640
Nelson showed that an antagonist of folic acid produced malformations in the fetus.1 These were preventable by adding folic acid to the diet. In 1960 J. B. Thiersch showed that the administration of a metabolic antagonist of folic acid (aminopterin) to pregnant women was followed by the birth of deformed infants. You ask, "Are there any risks in folic acid supplementation, and if so, are they the same as the two folic acid dosages" (4 mg and 0.36 mg). The risks of vitamin supplementation at the lower dose are imaginary. Risks come from deficiencies of vitamins, not from supplying them in quantities that are in normal diets. Everyone is entitled to receive the required amounts of vitamins daily. It makes sense to supplement the diet with a daily allowance of folic acid,
such as the US recommended dietary allowance of 0-4 mg. We do withold vitamin D from children to see whether rickets will develop. Yet some seem to feel, illogically, that vitamins should be prescribed only in the case of nutritional deficiencies. The MRC Vitamin Study group’s recommendation on folic acid in the diet "of all women who may bear children" is excellent-and about 40 years overdue. not
Erythrocyte folate
in fetal blood.
. fetuses with NTD (n = 17). A =fetuses without NTD (n=45).
Department of Integrative Biology, University of California, Berkeley, Oakland, California 94608, USA
later in pregnancy for reasons such as determination of the lecithin/sphingomyelin ratio. The folate concentrations of the pregnant women with affected fetuses were all normal2 (218-3 [SD 115-2] ng/ml) and nutritional status assessed independently did not differ between the groups. By the one-tailed t test we could not find a significant difference in serum or in erythrocyte folate concentrations between the NTD and control groups of fetuses, and the figure shows data for erythrocyte folate. Ferritin and vitamin B12 measured as controls, did not differ between either group. Serum and erythrocyte folate values were in general much higher in the fetuses than in the mothers, suggesting a high demand for this vitamin in the growing fetus. Even though NTD originate earlier in gestation, we chose to study folate concentrations at various gestational ages immediately after the first sonographic diagnosis of anencephaly or spina bifida because enzymic or placental transfer differences should be unchanged throughout gestation and also because nutritional behaviour is fairly constant.3 Our finding of no relation between NTD and low folate values in fetal blood does not contradict the MRC trial results but shows that an easy explanation for the protective effect of folic acid cannot be provided yet and that further research to define the role of micronutrients in the development of NTD is required. Zentrum fur Frauenheilkunde, Westf Wilhelms-Universitat, D-4400 Munster, Germany
WOLFGANG HOLZGREVE SEVGI TERCANLI
Institut fur Ernahrungswissenschaft, Rheinische Friedrich-Wilhelms-Universitat Bonn
KLAUS PIETRZIK
1. Waxman
S, Schreiber C, Herbert V. Radioisotopic assay for measurement of serum Blood 1971; 38: 219-28 2. Bailey LB, Mahan CS, Dimperio D. Folacin and iron status m low-income pregnant adolescents and mature women. Am J Clin Nutr 1980, 33: 1997-2001. 3. Molloy AM, Kirke P, Hillary I, Weir DG, Scott JM. Maternal serum folate and vitamin B12 concentrations in pregnancies associated with neural tube defects. Arch folate
status.
Dis Child 1985; 60: 660-65.
SIR,-Your July 20 editorial stimulates some further comments the history of folic acid deficiency. In 1931 Lucy Wills reported in the British Medical Journal that pregnant women in India on a diet largely of wheat had "tropical macrocytic anaemia" that could on
be
effectively
treated with yeast extract; this
was
shown later
to
supply folic acid. She also found that the antipemicious-anaemia factor of concentrated liver extracts, subsequently identified as vitamin Blz, was ineffective. Wills did not record the occurrences of birth defects, only the responses in her patients to their treatment in pregnancy. Folic acid was found to prevent hydrocephalus by A. G. Hogan and colleagues, in studies with rats, published in Proc Soc Exp Biol Med (1950). A series of experiments on rats by Marjorie
1. Nelson MM. In: Rhoads AAAS, 1955: 107-28.
CP, ed. Antimetabolites and
THOMAS H. JUKES cancer.
