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contributing factor to the poorer results, although we do not deny that other factors may have played a part.With these reservations the three principal conclusions may be restated in relation to extradural haematoma. (a) Delay in surgical evacuation of extradural haematomas leads to increased morbidity and mortality. Specifically it appears that delays exceeding two hours are unacceptable. (b) Direct admission of patients to neurosurgical beds from the accident and emergency unit decreased the delay time. The major delay time in the earlier period occurred in hospital and not before admission. (c) Direct admission of patients to neurosurgical beds in the later period was associated with a decline in morbidity and major mortality. That this decline was due to shorter delays is suggested by (b) but may have been contributed to by other factors.It therefore seems reasonable to conclude that direct admission of head-injured patients immediately to the primary care of the neurosurgical team is a good policy. It is, of course, possible only in cities where a neurosurgical department is immediately available and staffed to deal with head injuries in this way. Nevertheless, evacuating an extradural haematoma is not difficult, nor is diagnosing its presence and site if a history of the trend of events from injury, especially conscious level, is always obtained. A telephone consultation service round the clock must be available to district hospitals from the nearest neurosurgical department and backed up with a flying-squad service" to deal with the more complicated problems of surgical technique. Training district hospital and accident and emergency surgeons for three to six months in a head and spinal injuries service as part of a neurosurgical department at the senior house officer/ registrar level has been part of the organisation in Edinburgh for 10 years. Its value is in no doubt.The Kvarnes, T L, and Trumpy, J H, Acta Neurochirurgica, 1978, 41, 223. 7Jamieson, K G, and Yelland, J D N,3Journal of Neurosurgery, 1968, 29, 13. 8 Hooper, R, British Journal of Surgery, 1960, 47, 71. 9 Lewin, W, Proceedings of the Royal Society of Medicine, 1954, 47, 865. 10 Gallagher, J P, and Browder, E J, Journal of Neurosurgery, 1968, 29 Hyponatraemia and severity and outcome of myocardial infarction C T G FLEAR, P HILTON British MedicalJournal, 1979, 1, 1242-1246 Summary and conclusions A total of 235 consecutive patients admitted to a coronary care unit were investigated for serum electrolyte and urea concentrations; activities of aspartate aminotransferase, lactate dehydrogenase, and lactate dehydrogenase isoenzymes; electrocardiographic changes; clinical state; and outcome. Hyponatraemia, hypochloraemia, and uraemia were common in patients with confirmed myocardial infarctions, the degree of infarction correlating well with all the above indices of

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Summary: In experiments on 8 healthy young male volunteers, the ingestion of a large meal was found to cause plasma osmolality to rise from 288.8 + 0.8 (mean + s.e. mean) to 295.6 + 0.9 mmol/kg at 4 hours (P <0.001). There was an accompanying rise in plasma sodium (Na) from 141.9 + 0.8 to 144.6 + 0.8 mmol/l, also at 4 hours (P < 0.01), but little change in other plasma electrolytes. Serum total amino acids rose slightly, non-esterified fatty acid fell minimally and changes in blood glucose concentrations were unremarkable. Thirst was experienced at plasma osmolality of 294.8 + 0.7 mmol/kg. Repeating the experiment either without food, or with the salt content of the meal only, was without effect on plasma Na, other solutes or osmolality. Postprandial hypersomolality and hypernatraemia is probably due to movement of water from the vascular compartment to the gut, or into cells. Plasma osmolality is best measured in the fasting state. IntroductionIn health, plasma osmolality is tightly controlled by well-defined homeostatic mechanisms (Baylis 1983). We postulated, however, that absorption of solutes produced within the gastrointestinal tract after large meals, by digestion of food, might increase plasma osmolality. This paper reports our investigation of this hypothesis. Relative hyperosmolality after meals was confirmed, but it appeared to be due to net loss of water from the extracellular fluid (ECF), rather than the addition of absorbed exogenous 'osmoles' to the ECF.

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