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A Zyluk

Publications and source records attributed to A Zyluk.

30 records · Page 2Linked to original sources

[Iatrogenic causes of post-traumatic reflex sympathetic dystrophy].

It is suspected that some faults in the course of the treatment of traumas such as: reduction of fractures without sufficient anaesthesia, repeated reductions, tightness of casts, immobilization of fingers, ignoring patients' complaints of the pain and swelling about or painful rehabilitation may have effect on the development of the post-traumatic reflex sympathetic dystrophy. These opinions have not been confirmed by clinical trials. The incidence of above mentioned factors was analysed retrospectively in 165 patients with post-traumatic reflex sympathetic dystrophy within upper extremity and in 86 patients following fracture of distal radius without features of the condition (control group). It was found that the patients with reflex sympathetic dystrophy significantly more frequently complained of pain and swelling in the course of the treatment of trauma in the cast and they were subjected more frequently to painful rehabilitation after removing the cast. These factors appeared to have an effect on developing the reflex sympathetic dystrophy (comparing with the control group). The role of remaining factors that are often considered as significant in the development of reflex sympathetic dystrophy--painful and repeated reductions of fractures as well as immobilization of fingers-was not confirmed.

Arm Injuries↗

The reasons for poor response to treatment of posttraumatic reflex sympathetic dystrophy.

One hundred twelve patients with posttraumatic reflex sympathetic dystrophy were treated using 4 methods: regional intravenous blocks with lignocaine and methylprednisolone, mannitol i.v. (free-radical scavenger), calcitonin i.m. and physical therapy (program of exercises). Good results occurred in 73 cases (65%), moderate in 27 (24%) and poor results (persistence of spontaneous pain and/or malfunction of the hand) in 12 (11%). The method of treatment had no significant influence on the frequency of poor results. The following factors were analyzed in order to assess their influence on the results of the treatment: age, sex, psychological status, type and severity of the initial injury, duration and stage of the disease, initial deficiency of finger flexion, presence of changes on x ray and bone scans; the results were subjected to statistical analysis ("z" test comparing frequency for two independent trials). The incidence of poor results was significantly higher in patients with duration of reflex sympathetic dystrophy longer than 12 months, in the second and third stages of disease, and in cases with coexisting nerve injuries or compression as a consequence of initial trauma. The other factors analyzed had no significant influence on the unfavourable result of the treatment of reflex sympathetic dystrophy.

Adult↗

Results of the treatment of posttraumatic reflex sympathetic dystrophy of the upper extremity with regional intravenous blocks of methylprednisolone and lidocaine.

The results of the treatment of 36 patients with posttraumatic reflex sympathetic dystrophy of the upper extremity with regional intravenous blocks of methylprednisolone and lidocaine are presented. The extremity is exsanguinated and a tourniquet is applied. A solution of methylprednisolone, lidocaine and heparin is injected. The duration of the block is 20-25 minutes. After the limb is anesthetized the affected joints can be manipulated in a progressive, controlled fashion. With a 1-year follow-up the response to treatment in 25 patients (69%) was considered as good (relief of spontaneous pain, no limitation in finger movement), in 8 as moderate (22%) and in 3 as poor (9%--the symptoms were unaltered or worse). Physiotherapy was applied in all patients (program of finger exercises, whirlpool therapy). Complications in 2 cases were transient superficial thrombophlebitis of the forearm; in 2 other patients the block was interrupted because of severe pain in the limb. We found this method simple, easy to perform, safe and inexpensive; the results are comparable to other established methods of the treatment i.e. sympathetic blocks or calcitonin.

Adult↗

[Diagnostic criteria for post-traumatic algodystrophy].

Algodystrophy (reflex sympathetic dystrophy, Sudeck's atrophy) is a clinical syndrome, developing in most cases as a consequence of trauma and characterized by pain, swelling, tenderness, vascular and sudomotor instability trophic changes of the skin and stiffness. There are several controversial issues concerning algodystrophy in the literature: incidence of the condition (from 0.03% to 95% in various studies), the value of the diagnostic tests in its recognizing and efficacy of the various methods of the treatment. The causes of these discrepancies were discussed: various diagnostic criteria, its unrestricted use by authors and specificity of the natural history of the condition were considered as the main reasons. The features of algodystrophy and its importance in recognizing of the disorder were described in detail; the diagnostic value of the radiographic, static and dynamic scintigraphic examination and diagnostic sympathetic block were also discussed. Several clinical classifications of algodystrophy were presented; the usefulness of these classifications in providing more accurate assessment of the clinical groups and in facilitating of comparison between studies were underlined.

