1/7. colchicine neuromyopathy: a report of six cases.colchicine has been in use for therapeutic purposes for many years. It can, however, cause subacute onset muscle and peripheral nerve toxicity in patients with chronic renal failure. In this report we describe 6 patients who developed neuromyopathy after the administration of colchicine. All patients presented with proximal muscle weakness, elevated serum creatine kinase (CK) levels, and neuropathy and/or myopathy on electromyography (EMG). The diagnosis of colchicine toxicity was confirmed in all cases by the normalization of CK levels and EMG after discontinuation of the drug. Toxicity developed in 4 renal failure patients on therapeutic doses of the drug, while one patient took a massive dose for suicidal reasons, and the other was on high-dose therapy. patients using colchicine--especially those with renal failure--should be warned about the side effects of the drug and physicians should be careful in the administration of the drug.- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
2/7. The pulmonary physician in critical care * illustrative case 4: neuromusculoskeletal disorders.The case history is presented of a patient admitted to the ICU with ventilatory insufficiency following thoracotomy for thymic resection. The role of non-invasive ventilation for weaning in patients following phrenic nerve injury is discussed.- - - - - - - - - - ranking = 4keywords = physician (Clic here for more details about this article) |
3/7. Clinical value of electrodiagnostic studies in neuromuscular disorders.EMG and conduction studies provide the physician with a precise means of defining the multiple diseases affecting the peripheral motor-sensory unit. These studies frequently provide clues that may be useful in arriving at the appropriate therapeutic decisions and in determining prognosis. Normal results may also support a suspected clinical diagnosis of inorganic illness, providing no evidence of central nervous system disease can be defined. Like any other test, however, results of EMG may be false-negative in bona fide neuromuscular disorders. This is particularly true early in a disease process; in neuropathies restricted primarily to small, unmyelinated nerve fibers; and in certain of the less virulent diseases of muscle and muscle energy metabolism.- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
4/7. Potentiation of magnesium-induced neuromuscular weakness by gentamicin.A term neonate with hypermagnesemia secondary to maternal administration of MgSO4 for pre-eclampsia had a respiratory arrest after receiving gentamicin im. The neuromuscular tracings and sequential physician exams done before and after administering gentamicin suggest aminoglycosides may potentiate a magnesium-induced impairment of neuromuscular transmission and cause muscular weakness in neonates.- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
5/7. emetine myopathy in a patient with an eating disorder.OBJECTIVE: To alert physicians to the dangers of a readily available, non-prescription drug by describing the clinical and pathological features of myopathy due to chronic poisoning with ipecac syrup in a patient with an eating disorder. CLINICAL FEATURES: A 27-year-old woman presented in 1991 with a right foot drop, followed a few months later by progressive severe neck and limb weakness associated with dysphagia, faecal incontinence and diffuse body ache. It emerged that she had been consuming increasing quantities of ipecac syrup (up to 200 mL per week) for three months to induce vomiting and weight loss. The serum creatine kinase activity was slightly elevated and electromyographic examination results were in keeping with a necrotising proximal myopathic process. Muscle biopsy showed vacuolar degeneration with myofibrilolysis and fine cytoplasmic body formation, consistent with a diagnosis of emetine myopathy. INTERVENTION AND OUTCOME: The patient was advised to stop taking ipecac and observed for the next few months. The symptoms resolved gradually and strength returned to normal in four months. CONCLUSION: Chronic emetine toxicity, with its potentially catastrophic consequences, should be remembered in the evaluation of neuromuscular symptoms in young women, in whom eating disorders are common and often unrecognised.- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
6/7. Approach to generalized weakness and peripheral neuromuscular disease.A large number of intellectually engaging and potentially serious neuromuscular diseases have been presented. The emergency medicine physician must be able to recognize those entities that have the potential to clinically deterioration. The evaluation of weakness requires a comprehensive, broad-based differential that is driven by the history and physical. Diagnostic testing is determined by the clinical suspicion as is the urgency for further work-up. The following are the final diagnoses of the eight illustrative cases that were presented at the beginning of this article. Case 1. This unfortunate woman had a metabolic myopathy that was only diagnosed after enzymatic analysis of a muscle biopsy. Her genetic defect, carnitine palmitoyltransferase deficiency, is unusual as it does not present until late in adolescence or slightly later in life. It is a defect in lipid metabolism in which long-chain fatty acids are unable to gain entrance into the mitochondrion for oxidative degradation. The defect is apparent only after prolonged exercise or fasting. In this patient, rhabddomyolysis led to acute renal failure that resolved without requiring temporary dialysis. Case 2. This patient had an elevated CPK-MM. Her EMG showed myopathic changes and her nerve conduction studies were normal. She had a positive test for antinuclear antibodies. A biopsy of her quadriceps muscle revealed lymphocytic infiltration of the muscle fibers that showed some focal myocyte degeneration. The diagnosis of dermatomyositis was made based on the findings noted previously and the heliotrope hue of her periorbital skin. A search for an occult neoplasm was negative. She responded moderately to a course of high-dose prednisone. Case 3. The laboratory test that confirmed this diagnosis was the potassium of 2.4 mEq/L. The remainder of the electrolytes were normal. Infusion of 20 mEq of potassium over 2 hours led to a prompt return of normal muscle strength. The final diagnosis was hypokalemic periodic paralysis. In this disease there is an inherited defect in the ability of the myocyte to maintain a normal transmembrane potential. The defect is latent until there is a precipitating factor, such as an high carbohydrate meal or prolonged immobility. There is also a form seen with thyrotoxicosis and is essentially cured when the patient becomes euthyroid. The disease is seen most frequently in Asian males, although it is reported in most ethnic groups. Prophylaxis in these patients is with acetazolamide which raises the serum potassium indirectly by causing a metabolic acidosis. triamterene and spironolactone have also been successfully used on occasion. This patient turned out to have thyrotoxicosis as well. Case 4. This man had both cranial motor and peripheral muscular dysfunction. There was no evidence of nonmotor cranial nerve dysfunction, nor was there evidence of any peripheral sensory deficits. The diagnosis of myasthenia gravis was established by the rapid and transient response of this patient to 2 mg of edrophonium. He was found to have antiacetylcholine receptor antibodies and was also thyrotoxic. He had a stormy course requiring intubation and prolonged ventilation. Eventually, he underwent thymectomy and is stable on pyridostigmine. Case 5. Initially suspected to be hysteria, this patient and his relatives had botulism from home-canned peppers. The index case required prolonged intubation and ventilation. The patients were treated with polyvalent antiserum and gastric lavage to remove the residual contaminated food which was still in their stomachs due to the gastric atony seen with this disease. The botulinus toxin prevents the release of acetylcholine molecules from their storage vesicles in nerve terminals. Thus, this disease is the opposite of the cholinergic syndrome seen with organophosphate insecticide poisonings except that cognitive functioning is not impaired in botulism. Case 6. This is a celebrated case that took a great deal of sleuthing- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |
7/7. Isolated venlafaxine-induced serotonin syndrome.serotonin syndrome is a potentially fatal complication of serotonergic drug therapy. Usually, serotonin syndrome occurs with the concomitant use of two serotonergic drugs; this case report describes a patient with a classic presentation of serotonin syndrome induced solely by a venlafaxine overdose. Emergency physicians need to be aware that the serotonin syndrome may occur not only with serotonergic drug combinations but also with overdoses of a single potent serotonergic agent such as venlafaxine.- - - - - - - - - - ranking = 1keywords = physician (Clic here for more details about this article) |