Cases reported "Myoglobinuria"

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1/4. Malignant hyperpyrexia and Duchenne muscular dystrophy: A case report.

    We report a patient with Duchenne muscular dystrophy who developed malignant hyperpyrexia during general anaesthesia. During anaesthesia bradycardia was followed by ventricular fibrillation, on which ventricular flutter supervened and a body temperature rise of 0.6 degrees C for 15 minutes, myoglobinuria and elevation of CPK level were observed. The caffeine sensitivity test of biopsied muscle fibers revealed an increase in sensitivity, although there was no sign of muscle rigidity during or after anaesthesia. diagnosis of Duchenne muscular dystrophy was first established after the development of malignant hyperpyrexia in the present case as well as in previously reported cases. Determination of serum CPK is very important before general anaesthesia.
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2/4. strabismus as a possible sign of subclinical muscular dystrophy predisposing to rhabdomyolysis and myoglobinuria: a study of an affected family.

    Administration of succinylcholine to normal individuals results in alterations in muscle membrane integrity expressed as a slight increase in the concentrations of creatine phosphokinase (CK) in serum and appearance of small amounts of myoglobin in the urine, but without clinical symptoms. Subjects with strabismus due to congenital muscular dystrophy may develop more significant rhabdomyolysis expressed as muscle stiffness and weakness, massive myoglobinuria, marked elevation of serum CK and other enzymes, metabolic acidosis, tachycardia and moderate elevation of body temperature. In some cases grave malignant hyperthermia with significant hypoxia, metabolic acidosis, tachycardia and marked abnormalities in serum electrolyte concentrations may cause irreversible damage to the central nervous system and other vital organs and death. A case of difficult anaesthesia for a six year old boy belonging to family affected with muscular dystrophy is presented. More attention must be given to preoperative examination (anamnesis, serum enzymes) or ophthalmological patients and more careful monitoring during anaesthesia and in the early postoperative period must be instituted to prevent and treat complications induced by succinylcholine and volatile anaesthetic agents.
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keywords = anaesthesia
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3/4. myoglobinuria following the use of succinylcholine.

    Eight hours following tympanoplasty performed under general anaesthesia (sodium pentothal and trichloroethylene), a 30 year old male complained of muscular weakness and dark coloured urine. urinalysis revealed myoglobin pigment. A rise in BUN (47mg%), serum creatinine (5.7mg%), creatinine phosphokinase (15,500 U/L) and CPK-MB fraction (4690 U/L) was noticed 36 hrs later. The patient developed acute renal failure, and recovered after haemodialysis. From a history of use of succinylcholine as a muscle relaxant during operation, myoglobinuria appears to be secondary to muscle damage caused by succinylcholine.
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keywords = anaesthesia
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4/4. succinylcholine-induced cardiac arrest in children with undiagnosed myopathy.

    Two paediatric cases are reported in which unexpected, life-threatening arrhythmias occurred. Routine induction of general anaesthesia with thiopentone, 5 mg.kg-1, in one and with halothane in the other, and succinylcholine 1.25-1.5 mg.kg-1 i.v. was followed by the development of wide complex tachyarrhythmia with hypotension in the first case and asystole in the second case despite pre-treatment with atropine in both cases. The first patient was resuscitated with tracheal intubation, 100% oxygen, manual ventilation and intravenous lidocaine and bicarbonate. The second patient required intubation, manual ventilation, 12 min of CPR and i.v. calcium, epinephrine and bicarbonate, as well as DC counter shock. Neither patient received dantrolene. Early recovery in both patients was uneventful with no neurological sequelae. Subsequent investigations revealed the presence of a dystrophin-deficient muscular dystrophy, duchenne muscular dystrophy and Becker muscular dystrophy respectively, previously unsuspected, in both patients. The aetiology of the observed arrhythmias was presumably hyperkalaemia, secondary to succinylcholine-induced rhabdomyolysis. It is suggested that when faced with sudden, life-threatening arrhythmias following succinylcholine at induction of anaesthesia for paediatric patients, clinicians should include occult myopathy in the differential diagnosis, and thus consider the aggressive management of hyperkalaemia in addition to basic resuscitative efforts.
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