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Tropical Conditions with Special Reference to an Immigrant Population

peculiarity, believing that his work on coronary thrombosis would be more enduring. Sickling occurs in the presence of reduced oxygen tension and in vitro a solution of Hb S becomes a semisolid gel in such an atmosphere and it is presumed that this phenomenon produces distortion of the red cell. Hb S is widespread, being found throughout tropical Africa, in America and the Far East. The gene is perpetuated because of its tendency to afford some protection from the more severe attacks of malignant falciparal malaria. Increased breakdown of erythrocytes may lead to formation of gall-stones and erythropoiesis to hepatosplenomegaly, although in the homozygous disease recurrent infarction results in a small spleen. The presence of a large spleen in the older child or adult generally indicates a sickle heterozygote, e.g. Hb SC or Hb-thalassiemia. Cardiomegaly is present in about 80% of children with homozygous sickle cell disease from about 6 months of age. Possible causes are haemolytic anemia, obliterative pulmonary vascular disease and ischemic heart disease. Young children from late in the first year of age often present with the painful, swollen digits of sickle cell dactylitis (the 'hand-foot syndrome') resulting from bone infarction (Watson et al. 1963). The erythroid hyperplasia being less than in thalassimia, there is lesser widening of the diploe and the 'hair on end' appearance is extremely rare. Vascular obstruction may produce renal papillary necrosis in both the trait and the disease. Infarction of the femoral head is found about 5 times more often in Hb SC disease than in homozygous (SS) sickle cell disease (Chung & Ralston 1969), whilst in the trait it is exceptional. Bone infarction affects multiple bones and some radiographic change in the spine is common. Alteration of vertebral body shape is of three types: biconcave, as in thalasszemia; anterior wedging rarely; and the classical, squared depression of the centre of the vertebral end-plate (Fig 2) which, when present, usually indicates sickle-cell disease, although it has been described in thalassemia (Cassady et al. 1967). Reynolds (1966) has suggested that it is due to obstruction of the main arterial supply to this region, and that the less common, but analogous, appearance seen in the hands has the same mechanism of production (Fig 3). I believe that the dense plate in the floor of the depression represents a growth arrest line. Osteomyelitis in sickle-cell disease is several hundred times as common as in the normal subject in the first two years of life. In Africa, it is predominantly due to salmonella infection, and probably results from microinfarcts of the bowel wall leading to bacterxmia. Clinical and radiological differentiation between a massive bone infarct and osteomyelitis is often difficult. In 1950, Wigh & Thompson reported linear lucencies in the bone cortex in salmonella osteomyelitis, but the value of the observation is limited as they are not often seen and may take 4-5 weeks to appear. As radiologists, we may have the opportunity to be the first to suggest the diagnosis of sicklecell disease, and by so doing may protect the patient from conditions that would lead to increased morbidity, if not to death.