CARDIOVASCULAR RENAL DISEASE

With the strennousness of this era, this disease or condition, which may be regarded as one of the accompaniments of normal old age, has become of grave importance, and nowadays frequently develops in early middle life. If it is diagnosed in its incipiency, and the patient follows the advice given him, the progress of the disease will generally be inhibited, and a premature old age postponed.

In the beginning the symptoms and signs of this disease are generally those of hypertension, and the treatment and management is that advised in hypertension. If the kidneys show irritation, as manifested by the presence of albumini and casts in the urine, or if they show insufficiency in the twenty-four-hour excretion of one or more salts or other excretory product, the diet and life must be more carefully regulated than advised in hypertension, and the treatment becomes practically that of chronic interstitial nephritis.

Sooner or later, in most instances of this disease, whether hypertension, chronic endarteritis or interstitial nephritis or any combination of these conditions is most in evidence, the heart will hypertrophy. As long as the circulation in the heart itself is good and not impaired by coronary sclerosis, and as long as this slowly developing chronic myocarditis has not advanced far, cardiac symptoms will not be in evidence; but if these conditions occur, or if the blood pressure is so greatly increased as to damage the aortic valve or strain and dilate the left ventricle, symptoms rapidly appear, and the heart must be carefully watched. Subsequently, as the disease advances, if the patient does not die of angina pectoris, apoplexy or uremia, the symptoms of cardiac decompensation will develop. As the heart begins to fail, a dilatation of the right ventricle causes passive congestion of the kidneys, and the chronic interstitial nephritis may progress more rapidly. It is often difficult to decide which is more in evidence, heart insufficiency or kidney insufficiency. The more the heart fails, the more albumin will generally appear in the urine, and the lower the blood pressure, especially the diastolic. The more insufficient the kidneys, the higher the blood pressure, especially the diastolic. The location of the edema will aid in deciding which condition is most in evidence. If the edema is pendent in feet, legs and perhaps genitals when the patient is up, with its disappearance at night, and more or less backache and pitting of the back in the morning, it is the heart that is most rapidly failing. If there is more general edema, the hands and face puffing, and there are considerable nausea and vomiting, headache and drowsiness, and perhaps muscular twitchings, with neuralgic pains, the most serious trouble at that particular time lies in the kidney insufficiency. Kisch [Footnote: Kisch: Med. Klin., Feb. 27, 1916.] sums up the procedural symptoms and signs of cerebral hemorrhage. The heart is generally enlarged and hypertrophied. The patient is likely to be overweight or adding weight, and to suffer from intestinal indigestions. Signs of sclerosis of the blood vessels of the brain are evidenced by transient dizziness; headaches; impaired sleep; loss of memory, especially for names and words; slight disturbances of speech, momentary perhaps, and more or less temporary localized numbness of the hands or feet, or arms or legs, with perhaps flushing of some part of the body, or little localized spasms of vessels of other parts of the body, causing chilliness.

There is also a marked hereditary tendency to apoplexy.

Cadwalader, [Footnote: Cadwalader, W. R.: A Comparison of the Onset and Character of the Apoplexy Caused by Cerebral Hemorrhage and by Vascular Occlusion, The Journal A. M. A., May 2, 1914, p. 1385.] after considerable investigation, has come to the conclusion that large hemorrhages into the brain are the rule in apoplexy, and that small hemorrhages are rare, and he is inclined to think that even small, as well as large hemorrhages, are more frequently fatal than supposed. In other words, he thinks that many of the nonfatal hemiplegias are caused by vascular obstruction and softening and not by hemorrhage. He finds that sudden death, or death within a few minutes, does not occur from hemorrhage, even if the hemorrhage is large, though a rapidly developing and persistent coma usually indicates a hemorrhage. If the coma is not profound and is slow in its onset, with symptoms noticed by the patient, and cerebral disturbance, he believes it to be caused generally by softening of the cerebral center, due to some obstruction of the blood flow, and not to hemorrhage. While occasionally a slowly increasing loss of consciousness may be due to hemorrhage, he thinks it is doubtful if real hemorrhage ever occurs without loss of consciousness, while softening of some part of the cerebrum may occur without unconsciousness. He thinks that the size of the hemorrhage is of more importance than its situation in causing the profoundness of the symptoms, but he repeats that nonfatal cases of hemiplegia are generally caused by vascular occlusion and subsequent softening, and not by hemorrhage.