sympathetic dystrophy, upper and lower extremity: diagnosis and management. In: American Academy of OrthopaedicSurgeons InstructionnlCourseLectures, 26. St. Louis, C.V. Mosby, 1977: 163-178. LIDSTROM, A. (1959). Fractures of the distal end of the radius. A clinical and statistical study of end results. Acta Orthopaedica Scandinavica, Supplement 41. MCCARTY, D. J., GATTER, R. A. and PHELPS, P. (1965). A Dolorimeter for Quantification of Articular Tenderness. Arthritis and Rheumatism 8: 4: 551-559. MITCHELL, S. W., MOREHOUSE, G. R. and KEEN, W. W. Gunshot wounds and other injuries of nerues. Lippincott, Philadelphia, 1864. PLEWES, L. W. (1956). Sudeck’s atrophy in the hand. Journal of Bone and Joint Surgery, 38B: 195-203. POOL, C. (1973). Colles’ fracture. A Prospective Study of Treatment. Journal of Bone and Joint Surgery 55B: 3 : 540-544. STEWART, H. D., INNES, A. R. and BURKE, F. D. (1965). The Hand Complications of Colles’ fractures. Journal of Hand Surgery, 10B: 1: 103106.

Accepted: 140ctober 1988 Mr. R. M. Atkins, Consultant Senior Lecturer, Royal Infirmary, 0

Department

of Orthopaedic

Surgery,

Bristol

Bristol BS2 8HW.

1989 The British

Society

for Surgery

of the Hand

0266-7681/89/0014-0161/$10.00

THE

JOURNAL

OF HAND

SURGERY