Washington, DC:
Lumbar puncture in cerebral malaria SiR,—The upper limit of normal for cerebrospinal fluid (CSF) pressure at lumbar puncture (LP) is lower in infants (< 80 mm CSF) and children (< 90 mm CSF) than in adults (< 210 mm). In adults with cerebral malaria, opening pressures at LP are usually (80% of the time) within the normal range.’ By contrast, recent studies have shown that LP opening pressures in children with cerebral malaria are usually raised.2-4 In the Kenyan study,2opening pressures were strikingly increased, especially in fatal cases. Mean (95% CI) pressures were 281 (209-353) mm CSF in children who subsequently died (n = 5), compared with 213 (183-243) mm CSF in those who survived
(n = 21). Raised intracranial
pressure and
to be responsible for the observed
coning thought signs, brainstem compression, were
neurological
and death. The Kenyan workers now believe that the risks of immediate LP in young children with cerebral malaria outweigh the diagnostic benefit. They delay diagnostic LP in suspected cerebral malaria while giving empirical antibiotic treatment to cover the possibility of coincident
meningitis. My colleagues and I have studied childhood cerebral malaria prospectively in The Gambiaand in Thailand (Dr F. Nosten and Dr F. ter Kuile, personal communication). We can confirm that LP opening pressures are usually increased, but not to the same extent as reported from Kenya and, as in more recent studies from The Gambia and Malawithere were no significant differences between survivors and fatal cases. The results of these four studies were similar and pooled data are shown in the figure. The mean (95 % CI) opening pressure was 60 (24-96) mm CSF lower in survivors (n 70) and 126 (43-209) mm CSF lower in fatal cases (n 26) than in the Kenyan studies (p < 0’001). Systemic arterial blood pressures were similar in all these series, and therefore the estimates of cerebral perfusion pressure (mean arterial pressure minus opening pressure) were significantly lower in the Kenyan series: mean (SD) 53 (14) mm Hg compared with 69 (17) mm Hg (p < 0001). Mortality among children with viral and bacterial infections of the central nervous system (CNS) seems to correlate with the degree of increased intracranial pressure,s,6 but in these infections LP opening pressures are much higher, and cerebral perfusion pressures lower, than in children with cerebral malariaIntracranial pressure fluctuates in CNS infections and opening pressures at LP do not reliably predict maximum intracranial pressures measured directly by subdural and intraventricular catheters or pressure transducers. Nevertheless, if raised intracranial pressure is an important cause of death in childhood cerebral malaria, as has been suggested, it is surprising that opening pressures are no higher in fatal cases than in survivors, especially since the neurological signs attributed to raised =
=
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
Nelson showed that an antagonist of folic acid produced malformations in the fetus.1 These were preventable by adding folic acid to the diet. In 1960 J. B. Thiersch showed that the administration of a metabolic antagonist of folic acid (aminopterin) to pregnant women was followed by the birth of deformed infants. You ask, "Are there any risks in folic acid supplementation, and if so, are they the same as the two folic acid dosages" (4 mg and 0.36 mg). The risks of vitamin supplementation at the lower dose are imaginary. Risks come from deficiencies of vitamins, not from supplying them in quantities that are in normal diets. Everyone is entitled to receive the required amounts of vitamins daily. It makes sense to supplement the diet with a daily allowance of folic acid,
such as the US recommended dietary allowance of 0-4 mg. We do withold vitamin D from children to see whether rickets will develop. Yet some seem to feel, illogically, that vitamins should be prescribed only in the case of nutritional deficiencies. The MRC Vitamin Study group’s recommendation on folic acid in the diet "of all women who may bear children" is excellent-and about 40 years overdue. not
Erythrocyte folate
in fetal blood.
. fetuses with NTD (n = 17). A =fetuses without NTD (n=45).
Department of Integrative Biology, University of California, Berkeley, Oakland, California 94608, USA
later in pregnancy for reasons such as determination of the lecithin/sphingomyelin ratio. The folate concentrations of the pregnant women with affected fetuses were all normal2 (218-3 [SD 115-2] ng/ml) and nutritional status assessed independently did not differ between the groups. By the one-tailed t test we could not find a significant difference in serum or in erythrocyte folate concentrations between the NTD and control groups of fetuses, and the figure shows data for erythrocyte folate. Ferritin and vitamin B12 measured as controls, did not differ between either group. Serum and erythrocyte folate values were in general much higher in the fetuses than in the mothers, suggesting a high demand for this vitamin in the growing fetus. Even though NTD originate earlier in gestation, we chose to study folate concentrations at various gestational ages immediately after the first sonographic diagnosis of anencephaly or spina bifida because enzymic or placental transfer differences should be unchanged throughout gestation and also because nutritional behaviour is fairly constant.3 Our finding of no relation between NTD and low folate values in fetal blood does not contradict the MRC trial results but shows that an easy explanation for the protective effect of folic acid cannot be provided yet and that further research to define the role of micronutrients in the development of NTD is required. Zentrum fur Frauenheilkunde, Westf Wilhelms-Universitat, D-4400 Munster, Germany
WOLFGANG HOLZGREVE SEVGI TERCANLI
Institut fur Ernahrungswissenschaft, Rheinische Friedrich-Wilhelms-Universitat Bonn
KLAUS PIETRZIK
1. Waxman
S, Schreiber C, Herbert V. Radioisotopic assay for measurement of serum Blood 1971; 38: 219-28 2. Bailey LB, Mahan CS, Dimperio D. Folacin and iron status m low-income pregnant adolescents and mature women. Am J Clin Nutr 1980, 33: 1997-2001. 3. Molloy AM, Kirke P, Hillary I, Weir DG, Scott JM. Maternal serum folate and vitamin B12 concentrations in pregnancies associated with neural tube defects. Arch folate
status.