Humans↗

[Historical review of algodystrophy: part I].

The history of algodystrophy discerning, its recognition as a separate clinical entity and evolution of ideas about its nature is presented on the basis of historical and scientific literature. First cases resembling algodystrophy were described as early as in XVI and XVIII century. A more detailed description of limb dystrophy that followed gunshot injuries was reported by American surgeon Weir Mitchell in 1864, who coined this condition as "causalgia". In the year 1900 Paul Sudeck of Germany described radiological changes secondary, as he believed, to inflammatory process within the limb as patchy osteoporosis. His name is still attached to this syndrome in German and Polish literature. French neurosurgeon Rene Leriche believed, that the syndrome was caused by increased activity of the sympathetic nervous system and introduced a surgical periarterial sympathectomy. Oscar Steinbrocker of the United States separated particular form of algodystrophy known as shoulder-hand syndrome; later, he introduced the treatment of this condition with steroids.

History, 19th Century↗

[A historical review of algodystrophy: part II].

Second part of this paper deals with developing of the etiopathological concepts on algodystrophy. Variety of terms have been used to describe the syndrome during over hundred years. The name "reflex sympathetic dystrophy" introduced by J.A. Evans in 1946 is commonly used in English and American literature. French rheumatologists proposed the term "algodystrophy" in 1960; this seemed very satisfactory, because did not imply involvement of any particular tissue, localization or etiology but reflected the combination of pain and dystrophic changes. Current taxonomic concepts were also presented e.g. "complex regional pain syndrome". A discrepancies on the incidence rates of the condition were mentioned and their causes suggested. Current diagnostic criteria of the syndrome were presented. The contribution of Polish authors was reminded. In spite of considerable progress in understanding of the syndrome, its many aspects remain controversial or obscure.

England↗

[Post-traumatic painful ulnar nerve compression syndrome treated by wrapping the nerve with the vein: preliminary report].

Three cases of post-traumatic painful ulnar nerve compression syndrome are presented. Previous treatment both conservative and surgical (neurolysis) proved unsatisfactory. The method described-wrapping of the nerve with the saphenous vein graft in the area of scarification-gave satisfactory outcome in 2 of 3 operated patients (significant resolution of pain and improvement of sensation) in one year follow-up. In one patient surgery failed. The method presented might be considered in refractory cases of painful nerve compression syndrome due to its entrapment within scarred tissue after injury or previous surgery.

Arm Injuries↗

[Algodystrophy after distal radius fractures].

Algodystrophy is a severe complication of distal radius fractures; its incidence balances from 0.02% to 37% reported from various papers. In order to ascertain its incidence and clinical picture, the following features in 100 patients 2-4 months after distal radius fracture were examined: pain in the hand, swelling, vasomotor and sudomotor instability, stiffness, trophic changes, shoulder complaints and changes on X-ray picture; the presence and intensity of each feature were noticed. There were 87 female and 13 male patients, aged from 36 to 88 years (average 60.6 years) in the group; 79% of patients complained of pain in affected hand (spontaneous or after loading) and 20% complained of pain and limitation of movement in the shoulder joint. Algodystrophy, diagnosed by the presence of at least 4 strongly expressed features was noted in 14% of patients. The syndrome developed more frequently in women than in men, in patients with displaced and manipulated fractures (particularly with fragmentation of the epiphysis) and in individuals wit poorly reduced fractures. The most specific for algodystrophy features were: deficiency of finger flexion greater than 3 cm, severe spontaneous pain, severe swelling and permanent redness of the hand; the author suggests, that algodystrophy after distal radius fracture is far more common condition than it is generally believed.

Adult↗

[Inflammation theory for etiopathogenesis of algodystrophy].

Algodystrophy (reflex sympathetic dystrophy, Sudeckłs atrophy) is the condition of still unclear pathogenesis. Paul Sudeck, who described the syndrome was convinced of its inflammatory nature; later research established the inducing role of the sympathetic nervous system for many years. This view has been questioned in the last decade. This paper presents some evidence of inflammatory explanation of the disorder: increased uptake of the immunoglobulin IgM labeled In111 in affected area, followed by increased vascular permeability for macromolecules, and impaired metabolism of the high energy phosphates following the impaired oxygen extraction in the affected extremity. Free oxygen and hydroxyl radicals injurious role in the course of algodystrophy is also established by beneficial treatment with the use of free radicals scavengers (mannitol, dimethyl sulfoxide, N-acetylcysteine) and by pathologic ultrastructural changes in muscle cells due to oxidative stress. The view of the inflammatory nature of acute stage of algodystrophy does not preclude a role of sympathetic nervous system but it better explains some clinical aspects of this phase of the condition and increases recognition of its complicated nature.

