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Real-time B-mode ultrasonography was combined with a pulsed Doppler ultrasound technique for transcutaneous measurement of human fetal blood flow in the aorta and intra-abdominal part of the umbilical vein. The target vessel was located and its diameter measured in the two-dimensional real-time image. The pulsed Doppler transducer was attached to the real-time transducer at a fixed angle. By processing the Doppler shift signals the instrument estimated the mean and maximum blood velocities and the integral under the velocity curves. This permitted calculation of the blood flow. The method was applied to 26 fetuses in normal late pregnancies. Mean blood flow in the descending part of the fetal aorta based on maximum velocity was 191 ml/kg/min. Mean flow in the intra-abdominal part of the umbilical vein was 110 ml/kg/min. This method of measurement is non-invasive and opens new perspectives in studying fetal haemodynamics.

Treatment of hypertension with beta-blocking agents in three patients with moderately severe chronic renal failure was followed by rapid deterioration of renal function. In two of the patients the need for maintenance haemodialysis was accelerated but renal function in the third reverted to pretreatment levels after the drug was stopped. These findings suggest that until more is known about the effects of beta-blocking drugs they should not be given to patients with moderately severe renal failure.

The 14C-aminopyrine (14C-amidopyrine) breath test, carried out within 24-36 hours of an overdosage of paracetamol, was used to predict the extent of liver damage in 30 seriously poisoned patients. Mean 14CO2 excretion was 4.4% in 20 healthy control subjects; 5.5% in six patients who escaped injury; and 2.9%, 1.5%, and 0.2% in those with mild to moderate (12 patients), severe (eight patients), and fatal (four patients) liver damage respectively. This test proved to be a more reliable predictor of the extent of liver damage than plasma paracetamol concentration or half life or the results of conventional liver function tests and may enable treatment of hepatic failure to be started at an early stage.

Of 41 cases of acute paracetamol poisoning one died of gastrointestinal haemorrhage and acute massive necrosis of the liver, three became jaundiced, and 13 others had biochemical evidence of hepatocellular damage. Liver damage is a toxic effect which is present in most patients who ingest more than 15 g. of paracetamol. One patient with liver damage survived renal failure due to acute tubular necrosis. It is suggested that the renal lesion was also the result of paracetamol overdosage.Profound hypoglycaemia and metabolic acidosis may also complicate severe poisoning. Plasma levels of para-aminophenol fall rapidly, and procedures currently used to enhance the elimination of the drug cannot be expected to prevent development of hepatic damage.

Prolonged coma due to acute overdosage with hypnotic drugs is shown to be associated with a pronounced increase in the activity of serum creatine kinase and in the concentration of fibrin degradation products and with less pronounced abnormalities of other serum enzymes and of other indices of coagulation and fibrinolysis. Evidence is presented that skeletal muscle damage occurs and that this is related to the coagulation abnormality. These findings probably explain some of the non-specific features such as fever which commonly occur in recovery from severe poisoning.

In 27 patients nitrazepam (Mogadon) taken in acute overdosage produced no untoward effects except drowsiness, even when 80 tablets were consumed. A double-blind trial in patients in general medical wards established that nitrazepam was as effective as butobarbitone as a hypnotic. It is concluded that nitrazepam is a safe and effective hypnotic.