Browsing by Author "Schoeman, J. F."

Now showing 1 - 4 of 4
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    Cerebral oedema with coning in diabetic keto-acidosis : report of 2 survivors
    (Health & Medical Publishing Group, 1991) Kalis, N. N.; Van der Merwe, P.-L.; Schoeman, J. F.; Smith, R. M. L.
    Two children presented with a first episode of diabetic keto-acidosis. Initially both patients made a good clinical and biochemical recovery, but suddenly developed neurological signs consistent with a diagnosis of tentorial herniation. Cranial computed tomography showed signs of cerebral oedema in both cases with evidence of uncal and tentorial herniation in 1 patient, which resolved after the appropriate treatment. The excellent neurological outcome emphasises the need for early recognition and treatment of sudden onset brain oedema in diabetic keto-acidosis.
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    Magnetic resonance imaging of the cerebral malformation in Miller-Dieker syndrome. A case report
    (Health & Medical Publishing Group, 1988-12) Smith, J.; Schoeman, J. F.; Booysen, J. T.
    Absent or defective cortical gyri (lissencephaly) combined with a characteristic phenotypic appearance was first reported by Miller and Dieker in 1963 and the clinical, computed tomographic and pathological features of this syndrome have been extensively reviewed. We report on magnetic resonance imaging of the brain in a sporadic case of this syndrome.
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    Practical management of therapeutic diphenylhydantoin concentrations in children
    (Health & Medical Publishing Group, 1999) Smit, A.; Schoeman, J. F.; Seifart, H. I.; Parkin, D. P.
    Objective. Development of easy, practical methods for the management and optimisation of therapeutic diphenylhydantoin (DPH) concentrations in children. Design: Investigation of DPH concentration profiles and pharmacokinetic parameters in children with poorly controlled epilepsy. Subsequent determination of individual-specific DPH maintenance dosage and volume of distribution data suitable for use in routine therapeutic concentration management procedures. Setting. Department of Paediatrics and Child Health and Department of Pharmacology, University of Stellenbosch, Tygerberg Hospital. Subjects. Children of both sexes between the ages of 4 and 12 years with poorly controlled epilepsy receiving DPH as sole medication. Results. In all subjects evaluated epilepsy was unsatisfactorily controlled because of inadequate DPH dosage regimens. Individual-specific maintenance dosage and volume of distribution data could be calculated for all individuals participating in the trial. The calculated data were suitable for use in routine management procedures and in no instance was it necessary to recalculate parameters in a 12-month follow-up period subsequent to evaluation. Conclusions. Therapeutic DPH concentration profiles can be managed satisfactorily in children if individual-specific DPH pharmacokinetic parameters are derived and skilfully applied.
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    The simultaneous determination of cerebrospinal fluid and plasma adenosine deaminase activity as a diagnostic aid in tuberculous meningitis
    (Health & Medical Publishing Group, 1986-04) Donald, P. R.; Malan, Christina; Van der Walt, Adri; Schoeman, J. F.
    The simultaneous determination of cerebrospinal fluid (CSF) and plasma adenosine deaminase (ADA) activity was evaluated as a diagnostic aid in tuberculous meningitis (TBM). CSF and plasma ADA activity were determined in four groups of patients: (i) a 'no meningitis' group of 174 children investigated for possible meningitis, but found to be uninfected; (ii) an aseptic meningitis group of 40 children; (iii) a bacterial meningitis group of 31 children; and (iv) a TBM group of 27 patients (24 children and 3 adults). CSF ADA alone was determined in a further 23 children with aseptic meningitis, 19 with bacterial meningitis and 13 children and 7 adults with TBM. Both the CSF/plasma ADA ratio and the absolute CSF ADA activity were raised in TBM (mean values 0.24 and 12.61 U/l respectively) and bacterial meningitis (mean values 0.59 and 15.43 U/l respectively), but not in the aseptic meningitis group (mean values 0.06 and 2.00 U/l) or the 'no meningitis' group (mean values 0.04 and 1.51 U/l). Both values will distinguish TBM from aseptic meningitis, but do not appear to hold any marked advantages over conventional CSF criteria in the diagnosis of TBM.