DIPHTHERITIC HEART FAILURE The fatalities in diphtheria are always more or less dependent. on toxic changes in the heart, some cases being pure instances of heart failure, such an event occurring either in the a-cute stage or in conva lescence, suddenly and unexpectedly, or slowly with typical signs. The ultimate cause is still the subject of much controversy. Apparently well grounded and hard to refute is the theory of Eppinger, of a separa tion of the fibrils of the heart muscle from their sheath,—a myolysis from toxic oedema.
Because of the reduced strength of the heart, thrombosis and con secutive embolism may occur, immediately preceding and hastening death.
Heart failure in the acute stage is seen only in the severest form of diphtheria. It may occur without any warning or there may be pre monitory symptoms of failing circulation in progressive weakness of the pulse, coldness of the extremities, cadaveric pallor with a cyanotic tint, swelling of the liver and dilatation of the heart.
Death in convalescence may likewise he sudden and unexpected or be heralded by the typical symptoms. It may occur not only after attacks of severe diphtheria apparently running a favorable course hut also occasionally in relatively mild attacks. The patients may feel well and have good appetites, looking bright, improving in color and gaining strength. Then following on some slight bodily exertion, like gutting out of bed, having a movement of the bowels, or eating a hearty meal, this catastrophe occurs. With great pallor and involuntary dis charge of stools and urine, the patients sink back quietly, but some times with several cries and complaints of pain referred to the abdomen (embolism of the abdominal aorta, Muffin).
In other cases, especially in older children, the heart failure occurs with prodromes of greater or less duration: the pulse becomes small, compressible, irregular, rapid, with periods of marked slowness espe cially shortly before death. The area of cardiac dulness is increased to the right, and at times to the left, the apex-beat is weak and the sounds are feeble, the first being impure or even rough and blowing; toward the end there is gallop-rhythm. Profound amnia, complete anorexia and apathy deepening to somnolence set in, with unconsciousness before death. As in the acute heart failure, the end may be ushered in with restlessness and attacks of pain, and sometimes with unilateral paralyses the results of embolism (of the abdominal aorta, of the cerebral arteries, or of those of the extremities).
The period of danger may in rare cases last for a long time without these grave complications, or it may speedily subside. The improvement, however, is frequently not substantial nor lasting and the patients later succumb to an insurmountable weakness, the diphtheritic marasmus.
When the termination is recovery the albumin first disappears (Unruh), and later, the heart weakness and rapidity of the pulse. The disappearance of the albumin in such eases may then be considered a favorable sign.