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  1. Davey DG
    Br Med Bull, 1951;8:37-46.
    DOI: 10.1093/oxfordjournals.bmb.a074052
    Until the early thirties the chemotherapy of malaria was comparatively simple, even if unsatisfactory. Quinine, inherited from the seventeenth century, still held sway, and directions for its use were fairly straightforward, although the experts, of course, each had a particularly favoured way of using it A second drug, plasmoquine (pamaquin)1, heralded with an appropriate fanfare because it was the first synthetic drug for malaria, appeared in 1926, but in the early thirties it was still in an experimental stage, and in any event no one suggested that it would rival quinine or that it would have more than special uses ancillary to quinine. Then, in 1931, atebrin (mepacrine) was announced, and as research with it proceeded, particularly by Field and his colleagues in Malaya, it became clear that the role of quinine was being challenged. If war had not broken out in 1939 the outcome of the challenge would, perhaps, never have been properly known, for the Germans had pushed on from atebrin and developed resochin (chloroquine) and sontochin (sontoquine) both of which were receiving field trials when war came. © 1951, Oxford University Press. All rights reserved.
    Matched MeSH terms: Malaria/therapy
  2. WALLACE MF
    Med J Malaya, 1954 Mar;8(3):251-9.
    PMID: 13164695
    Matched MeSH terms: Malaria/therapy*
  3. FIELD JW, STRAHAN JH, EDESON JF, WILSON T
    Med J Malaya, 1954 Jun;8(4):303-17.
    PMID: 13193268
    Matched MeSH terms: Malaria/therapy*
  4. WILSON T, EDESON JF
    Med J Malaya, 1954 Dec;9(2):115-31.
    PMID: 14355275
    Matched MeSH terms: Malaria/therapy*
  5. EDESON JF, TURNER LH, LAING AB
    Med J Malaya, 1955 Jun;9(4):260-4.
    PMID: 13253125
    Matched MeSH terms: Malaria/therapy*
  6. EDESON JF, WILSON T, TURNER LH, LAING AB
    Med J Malaya, 1955 Jun;9(4):252-9.
    PMID: 13253124
    Matched MeSH terms: Malaria/therapy*
  7. Karnad DR, Nor MBM, Richards GA, Baker T, Amin P, Council of the World Federation of Societies of Intensive and Critical Care Medicine
    J Crit Care, 2018 Feb;43:356-360.
    PMID: 29132978 DOI: 10.1016/j.jcrc.2017.11.007
    Severe malaria is common in tropical countries in Africa, Asia, Oceania and South and Central America. It may also occur in travelers returning from endemic areas. Plasmodium falciparum accounts for most cases, although P vivax is increasingly found to cause severe malaria in Asia. Cerebral malaria is common in children in Africa, manifests as coma and seizures, and has a high morbidity and mortality. In other regions, adults may also develop cerebral malaria but neurological sequelae in survivors are rare. Acute kidney injury, liver dysfunction, thrombocytopenia, disseminated intravascular coagulopathy (DIC) and acute respiratory distress syndrome (ARDS) are also common in severe malaria. Metabolic abnormalities include hypoglycemia, hyponatremia and lactic acidosis. Bacterial infection may coexist in patients presenting with shock or ARDS and this along with a high parasite load has a high mortality. Intravenous artesunate has replaced quinine as the antimalarial agent of choice. Critical care management as per severe sepsis is also applicable to severe malaria. Aggressive fluid boluses may not be appropriate in children. Blood transfusions may be required and treatment of seizures and raised intracranial pressure is important in cerebral malaria in children. Mortality in severe disease ranges from 8 to 30% despite treatment.
    Matched MeSH terms: Malaria/therapy*
  8. Lau YL, Tan LH, Chin LC, Fong MY, Noraishah MA, Rohela M
    Emerg Infect Dis, 2011 Jul;17(7):1314-5.
    PMID: 21762601 DOI: 10.3201/eid1707.101295
    Matched MeSH terms: Malaria/therapy
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