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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle membrane injury is a predictable consequence of extreme exertion. The risk is compounded if an untrained individual performs eccentric exercise in a hot environment, or there is any preceding infectious disease, drug ingestion or an underlying metabolic disorder. Once the integrity of the membrane is breached, a constellation of physiological changes follows. Cell contents leak out and extracellular components leak in. Muscle pain and weakness ensue. Myoglobin is but one substance that is liberated into the bloodstream. When dehydration, hypovolaemia and acidosis are added to the myoglobin load, the kidney may respond by ceasing its excretory and metabolic functions. This is the most serious consequence of rhabdomyolysis, and may be life threatening. The clinical setting, in combination with laboratory features of a grossly elevated creatine kinase, orthotoluidine positive urine and granular casts provides a rapid and accurate means of diagnosis in most cases. Management principles include aggressive fluid replacement, early use of cation exchange resins and dialysis for electrolyte control, plus fasciotomy for relief of compartment syndrome and limb preservation. Following this protocol, the prognosis is excellent. Prior conditioning clearly reduces the incidence of exercise-related muscle injury. Future research should concentrate on the rate at which training loads can be safely increased.
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PMID:Rhabdomyolysis, myoglobinuria and exercise. 306 36

Weakness of dorsiflexion of the foot is a common complication of proximal tibial osteotomy and it has been suggested that this may be caused by an anterior tibial compartment syndrome. A prospective study of 20 patients undergoing tibial osteotomy was undertaken, in which compartment pressures were recorded and related to clinical signs. In 10 of the patients, the operation site was drained, and in 10 no drainage was employed. The undrained group showed significant elevation (greater than 45 mmHg) of the anterior compartment pressure in seven patients, and five of these had transient clinical signs. Only one patient had any permanent deficit, a minor asymptomatic weakness of extensor hallucis longus. In the drained group the pressures remained below 30 mmHg in all except two patients, who both had only a minor pressure rise and no significant early clinical signs. However, two patients from this group later developed weakness of dorsiflexion, probably due to common peroneal nerve injury, the cause of which is not clear.
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PMID:Weakness of foot dorsiflexion and changes in compartment pressures after tibial osteotomy. 373 17

Three patients exhibited variable weakness of toe extensors after trivial injuries. The first patient suffered an acute, partial anterior compartment syndrome during a prolonged motorbike ride; the second a traction injury of the deep peroneal nerve while slipping during a racquetball game. The third patient developed a compression injury of the peroneal nerve on the basis of a generalized demyelinating polyneuropathy. The major clues for diagnosis and management came from electromyographic (EMG) examination.
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PMID:Toe extensor weakness resulting from trivial athletic trauma. Report of three unusual cases. 713 53

Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.
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PMID:Volkmann's ischemic contracture of the foot and ankle: evaluation and treatment of established deformity. 755 Sep 46

A 38-year-old male presented to the emergent department complaining of bilateral leg numbness and weakness after waking from a sleep. Finding himself on the floor, he attributed this problem to falling out of bed. His subsequent course was complicated by progressive leg swelling, shock, profound hemoconcentration and renal failure. He received large volume of crystalloid and fasciotomy in the emergent department and then admitted. He ultimately recovered well. Crush syndrome without obvious compressive trauma or substance induced sleep is highly unusual. Early recognition is important because a delay of more than 6 hours in giving adequate volume support will lead to renal failure. Ischemic muscle times of greater than eight hours inevitably lead to residual disability. It remains imperative therefore, to recognize the presence of a compartment syndrome secondary to fluid sequestration early, either clinically or using compartment pressures. A fasciotomy within this eight hour window may still lead to complete recovery.
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PMID:Crush syndrome--delayed diagnosis due to a lack of apparent injury mechanism--a case report. 806 45

Chronic compartment syndrome (CCS) is a recognized cause of recurrent leg pain in the exercising patient. Decreased muscle function has been implied in this condition. This study compared the ankle dorsiflexion torque of 10 CCS patients with that of 18 control subjects during 20 repeated, maximal, isokinetic contractions at 60 degrees/sec. Peak torque, relative peak torque, and endurance data were collected. Results showed significantly lower peak torque and relative peak torque in the CCS group (p < or = 0.05), supporting the implication of muscle weakness in CCS. Paradoxically, endurance was significantly higher in the CCS group (p < or = 0.01), and there was a significant (p < or = 0.01), negative correlation (r = -0.50) between peak torque and endurance. The relationship between the findings and CCS is discussed. Strengthening may be useful in very mild cases or in postfasciotomy patients.
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PMID:Muscle function in chronic compartment syndrome of the leg. 826 60

