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Two patients are reported in whom fatal alveolar pulmonary haemorrhage occurred after pulmonary embolectomy. Possible causes and methods of prevention are discussed.Pulmonary haemorrhage after embolic occlusion of a pulmonary artery usually follows the infarction of lung parenchyma. This complication is particularly prevalent in patients suffering from chronic congestive cardiac failure. The usual finding in such cases is obstruction of a segmental or smaller artery with infarction of the parenchyma supplied by it. The haemorrhage itself is usually slight and unimportant as regards eventual prognosis.Parenchymal bleeding following obstruction of the main branches of the pulmonary artery, without overt evidence of infarction, and severe enough to cause death at a time when the obstructing embolus has been removed, is a rare eventThe purpose of this communication is to describe two patients in whom fatal pulmonary haemorrhage occurred following the removal of the obstructing clot. This complication of pulmonary embolectomy is relevant, as several nonoperative methods of treating acute pulmonary embolism have recently been introduced. CASE HISTORIES CASE 1 Mrs. R. S., aged 55 years, had a right partial nephrectomy for renal calculus. There was no previous history of cardiac disease. On the fifth postoperative day thrombophlebitis occurred in the left leg. A few hours later chest pain, dyspnoea, and a fall in blood pressure occurred. Heparin therapy was started, but 22 hours later there was a further episode with dyspnoea, cyanosis, and hypotension. An electrocardiogram showed acute right heart strain ( Fig. 1). A pulmonary angiogram (Fig. 2) showed a complete blockage of the right main pulmonary artery and a further block in the artery to the left lower lobe.In view of continued deterioration despite routine medical treatment, emergency pulmonary embolectomy with cardiopulmonary bypass was carried out 34 hours after the initial embolus. A large coiled clot was removed from the right main pulmonary artery, and smaller fragments from the left lower lobar artery. The total time on full bypass was 20 mirnutes. While weaning off bypass there was a massive exudation of haemorrhagic pulmonary oedema fluid from the endoctracheal tube. This rapidly resembled pure blood and appeared to come from the right lung, which looked congested and infarcted. The left lung became flooded, despite attempts to exclude the right with a Carlen's tube. It proved impossible to oxygenate the arterial blood, and the patient died from cardiac arrest.Necropsy showed a healthy heart and coronary vessels. There was antemortem thrombus in the left femoral vein. Fluid blood was present in the right bronchial tree. The right lung was soft and haemorrhagic with antemortem thrombus in the smallest arteries, but the major pulmonary vessels were normal. Histological examination confirmed infarction of the parenchyma (Fig. 3). An incidental finding was a recent right adrenal haemorrhage (Fox, 1969). CASE 2 Mr. J. W., aged 53 years, had suffered from myelo...

When one considers the many types of chemical compound used in modern therapeutics, it is not surprising that some of these modify the action of muscle relaxants. In general such substances may interfere with neuromuscular transmission, or may influence relaxants by actions at other sites. Some such side effects are well known. Others, based on animal experiments on many different species and under varying conditions, are more difficult to assess precisely. Nevertheless, it would be unwise for the anaesthetist to ignore the possible risks they suggest. Although it is difficult to classify drugs accurately according to their pharmacological action at the neuromuscular junction, they may be grouped under the following headings. It must, however, be remembered that one drug may have several effects. (1) Drugs influencing the release or metabolism of acetylcholine. (2) Drugs altering the sensitivity of the motor endplate. (3) Drugs affecting the metabolism and excretion of muscle relaxants. DRUGS INFLUENCING THE RELEASE OR METABOLISM OF ACETYLCHOLINE Magnesium. Magnesium ions block the release of acetylcholine at the neuromuscular junction. They may also stabilize the endplate, making it resistant to the effects of acetylcholine. These actions, together with the accelerating action of magnesium ions on the action of the true cholinesterases (del Castillo and Engbaek, 1954), potentiate the actions of the antidepolarizing relaxants which in turn will also potentiate the action of magnesium. However, high enough concentrations of this ion are unlikely to be encountered except perhaps in the magnesium treatment of eclampsia. The neuromuscular block produced by magnesium is reversed by calcium ions.

Post-exposure nerve agent treatment usually includes administration of an oxime, which acts to restore function of the enzyme acetylcholinesterase (AChE). For immediate treatment of military personnel, this is usually administered with an autoinjector device, or devices containing the oxime such as pralidoxime, atropine and diazepam. In addition to the autoinjector, it is likely that personnel exposed to nerve agents, particularly by the percutaneous route, will require further treatment at medical facilities. As such, there is a need to understand the relationship between dose rate, plasma concentration, reactivation of AChE activity and efficacy, to provide supporting evidence for oxime infusions in nerve agent poisoning. Here, it has been demonstrated that intravenous infusion of HI-6, in combination with atropine, is efficacious against a percutaneous VX challenge in the conscious male Dunkin-Hartley guinea-pig. Inclusion of HI-6, in addition to atropine in the treatment, improved survival when compared to atropine alone. Additionally, erythrocyte AChE activity following poisoning was found to be dose dependent, with an increased dose rate of HI-6 (0.48mg/kg/min) resulting in increased AChE activity. As far as we are aware, this is the first study to correlate the pharmacokinetic profile of HI-6 with both its pharmacodynamic action of reactivating nerve agent inhibited AChE and with its efficacy against a persistent nerve agent exposure challenge in the same conscious animal.

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