Free Radicals↗

[Clinical estimation of late treatment results in posttraumatic Sudeck's dystrophy treated with mannitol, calcitonin and exercise therapy].

The author presents late results of treating 60 patients with posttraumatic Sudeck's dystrophy of upper extremity. The treatment was conducted by 3 methods: 30 patients were receiving mannitol for 1 month, 15 subjects were given calcitonin intramuscularly for 1 month, and programmed rehabilitation according to Mucha's scheme was applied in 15 patients. The results were estimated within the period of 1/2--2 years since the commencement of therapy. The evaluation of the results was accomplished by 3-degree classification namely: good, fair, poor. Main attention was focussed on the rest pain regression and improvement of the hand grasping function. In the total group of 60 patients under treatment, there were 38 persons with good results (62%), in 16 the result was fair (27%) and in 6 persons the outcome was poor (11%). It has been recorded that the treatment during the I stage of disease by all the three methods used was uniformly effective. In the treatment of the II stage the most efficacious was mannitol (statistically significant). Mannitol best influenced the improvement of hand grasping strength after the treatment, as well as regression of DS typical changes in RTG and bone scan. It has been also ascertained that for achievement of good results--regardless of the therapeutic method--the greatest influence was exerted by: the time shorter than 3 months elapsing from the trauma to the onset of the treatment, initial deficit in flexion of the fingers smaller than 3 cm, the presence of typical for DS changes in bone scintigraphy as well as I stage of the disease.

Calcitonin↗

[Shoulder-hand syndrome in patients after stroke].

Basing on the literature, the information on the shoulder-hand syndrome in stroke patients is presented. The syndrome is believed to be a clinical form of algodystrophy of the upper extremity. The main signs and symptoms include pain and considerable reduction of movement in shoulder joint, wrist and hand. The condition usually develops 1-6 months after stroke with pain and loss of range of motion in the shoulder at the beginning; then the distal part of the extremity is involved. The syndrome is considered to develop in three consecutive phases: I--acute, II--dystrophic and III--atrophic. Besides classical clinical form, affecting distal and proximal part of extremity, the incomplete forms confined only to one of this parts may exist. The prevalence of the condition is rated at 12.5-27% in stroke patients. It is believed that the development of the syndrome is related to altered biomechanics of the hemiplegic shoulder. Stability of the joint is considerably affected due to paresis or palsy of shoulder girdle muscles what results in partial subluxation of humeral head. Repeated microtraumas of shoulder joint may cause chronic pain and may initiate development of abnormal, regional sensory-sympathetic reflex arch, or--according to the other concept--it results in "sensitization" of neurons in the dorsal horn; this state may alter dorsal horn central mechanisms processing sensory and painful stimuli. The diagnosis of the syndrome is based on clinical ground. Three-phase bone scintigraphy is believed to be the most useful additional diagnostic test. The diagnostic and predictive value of this technique is presented. For all advantages of scintigraphic examination, it does not need to be performed in the majority of stroke patients since the presence of typical signs and symptoms is usually sufficient to make a diagnosis. The treatment of shoulder-hand syndrome included administration of steroids with satisfactory response. The role of proper physical therapy in improving of the results of treatment as well as in prophylactics of the syndrome is emphasised. Considering the fact that many of stroke patients may have contraindications to steroid therapy, other methods of effective treatment are proposed.

Cerebrovascular Disorders↗

[Shoulder-hand syndrome after stroke: a case report].

A case of shoulder-hand syndrome (algodystrophy, reflex sympathetic dystrophy) in a stroke patient is presented. Six weeks after stroke the condition started with pain, swelling and considerable reduction of movements of the hand and wrist followed by involvement of shoulder joint a few days later. Initially, the complaints were attributed to excessive rehabilitation, however, when cessation of exercises and anti-inflammatory treatment failed to improve, the diagnosis of shoulder-hand syndrome was suspected. Three phase bone scintigraphy performed 2 weeks after the onset of symptoms revealed features of possible algodystrophy. X-ray revealed no significant changes. The patient satisfactory responded to nasal salmon calcitonin treatment 300 units daily during 4 weeks. The reassessment performed 3 months after the onset of disease showed regression of most signs and symptoms as well as satisfactory range of motion of the hand and shoulder. Bone scintigraphy revealed typical algodystrophy pattern (diffusely increased periarticular uptake). The cause of such evolution of scintigraphic changes as well as some implications of nasal calcitonin administration were discussed.

Administration, Intranasal↗