Peripheral nerve lesions are uncommon but serious injuries which may delay or preclude an athlete's safe return to sports. Early, accurate anatomical diagnosis is essential. Nerve lesions may be due to acute injury (e.g. from a direct blow) or chronic injury secondary to repetitive microtrauma (entrapment). Accurate diagnosis is based upon physical examination and a knowledge of the relative anatomy. Palpation, neurological testing and provocative manoeuvres are mainstays of physical diagnosis. Diagnostic suspicion can be confirmed by electrophysiological testing, including electromyography and nerve conduction studies. Proper equipment, technique and conditioning are the keys to prevention. Rest, anti-inflammatories, physical therapy and appropriate splinting are the mainstays of treatment. In the shoulder, spinal accessory nerve injury is caused by a blow to the neck and results in trapezius paralysis with sparing of the sternocleidomastoid muscle. Scapular winging results from paralysis of the serratus anterior because of long thoracic nerve palsy. A lesion of the suprascapular nerve may mimic a rotator cuff tear with pain a weakness of the rotator cuff. Axillary nerve injury often follows anterior shoulder dislocation. In the elbow region, musculocutaneous nerve palsy is seen in weightlifters with weakness of the elbow flexors and dysesthesias of the lateral forearm. Pronator syndrome is a median nerve lesion occurring in the proximal forearm which is diagnosed by several provocative manoeuvres. Posterior interosseous nerve entrapment is common among tennis players and occurs at the Arcade of Froshe--it results in weakness of the wrist and metacarpophalangeal extensors. Ulnar neuritis at the elbow is common amongst baseball pitchers. Carpal tunnel syndrome is a common neuropathy seen in sport and is caused by median nerve compression in the carpal tunnel. Paralysis of the ulnar nerve at the wrist is seen among bicyclists resulting in weakness of grip and numbness of the ulnar 1.5 digits. Thigh injuries include lateral femoral cutaneous nerve palsy resulting in loss of sensation over the anterior thigh without power deficit. Femoral nerve injury occurs secondary to an iliopsoas haematoma from high energy sports. A lesion of the sciatic nerve may indicate a concomitant dislocated hip. Common peroneal nerve injury may be due to a direct blow or a traction injury and results in a foot drop and numbness of the dorsum of the foot. Deep and superficial peroneal nerve palsies could be secondary to an exertional compartment syndrome. Tarsal tunnel syndrome is a compressive lesion of the posterior tibial nerve caused by repetitive dorsiflexion of the ankle--it is common among runners and mountain climbers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Peripheral nerve injuries in athletes. Treatment and prevention. 837 68

We retrospectively reviewed the results of operative treatment of chronic Monteggia lesions (Bado type I or the equivalent) with anterior radiocapitellar dislocation in seven patients. The mean age at the time of the reconstruction was six years and nine months (range, eleven months to twelve years), and the mean time from the injury to the operation was twelve months (range, five weeks to thirty-nine months). The mean duration of follow-up was four years and six months (range, two years to eleven years and three months). There were fourteen complications, including malunion of the ulnar shaft in one patient; residual radiocapitellar subluxation in two patients (one anterior and one posterolateral); radiocapitellar dislocation (dynamic anterior subluxation of the radial head in supination) in one patient; transient ulnar-nerve palsy in three patients (with residual weakness in two); partial laceration of the radial nerve in one patient; loss of the fixation in two patients; and non-union of the ulnar osteotomy site, compartment syndrome, conversion reaction, and possible fibrous synostosis of the forearm in one patient each. The patients lost a mean of 36 degrees of pronation and a mean of 27 degrees of supination of the forearm compared with the contralateral, uninjured extremity. Two patients demonstrated a loss of flexion of the elbow of 8 and 13 degrees and three had a loss of extension (mean, 15 degrees) compared with the contralateral side. There were three good, two fair, and two poor results.
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PMID:Chronic Monteggia lesions in children. Complications and results of reconstruction. 881 46

A variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by: 1) which leg compartments have been affected and to what degree extrinsic flexor or extensor "overpull" is exhibited, 2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles, 3) which foot compartments have been affected and to what degree intrinsic "overpull" is exhibited, and 4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Nonoperative therapy attempts to obtain or preserve joint mobility, increase strength, and provide corrective bracing and accommodative foot wear. Operative management is undertaken for treatment of residual nerve compression or refractory problematic deformities. Established surgical protocols are performed in a stepwise fashion, and include: 1) release of residual or secondary nerve compression; 2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy; 3) tendon transfers or arthrodesis to increase function; and 4) osteotomy or amputation for severe, non-salvageable deformities.
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PMID:Ischemic contracture of the foot and ankle: principles of management and prevention. 886 51

We reviewed 25 patients with tibial diaphyseal fractures which had been complicated by an acute compartment syndrome. Thirteen had undergone continuous monitoring of the compartment pressure and the other 12 had not. The average delay from injury to fasciotomy in the monitored group was 16 hours and in the non-monitored group 32 hours (p < 0.05). Of the 12 surviving patients in the monitored group, none had any sequelae of acute compartment syndrome at final review at an average of 10.5 months. Of the 11 surviving patients in the non-monitored group, ten had definite sequelae with muscle weakness and contractures (p < 0.01). There was also a significant delay in tibial union in the non-monitored group (p < 0.05). We recommend that, when equipment is available, all patients with tibial fractures should have continuous compartment monitoring to minimise the incidence of acute compartment syndrome.
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PMID:Acute compartment syndrome in tibial diaphyseal fractures. 868 51


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