CIRCULATORY FAILURE IN ACUTE INFECTIONS

In the circulatory failure which occurs in acute infections such as lobar pneumonia, two factors are at work : central, due to failure of the poisoned heart muscle, and peripheral, due to dilatation of the poisoned small vessels. Exhaustion of the adrenals, or their destruction by haemorrhage into their substance as in the Waterhouse-Friderichsen syndrome, plays an important role in the syndrome of toxasmic shock. This peripheral failure is generally more important than central (cardiac) failure. Even in diphtheria, many of the deaths are due to peripheral failure, though in some cases the specific action of the toxin on the heart causes sudden (cardiac) death, often many days after the subsidence of the acute infection.
Once circulatory failure has developed, the prospects of successful treatment are not good. It is then too late for efficient specific therapy, and measures calculated to stimulate the heart or the peripheral vessels are disappointing. The treatment of toxasmic circulatory failure lies in its prevention by early and adequate treatment of the causal infection. In diphtheria, for example, timely administration of antitoxin greatly reduces the incidence of dangerous circu¬latory failure. Similarly in pneumonia, early and efficient specific treatment with antibiotics lessens the risk of later intractable toxsemic effects. In diseases for which no specific treatment exists, or in which failure develops during a long illness, general measures to reduce toxasmia are employed to the best of our ability.
In view of the adrenal factor referred to above, there are logical grounds for using corticosteroids as replacement therapy despite the known disadvantage of their depressant action on the immunity responses of the body. In practice their use has been justified by the results, and hydrocortisone is probably our most potent weapon in combating toxasmic shock. Intramuscular hydrocor¬tisone, o-i to 0-2 g. daily should be given for its depot action, while for its speedy effect the w^ter-soluble hydrocortisone hemisuccinate should be given intravenously. The dosage should be 10 mg. per hour, best given as say i.o mg. added to a pint of dextran infusion fluid, given by drip. An appropriate anti¬biotic should be administered simultaneously in high dosage. While some apparently desperate cases of toxasmic shock in acute infections may be rescued by hydrocortisone, the results of treatment of peripheral failure late in the course of an infection are unsatisfactory. In fact, once such failure has developed,death is likely in spite of all therapy, unless the natural body processes succeed in overcoming the infection, as in the crisis phenomenon of lobar pneumonia. Of drugs which act on the heart, digitalis is the most widely employed : its use in pneumonia, for example, was once traditional, though its value is now discredited. The old controversy as to its value is hardly relevant in these days of efficient antibotics.
Many other drugs enjoyed a reputation as cardiac stimulants, and were widely used in conditions of toxasmic circulatory failure—strychnine and diffusible stimulants. It is now recognized that they have no direct cardiac action and that we do not possess any drug which can whip an exhausted or poisoned heart to renewed activity.