641

measured

by a spectrophotometer 1100b (Perkin-Elmer). Red cell magnesium content was calculated as previously described.2 Magnesium values were:

Magnesium concentration (SD) in mmol/I The values did not differ between patients and controls. There is no general agreement about the best method to assess intracellular magnesium statusbut the most practical and common method is the measurement of serum and red cell concentration atomic by magnesium absorption spectrophotometry. Our results show that intracellular magnesium is much the same in patients and controls. In our patients the assessment of red cell magnesium did not help in CFS diagnosis, and its supplementation is therefore not necessary. The discrepancy between our results and those of Cox et al may be related to the different dietary habits in Mediterranean countries and in northern

Europe. R. DEULOFEU Service of Clinical Biochemistry, and Section of Tropical Medicine, Hospital Clínic i Provincial de Barcelona, 08036 Barcelona, Spain

Opening

pressures at lumbar puncture in children with cerebral malaria.

0, pooled data from The Gambia (1990) and Malaw’ (provided by Dr D Kwiatkowski and Dr M Molyneux) and The Gambia (1989)’ and Thailand Mean and 95% CI are compared with the recent series from Kenya (8).2 intracranial pressure2 are present for long periods in the acute phase of the disease. Many deaths from cerebral malaria take place within hours of admission to hospital. Inevitably, some deaths will follow shortly after a diagnostic LP by chance. To ascribe a cause of death in children who die from cerebral malaria is often difficult, but we have never been convinced that any patient deteriorated or died from coning as a result of LP. We will continue to do lumbar punctures on admission in all patients with suspected cerebral malaria. Wellcome-Mahidol University, Oxford Tropical Medicine Research Bangkok 10400, Thailand

Programme,

N. J. WHITE

1. Warrell DA, Looareesuwan S, Phillips RE, et al. Function of the blood-CSF barrier m human cerebral malaria: rejection of the permeability hypothesis. Am J Trop Med Hyg 1986; 35: 882-89. 2. Newton CRJC, Kirkham FJ, Winstanley PA, et al. Intracranial pressure in African children with cerebral malaria. Lancet 1991; 337: 573-76. 3. Waller D, Crawley J, Nosten F, et al. Intracranial pressure in childhood cerebral malari. Trans R Soc Trop Med Hyg 1991; 85: 362-64. 4. Kwiatkowski D, Molyneux M, Taylor T, Klein N, Curtis N, Smit M. Cerebral malaria. Lancet 1991, 337: 1281-82. 5. Goitein KJ, Amit Y, Musffi H. Intracranial pressure in central nervous system infections and cerebral ischaemia of infancy. Arch Dis Child 1983; 58: 184-86. 6 Williams CPS, Swanson AG, Chapman JT. Brain swelling with acute purulent meningitis. Pediatrics 1964, 55: 220-27.

Magnesium and chronic fatigue syndrome SiR,—Mr Cox and his colleagues (March 30, p 757) propose that magnesium deficiency could be a possible factor in symptoms and diagnosis of chronic fatigue syndrome (CFS). Magnesium supplements might therefore be beneficial in such patients. We have investigated basal thiacetazone concentrations before magnesium supplementation in 18 patients. The patients were diagnosed as having CFS according to Centers for Disease Control case definition.1 We evaluated plasma, serum, whole blood, and red cell magnesium in these patients and in 18 controls matched for age, sex, and socioeconomic status. Mean age of the 18 patients (4 males, 14 females) was 32 (SD 8-5) years. The controls were healthy volunteers from the hospital staff (4 males, 14 females) (mean age 31 [7’7] years). Magnesium concentration was

J. GASCON N. GIMÉNEZ M. CORACHAN

1. Holmes GP, Kaplan JE, Gantz NM, et al. Chronic fatigue syndrome: a working case definition. Ann Intern Med 1988; 108: 387-89. 2. Abraham GE, Michael MD, Lubran M. Serum and red cell magnesium levels in patients with premenstrual tension. Am J Clin Nutr 1981; 34: 2364-66. 3. Elin RJ. Assessment of magnesium status. Clin Chem 1987; 33: 1965-70.

Use of ketorolac in sickle-cell disease and vaso-occlusive crisis SiR,—The use of narcotics in sickle-cell disease for treatment of vaso-occlusive crisis is a double-edged sword, offering both analgesia and respiratory depression. I report the use of ketorolac in a patient with painful crisis and without deleterious side-effects. A 22-year-old black woman with mild haemoglobin sickle-cell disease and asthma presented with a two-week history of urinary tract infection, a one-day history of fever, and pleuritic right chest pain. She had been admitted for vaso-occlusive crisis at age 12 and underwent cholecystectomy two years earlier. On admission, her temperature was slightly raised. Oxygen saturation was 99-100% on room air. She had crackles at the right posteriorly, without wheezing or aegophony, and leucocytosis. Chest radiography revealed a right middle-lobe consolidation. The patient was admitted with a diagnosis of pneumonia and given ampicillin and sulbactam. Two days later, wheezing developed. Erythromycin, aminophylline, and methylprednisolone were added to her regimen. The next day she had bilateral leg pain and right shoulder pain requiring intravenous narcotics. Creatine phosphokinases were normal and viral cultures for influenza A were negative. The pain continued to be quite severe, requiring intravenous hydromorphone. Over the following four days, moderate abdominal distension developed with tympany, and she complained of constipation since the initiation of narcotic therapy. Abdominal distension and constipation worsened despite multiple interventions, leading to poor respiratory effort. A new left lower lobe infiltrate developed and supplemental oxygen was needed. At this time, narcotic therapy was discontinued and the patient was begun on intravenous ketorolac for pain relief. Her pain was well controlled. Two days later, with the continued help of normal saline enemas, she began to defaecate and to walk again. Her respiratory distress progressively decreased. She was discharged one week later on oral antibiotics. The use of narcotics for pain control in this patient contributed substantially to her morbidity and certainly lengthened her hospital stay. Narcotic use has been associated with constipation, which can itself lead to hypoventilation and respiratory compromise. These conditions, in turn, can increase intrapulmonary sickling and lead to the development of acute chest syndrome.1-3 Narcotics also have addictive potential. Whether this patient had acute chest

Magnesium and chronic fatigue syndrome.

641 measured by a spectrophotometer 1100b (Perkin-Elmer). Red cell magnesium content was calculated as previously described.2 Magnesium values were:...
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