Dis Child 1985; 60: 660-65.
SIR,-Your July 20 editorial stimulates some further comments the history of folic acid deficiency. In 1931 Lucy Wills reported in the British Medical Journal that pregnant women in India on a diet largely of wheat had "tropical macrocytic anaemia" that could on
be
effectively
treated with yeast extract; this
was
shown later
to
supply folic acid. She also found that the antipemicious-anaemia factor of concentrated liver extracts, subsequently identified as vitamin Blz, was ineffective. Wills did not record the occurrences of birth defects, only the responses in her patients to their treatment in pregnancy. Folic acid was found to prevent hydrocephalus by A. G. Hogan and colleagues, in studies with rats, published in Proc Soc Exp Biol Med (1950). A series of experiments on rats by Marjorie
1. Nelson MM. In: Rhoads AAAS, 1955: 107-28.
CP, ed. Antimetabolites and
THOMAS H. JUKES cancer.
Washington, DC:
Lumbar puncture in cerebral malaria SiR,—The upper limit of normal for cerebrospinal fluid (CSF) pressure at lumbar puncture (LP) is lower in infants (< 80 mm CSF) and children (< 90 mm CSF) than in adults (< 210 mm). In adults with cerebral malaria, opening pressures at LP are usually (80% of the time) within the normal range.’ By contrast, recent studies have shown that LP opening pressures in children with cerebral malaria are usually raised.2-4 In the Kenyan study,2opening pressures were strikingly increased, especially in fatal cases. Mean (95% CI) pressures were 281 (209-353) mm CSF in children who subsequently died (n = 5), compared with 213 (183-243) mm CSF in those who survived
(n = 21). Raised intracranial
pressure and
to be responsible for the observed
coning thought signs, brainstem compression, were
neurological
and death. The Kenyan workers now believe that the risks of immediate LP in young children with cerebral malaria outweigh the diagnostic benefit. They delay diagnostic LP in suspected cerebral malaria while giving empirical antibiotic treatment to cover the possibility of coincident
meningitis. My colleagues and I have studied childhood cerebral malaria prospectively in The Gambiaand in Thailand (Dr F. Nosten and Dr F. ter Kuile, personal communication). We can confirm that LP opening pressures are usually increased, but not to the same extent as reported from Kenya and, as in more recent studies from The Gambia and Malawithere were no significant differences between survivors and fatal cases. The results of these four studies were similar and pooled data are shown in the figure. The mean (95 % CI) opening pressure was 60 (24-96) mm CSF lower in survivors (n 70) and 126 (43-209) mm CSF lower in fatal cases (n 26) than in the Kenyan studies (p < 0’001). Systemic arterial blood pressures were similar in all these series, and therefore the estimates of cerebral perfusion pressure (mean arterial pressure minus opening pressure) were significantly lower in the Kenyan series: mean (SD) 53 (14) mm Hg compared with 69 (17) mm Hg (p < 0001). Mortality among children with viral and bacterial infections of the central nervous system (CNS) seems to correlate with the degree of increased intracranial pressure,s,6 but in these infections LP opening pressures are much higher, and cerebral perfusion pressures lower, than in children with cerebral malariaIntracranial pressure fluctuates in CNS infections and opening pressures at LP do not reliably predict maximum intracranial pressures measured directly by subdural and intraventricular catheters or pressure transducers. Nevertheless, if raised intracranial pressure is an important cause of death in childhood cerebral malaria, as has been suggested, it is surprising that opening pressures are no higher in fatal cases than in survivors, especially since the neurological signs attributed to raised =
=
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
