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Pericardial effusion in myxedema
PERICARDIAI,
EFFUSION
IN MYYEl)ERtA
GEORGE T. HARRELL, M.D., WINSTON-SALEM, N. C., ASD CHRISTOPHER JOHXSTOS, M.D., IMzR2q N. C.
E
FFUSION into the pericardium and other YP~‘OLIS cavities is a complication of myxedema on which few data are available. Zondekl first described myxedema heart, disease as a clinical entity, and Gordon’ first proved that pericardial effusion might account for at least part of The occurrence of serous effusions the apparent cardiac enlargement. was noted at autopsy in cases of myxedcma as earl)- as 188K3 Taturn4 and Goldberg5 reproduced pericardial effusion in thyroideetomized sheep and goats. Freeman6 reported the first thoroughly described case of massive pericardial effusion in myxedema. Since his report, other illstances have been recorded.‘, 8 Although the case described by Merrill” resembled myxedema clinically, the basal metabolic rate was elevated. In the case reported by Cams and Lee,l” the presence of pericardial Two patients with untreated fluid was not demonstrated by aspiration. myxedema who came to autopsy at the Massachusetts &neral Hospital had pericardial effusion, although one was small in amount.ll Often the picture is complicated by the development of arteriosclerosis, espcciall) in the coronary arteries, if the myxedema remains untreated for a period of years. The following two cases, in both of which there was underlying artrriosclerotic heart disease, add a few data, including the first quantitative studies on the cholesterol content of the pericardial fluid, and are interesting because of the variation in response to the administ,ration ot’ thyroid substance. CASE 1.--X 5%year-old, white, farm housewife, was admit,ted to Duke Hospital October 1, 1938, complaining of weaknehs, intermittent rwelling of the abdomen, and slight dyspnea, of eighteen months ’ duration. The feet were always cold. The patient was pale, undernourished, breathing quietly, and not orthopneic. Speech was slow and the voice was hoarse. The tongue showed no papillary atrophy. The skin was dry and thickened. The breath sounds at the bases of the lungs were distant. The heart was enlarged, the precaordium quiet, the rate slow, and the sounds distant; the blood pressure was lZO/SO. The abdomen was rounded, shifting dullness was present, and the liver extended 8 cm. below the costal margin. Pitting edema was present over t,he sacrum, but not over the legs. The hemoglobin was 10.9 Gm., the erythrocytes numbered 2,ti00,00(), the color index was 1.3, and the mean corpuscular volume was 140 cubic micra. The urine contained no albumin. Gastric analysis showed 64 degrees of free HCI after the injection of histamine. The total serum protein was 6.4 per cent, with albumin 3.6 per cent, and globulin 2.8 per cent; the cholesterol was 530 mg. per rent. ‘I%? bafial metabolic N.
From the Department C. Received for publication
of Medicine. July
Duke
7, 1942. 505
rniversity
School
of Me(licine,
Durham,
C. pericarclial and small pleural Fig. l.-Case 1. A, Massive B, Complete disappearance of eff,usions on thyroid therapy D,, Improvement effusions after withdrawal of thyroid. therapy, after failure to improve on digitall%
I>. effusion, alone. R second
before therapy. CT Recurrence ?f tnne on thsroltl
HARRELL
AND
JOHNSTON
:
PERICARDIAL
EFFUSION
IN
MYXEDEMA
507
was orthopneic, and had physical and roentgenologic evidence of fluid in all the serous cavities (Fig. 2), peripheral edema, and signs of myxedema. The hemoglobin was 13 Gm., the ergthrocytes numbered 4,4OO,OtlO, the color index was 0.95, the mean corpuscular volume, 97.7 cubic micra the basal metabolic rate, minus 35 per cent, the vital capacity, 600 cc., the venous pressure, 190 mm. of water, and the serum were 5.0 per cent, with albumin 2.7 cholesterol, 270 mg. per cent; the serum proteins time was 19 seconds by the per cent and globulin 2.3 per cent, and the circulation The urine contained no albumin. The pericardial fluitl calcium gluconate method. contained 4.3 per cent of total protein and 94 mg. per cent of cholesterol.
