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We observed two cases of severe diabetic ketoacidosis with coma and shock. In one case, coma was present at admission and in the second occurred within 15 hours. In both cases, intracranial hypertension was confirmed with an extradural captor. These findings are in agreement with observations of brain oedema in diabetic ketoacidosis with coma. Clinical data suggest that brain oedema may occur after a latency period but that clinical expression is much more rare, perhaps favoured by treatment (excessive rehydratation, alkalinization, too sharp drop in blood glucose level). In our cases, despite major fluid infusion, shock persisted requiring norepinephrine. This shock could have been the expression of the severe ketoacidosis or have resulted from an underlying infection. In case of sudden onset coma, a regularly encountered manifestation of brain oedema, respiratory assistance and mannitol infusion must be instituted rapidly. With this type of management, it should be possible to improve the severe prognosis of brain oedema in diabetic ketoacidosis.

The index studied (simplified acute physiology score, or SAPS) is calculated from 14 measurable clinical and laboratory data obtained during the first 24 hours from admission. It was tested in a prospective study involving 280 consecutive patients treated in a 16-bed intensive care unit. Good correlations were found between SAPS and mortality rate and between SAPS and the two most widely used scoring systems: the Knaus index or APS (acute physiology score) and the Cullen index or TISS (therapeutic intervention scoring system), both evaluating therapeutic effectiveness. SAPS data being easy to collect, the simplified index could be used in many intensive care units or even applied to old case-records. Its main value lies in comparisons between two groups of patients with the same death probability and in evaluations of activities in intensive care units.

A broncho-alveolar lavage performed in a patient who developed pulmonary oedema a few hours after a caesarian section, produced foetal squamae which led to the diagnosis of amniotic fluid embolism.