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Localized sweating replacing cardiac pain

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Page 1: Localized sweating replacing cardiac pain

LOCALIZED SWEATING REPLACING CARDIAC PAIN”

EVELYN HOLT, M.D. NEW YORK, N. Y.

T HE following case is reported because it illustrates the occurrence of sympathetic reflex sweating in a patient with angina1 pain. It

is interesting to note that the sweating was strictly limited to the region where the patient had felt pain on effort for twenty-five years, but that the sweating occurred while the patient was at rest and not with the pain.

CASE REPORT

A.J.N., a retired clerk, aged 75 years, was admitted to the New York Hospital (service of Dr. L. A. Conner) ‘on November 20 and died on December 21, 1926. He had rheumatic fever at 25 and at 27 years, being sick for six or eight weeks with each attack, and later had two milder rheumatic attacks. He never had syphilis, but had gonorrhea twice as a young man. At the age of 30 he was told that his heart was affected, but he had no symptoms and considered himself in excellent health until the age of 50. From then until the time of his death he suffered from dyspnea and angina1 pain on exertion, and because of these symptoms he entered the New York Hospital eleven times, attended the out-patient department regularly, and .on two occasions was admitted to Roosevelt Hospital.

His first admission to the hospital was in November 1908, when he complained of precordial pain and tenderness brought on by exertion. At this time he had a transient auricular fibrillation and fairly well marked sclerosis of his peripheral arteries. The heart was somewhat enlarged and there were systolic murmurs at the apex and aortic area, and at times a diastolic murmur heard to the left of the sternum. He remained in the hospital for six weeks. His next admission was in December 1914, when he complained of severe precordial pain brought on by exertion and radiating down the left arm. Blood pressure was not elevated, arteriosclerosis was marked, and the auricular fibrillation had become permanent. He was re- admitted in 1916, 1917, 1918, 1919, 1920, 1921, 1924, and in March and November 1926, each time with the same complaints. On one admission he had a pulmonary embolus and au another an attack of jaundice. In November 1920 he was in the Neurological Institute because of a cerebral accident resulting iu right hemiplegia, from which he made an almost complete recovery. In December 1926, while in the hospital, the patient had a sharp chill followed by fever and associated with transient hematuria. Chills and fever recurred daily; no local evidence of infection could be found, but a staphylococcus aureus n’as recovered from the blood stream; the patient grew progressively worse aud died after two weeks. Permission for autopsy was not obtained.

The physical signs changed little in the last twelve years of the patient’s life. The blood pressure was never elevated; the heart was somewhat enlarged, with the apex in the 5th space 10.5 cm. to the left of the midline. The rhythm was totally irregular. Systolic murmurs were present at the apex and the aortic area, and at times a soft diastolic murmur was heard to the left of the sternum in the 2nd, 3rd

*From the Department of Medicine, Division of thz New York Hospital.

Cornell University and the First Medical

522

Page 2: Localized sweating replacing cardiac pain

HOLT : LOCALIZED SWEATING REPLACING CAR,DIAC PAIN ,523

or 4th space. Retinal and peripheral arteries showed evidence of sclerosis. The Wassermann reaction was negative on repeated examinations. The electrocardio- gram showed auricular fibrillation with left axis deviation and no abnormality of the ventricular waves. The records were practically identical over a period of ten years, a finding which was considered unlikely in the preseuce of any progressive disease of the coronary arteries.

On each admission to the hospital, and indeed on each visit to the clinic, the patient’s complaint was the same. On exertion he became short of breath and had severe pain and pressure under the sternum, in the left side of the chest, radiating donan the left arm and up into the left side of the neck. In 1914 the pain radiated to the jaw and left side of the face over the eye and was accompanied by a sense of pulsation in the left temporal region. Generalized sweating accompanied the more severe attacks of pain. In 1915 pain in the throat and hoarseness were not,ed with t.he pain. In 1921 the attacks were more frequent and were oft.eu fol- lowed by pain behind the left ear. Until lR?G the pain was always brought, on by effort and relieved by rest; it started under the sternum, spread over the left side of the chest, radiated to the left arm and left side of the neck, and was commonly associated with hyperaesthesia of the skin. In March 1926 the patient sta.tcLrl that he had had several attacks of pain at night, and on admission to the hospital t,he whole preeordial area was sensitive to light touch. On March 29 the following note wa.s made: “Last night patient had :I cerv profuse localized sweat limited to the area where angina1 pain occurs,-i.e. precordium, left shoulder and left arm. He has had similar experience two or three times before coming to hospital. Sweat occurs at night and is not accompanied bp pain.” At this time the pupils were equal and there was no flushing or other vasomotor disturhancc. AfWr six weeks of rest the patient went home and lvas fairly comfortable for six months, but in November he re-entered the hospital for the last time. On December t’ the following note was made: “About once in 34 hours, while sleeping and usually at night, patient complains of profuse sweating of the left side of &est, Left arm and left side of neck. It corresponds to the same area where he has prrviously corn plained Of angina1 pain. He rarely has pain with the sweating.” There was nrt change in the signs at this time, but a few days later the patient developed thr acute infection from which he died.

COMMENT

R case is reported in which localized sweating occurred, apparently as a substitute for angina1 pain. The sweating was limited to the region where 6he pain had previously been felt and was observed re- peatedly in the last year of the patient’s life. It was not accompanied by exophthalmos, dilatation of the pupil or other evidence of sympa- thetic involvement. Cardiac pain was present for the last twenty-five years of the patient’s life and was believed to be related to an old rheumatic valvular disease. The paGent had generalized arteriosclero- sis but no evidence of progressive coronary disease.