Coagulation activity and whole-blood viscosity were measured in the steady state, and serially during painful crisis, in eight patients with sickle-cell anaemia. Platelet and coagulation activation occurred in the steady state and became more pronounced early in crisis. Whole-blood viscosity increased during crisis in parallel with plasma fibrinogen. Similar changes were found in a parallel study of 20 patients with localized bacterial or viral infection who did not have sickle-cell anaemia. Reports of platelet activation, hypercoagulability, and hyperviscosity during painful crisis therefore reflect secondary changes arising from vascular stasis, precipitating infection, and an acute-phase protein reaction. Although secondary, these changes may contribute to vascular occlusion by an additive effect in vessels already partially occluded by sickled cells.

SYNOPSIS Plasma fibrinogen concentration and whole-blood viscosity, the latter measured at two shear rates (23 and 230 sec-1), were estimated during eight episodes of sickle-cell crisis and compared with values in 26 sickle-cell anaemia patients who were not in crisis. Painful crisis was associated with a significant increase in both plasma fibrinogen and whole-blood viscosity. Increased fibrinogen-erythrocyte interaction in vivo may be a significant contributory factor to raising blood viscosity and precipitating vaso-occlusive crisis in sickle-cell disease.The viscosity of whole blood is largely determined by the number of red cells (haematocrit) and by the deformability of individual red cells. Viscosity is also influenced by fibrinogen and other proteins which induce red-cell aggregation by protein-cell membrane interaction (Chien et al, 1967;Replogle et al, 1967;Rosenblum, 1969), and this is particularly important at low flow rates as in large veins, venules, and the microcirculation.The role of hyperfibrinogenaemia in vivo in increasing viscosity and leading to vaso-occlusive crisis in sickle-cell disease is not well defined although it has been suggested that the rise in fibrinogen during pregnancy and in acute infection may play a major role in precipitating crisis (Harris and Murphy, 1973). A study has therefore been made of plasma fibrinogen and whole-blood viscosity in children with sickle-cell disease to determine the changes which occur in vaso-occlusive crisis. Patients and methodsBlood was taken from 26 asymptomatic children (aged 3-16 years) attending a haematology outpatient clinic, of whom 18 had homozygous sicklecell anaemia (SS) and eight had sickle-cell/flthalassaemia. Blood specimens were also obtained from eight children (seven with SS) during admission for painful crisis. Routine bacteriological studies included blood, throat, and mid-stream urine cultures and the cytocentrifuge-NBT score Blood for viscosity studies was collected with minimal venous stasis into solid EDTA (1-8 mg/ml), with thorough mixing to avoid microclot formation, and measured within four hours of collection. Viscosity was measured using a Wells-Brookfield cone-plate microviscometer incorporating a 1-565°c one. Measurements were made at 37°C and at two shear rates corresponding to estimated physiological shear rates in veins and vessels of capillary diameter (23 sec-1) and large arteries (230 sec-1). Before viscosity measurements were made the blood was bubble oxygenated for 5 minutes and then mixed for 10 minutes on a roller-type blood mixer. When the temperature of the microviscometer sample-cup had reached 37°C, 0-8 ml of blood was introduced into the cup and the specimen was sheared at 23 sec-1 for 3 minutes to allow stabilization before a reading was taken. The sample was then sheared at the same rate for a further 2 minutes to give a second reading. The instrument was cleaned, a second 0-8 ml aliquot of the same blood sample was introduced, and a further two readings were taken at 23 sec-1. The value obtained f...

A serial study of coagulation activation and whole-blood viscosity was performed on 37 patients with local or systemic bacterial infection, malaria, or a viral infection. Thrombocytopenia, without consumption of coagulation factors, was the main feature of benign tertian malaria and viral infection, whereas in septicaemia and malignant tertian malaria it was associated with activation of coagulation and fibrinolysis. Patients with evidence of intravascular coagulation showed the highest levels of factor VIII related antigen which did not correlate with fibrinogen and probably reflected vascular endothelial cell damage rather than an acute-phase protein reaction. Hyperviscosity, which has been implicated in the pathogenesis of endotoxic shock and cerebral malaria, occurred in parallel with the acute-phase rise in plasma fibrinogen. There was, however, no evidence to implicate hyperviscosity as a major causative factor in the pathogenesis of septic shock or severe infective illness.

SYNOPSIS Accidental ingestion of sodium azide in 01I% solution by a patient and a laboratory technician in a haematological laboratory has demonstrated that very small quantities of sodium azide can give rise to toxic symptoms and that Isoton should be handled with care.

Equestrian accidents represent a significant proportion of HEMS missions. The majority of patients injured in equestrian accidents do not require HEMS intervention, however, a small proportion have life-threatening injuries, requiring immediate critical intervention. Further research is warranted, particularly regarding HEMS dispatch, to further improve accuracy of tasking to equestrian accidents.