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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during, and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Although the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.
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PMID:Induction of equine postanesthetic myositis after halothane-induced hypotension. 293 29

Right hind limb lameness, progressing to bilateral paraparesis, was observed in 56 of 610 (9%) beef cows. Lameness began 6 days to 4 weeks after vaccination in the right longissimus lumborum (loin) muscle with an Escherichia coli/Campylobacter bacterin in an oil adjuvant. Postmortem examination of 5 affected cows revealed a large inflammatory mass at the site of vaccination. In each cow, the mass spread through adjacent intervertebral foramina into the vertebral canal and compressed the lumbar portion of the spinal cord. Microbiologic procedures did not reveal a microbial agent in affected tissues or in an unopened bottle of bacterin from the same lot used in the herd. Histologic examination revealed pyogranulomatous inflammation of the vaccination site and adjacent epidural tissue, with inflammatory nodules centered around large clear spaces that probably represented remnant emulsion from the oil adjuvant in the bacterin. As evident in these cows, IM injection of irritating products may cause severe myositis. Vaccination into paravertebral muscles is risky because of possible extension of inflammation through intervertebral foramina.
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PMID:Myositis, lameness, and paraparesis associated with use of an oil-adjuvant bacterin in beef cows. 755 29

Ninety-three consecutive treadmill exercise stress test were performed for the assessment of peripheral vascular function. Thirty-one were for atypical claudication-like symptoms including pain on standing, relief on sitting and back pain. Pedal pulses were palpable in 24 patients. Twenty-five patients (81%) had a negative stress test, suggesting a non-vascular aetiology and this finding was subsequently confirmed in 24 of the 25. The final diagnoses were spinal stenosis 13, [CT = 3, myelogram = 5, neurosurgeon opinion = 4, MRI = 1], myositis 2, restless leg syndrome 2 and osteoarthritis 7. Four patients had symptoms due to a combination of peripheral occlusive arterial disease and spinal stenosis; the latter was considered the predominant disorder in all four. Of the original 31 patients with atypical symptoms, spinal stenosis was present in 13 (42%). Atypia- in the common syndrome of intermittent claudication should alert the surgeon to the possibility of spinal canal disorders. Further investigation may identify significant pathology spinal stenosis in particular.
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PMID:Spinal claudication versus arterial claudication. 869 57

Exertional compartment syndrome is characterized by intracompartmental pressures that rise transiently following repetitive motion or exercise, thereby producing temporary, reversible ischemia, pain, weakness, and, occasionally, neurologic deficits. The exact cause or pathogenesis remains unclear; a disturbance of microvascular flow caused by elevated intramuscular pressure leads to tissue ischemia, depletion of high-energy phosphate stores, and cellular acidosis. Anatomic contributing factors may include a limited compartment size, increased intracompartmental volume, constricted fascia, loss of compartment elasticity, poor venous return, or increased muscle bulk. The diagnosis is suspected based on history and confirmed with physical examination and intramuscular pressure evaluation before and after exercise (stress test). Differential diagnosis includes claudication or other vascular abnormalities, myositis, tendinitis, periostitis, chronic strains or sprains, stress fracture, other compression or systemic neuropathies, and cardiac abnormalities with angina or referred extremity pain. Initial treatment includes activity modification; refractory symptoms can be managed with elective fasciotomy.
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PMID:Exertional compartment syndrome of the upper extremity. 974 26

The effects on goats of Calotropis procera latex given by different routes of administration were investigated. The administration of latex at 1 ml/Kg body weight via the oral route or at 0.005 ml/Kg body weight/day via the intravenous or intraperitoneal route caused death of the goats between 20 minutes and 4 days. When the small dose of latex (0.005 ml/Kg body weight/day) was given by the oral route or intramuscular route no death among the goats occurred. Nervous signs, frequent urination, frothing at the mouth, dyspnoea and diarrhoea were the main features in goats given latex by the oral, intravenous or intraperitoneal route. Lameness was observed in goats given latex via the intramuscular route. Lesions were widespread congestion and haemorrhage, pulmonary cyanosis, enterohepatonephropathy, peritonitis (in goats receiving latex via i.p. route) and haemorrhagic myositis at the site of latex injection. These changes were accompanied by increases in the activities of serum GDH, LDH, ALP, GGT and AST and in the concentrations of cholesterol, urea and creatinine and decreases in the level of total protein.
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PMID:Studies on laticiferous plants: toxic effects in goats of Calotropis procera latex given by different routes of administration. 985 66

Up to 60 percent of adults report that they have had nocturnal leg cramps. The recurrent, painful tightening usually occurs in the calf muscles and can cause severe insomnia. The exact mechanism is unknown, but the cramps are probably caused by muscle fatigue and nerve dysfunction rather than electrolyte or other abnormalities. Nocturnal leg cramps are associated with vascular disease, lumbar canal stenosis, cirrhosis, hemodialysis, pregnancy, and other medical conditions. Medications that are strongly associated with leg cramps include intravenous iron sucrose, conjugated estrogens, raloxifene, naproxen, and teriparatide. A history and physical examination are usually sufficient to differentiate nocturnal leg cramps from other conditions, such as restless legs syndrome, claudication, myositis, and peripheral neuropathy. Laboratory evaluation and specialized testing usually are unnecessary to confirm the diagnosis. Limited evidence supports treating nocturnal leg cramps with exercise and stretching, or with medications such as magnesium, calcium channel blockers, carisoprodol, or vitamin B(12). Quinine is no longer recommended to treat leg cramps.
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PMID:Nocturnal leg cramps. 2296 30