Peripheral Gangrene in Myocardial Infarction

Abstract

Peripheral gangrene caused by the extreme vaso-constriction that accompanies severe circulatory failure in such a disease as cholera is well recognized. Its occurrence, however, as a complication of myocardial infarction is such an uncommon event, to judge from the literature, that the reporting of two cases seems to be justified. On admission he was severely dyspnoeic at rest. There was no cedema. He was pale and it was noted that the end of his nose was blue and cold. The pulse was impalpable at the wrist and the blood pressure was 80/60. The apex rate was 100 a minute and the rhythm was regular. The heart showed no clinical enlargement and the heart sounds were normal. There was no pericardial friction. There were loud moist sounds all over both lungs, especially towards the bases. The liver was not enlarged.He remained seriously ill with a heart rate of around 110 a minute until December 30th, when he seemed to be a little better, but it was found that the right foot had become cold and blue up to the level of the ankle, and was anmsthetic over the same area. No pulse could be felt at the ankle, though the femoral pulses were present on both sides. On this day also it was noted that the whole of the nose was blue, livid, cold and anesthetic, and that there was a clear line of demarcation with the normal skin at the base of the nose. The tips of the ears and the tongue were unaffected, but there were some blotchy blue areas on the hands. The fingers were unaffected. Anti-coagulant treatment was started on this day.On December 31st, the left foot became affected in exactly the same way, and the right foot remained blue, cold and anesthetic. The prothrombin time was 36 seconds and a normal control was 25 seconds.He remained gravely ill, and on January 3, 1949, a blood pressure reading of 60 mm. systolic with no diastolic end point was made: he died on this day. Electrocardiograms on the fourth and tenth day of the illness showed evidence of extensive myocardial infarction (Fig. 1).Necropsy. There was gangrene of the nose with a well-defined line of demarcation, and small bulli over the healthy skin at the junction. Both feet showed gangrene, with the skin black, swollen, and wrinkled (Fig. 2). The fingers and ears did not show gangrene.

Symmetrical Peripheral Gangrene—A Case Report and Brief Review

“…Symmetrical peripheral gangrene is described as multiple extremity ischemia at two or more sites in the absence of large vessel obstruction [1,2]. Possible etiological factors cited in literature include obstructive intracardiac lesions [3], sepsis [4], vasospastic conditions [5,6], small vessel obstruction [1], protein C deficiency [7], use of vasopressor agents [8,9], low cardiac output states [10,11], disseminated intravascular coagulation (DIC) [12,13], factor V Leiden mutation [14], and parenteral abuse of the sublingually available form of buprenorphine [15]. It is well established that the digital perfusion will drop to zero in presence of persistently low perfusion pressures of 35-60 mmHg [16].…”

Cutaneous Petechiae in Fatal Coronary Artery Disease

“…Peripheral vasoconstriction has been held to be responsible for referred cardiac pain by Roberts (1945) and has been demonstrated by variations of cutaneous temperature (Doret and Ferrero, 1951). An analogous mechanism is known to be responsible for the trophic lesions in the upper limb which are well-recognized clinical sequelae of acute cardiac pain and myocardial infarction (Askey, 1941;Kehl, 1943;Johnson, 1943;Steinbrocker, Spitzer, and Friedman, 1948;Hilker, 1949;Chitwood, 1950;Swan and Henderson, 1951). Apart from possibly initiating reflexes, which may cause spasm of the peripheral vessels, the coronary arteries themselves are subject to vasospastic stimuli from various organs of the body (von Bergmann, 1932;Greene, 1935;Gilbert, Fenn, and LeRoy, 1940;Freedberg, Spiegi, and Riseman, 1944).…”

Dynamics of Heart Failure

“…The place and nature of these reactions in the complex picture of acute left ventricular failure still remain to be clarified. We can all observe from time to time in the dying patient with left ventricular failure an intense peripheral constriction which may lead to actual gangrene of the tip of the nose and fingers (Swan and Henderson, 1951). lIn one such patient Dr. Graham Bull (unpublished) demonstrated that there was also a very gross reduction of renal blood flow to less than one-tenth the normal value.…”