Fig. P.-Case 1. A, Roentgenkymograph when patient was con irregular thyroid, showing absence of pulsations over the lower third of the heart pulsations over the great vessels, in.dicating recurrence of small pericarclial without impairment of ventricular contraction. B, Recurrence of massive and small pleural effusion after complete withdrawal of thyroil therapy; pulsations over the great vessels indicate feeble ventricular contractions.
doses of and good effusion pericardial the small
After rest in bed, restriction of fluids, and complete digitalization produced no response, 64 mg. of thyroid substance were administered daily, with a marked diurcsis of 8,700 cc. on the second day and a weight loss of 3 kg. in two days. On the eleventh and sixteenth days the thyroid dosage was increased, with the result that there was a second and third diuresis, each lasting three days. The edema, serous effusions, mental sluggishness, and coo&ress and thickening of the skin disappeared. CASF > d. 9-A Wyear-old white farmer was admitted to the Duke Hospital September 11, 1939, complaining of orthopnea and edema of one month’s duration. He had been seen in 1932, 1934, and 1937, when he had pellagra, anemia, and hypothyroidism, and had always responded promptly to therapy with desiccated thyroid, iron, and yeast.
The patient presented the classic appearance of myxedema. Signs of fluid were present at the bases of both lungs. The supracardiac dullness was greatly increased (Fig. 3), and the heart sounds were barely audible; the blood pressure was 168/114. The abdomen was distended and tympanitic, and the liver was enlarged. Pitting edema wzds present below the knees. The skin over the hands and feet was rough, dry, red, and scaling. The hemoglobin metabolic rate was
was 9 Gm., minus 39 per
the erythrocytes cent, the serum
numbered 3,100,000, proteins were ti.4 per
the basal cent, with
K. A. Fig. :3.-&w 1. A, Pwical’clial effusion aft.%, partial aspiration of fluid and PCplacement with air, before thyroid a,lministration and after failare of vitamin therapy. B, Small recurrent pleural effusion on right after thyroid therapy was discontinued. an(l clinical signs of myxedema ha<1 retumecl.
Of these two instances of pc~ricardial effusion in association with myxedrma, the first was nndouhtedl;v caused bg the myxedema itself, for the fluid disappeared undo thyroid replacement therapy, recurred after complete withdrawal of thyroid, did not disappear under digitalis therapy, and did respond a. second time to thyroid administration. The effusion in the second case did not respond to thyroid substance alone, on withdrawal of thyroid but also required digitalis, and did not recnr and digitalis. In each of these cases there was evidence of underlying arteriosclerotic heart disease. The more severely damaged heart (Case 2) did not respond to thyroid substance alone, and the second responsein
M
F----
*Guinea
F
SES
--z5410 -s--F
--i3F--E396-a--E'54s
AGE
pig
3 mo. 16 yr. 4 yr. J yr. 8 yr. inoculation.
s yr. 3 yr.
DURATION
-31 -35 -39 -3-i
-42 -45 t19
B. M. R. v0
A
Neg. Neg. lt Neg.
Trace Trace
URINE ALBUMIN
6.4 6.5
-___-50::
. .-l_.--_-~
6.4
__--
-. 2L--_.-~ -_--
TEIN
TOThI, PRO-
36 217 3.3 2.4
3.8
7.
ALB.
2.8 2.3 xi--4.1
---il--pp-
-236: -227
r---
--------p-p-~~___
BLOOD
319 270 156 292
357
278
I
Neg.
Neg.
Neg. Neg. Neg. Contam-Neg. inated Neg. Neg. Neg. Neg. p-p-Neg. -----
I
TABLE
72 109
4w 2600
75
-100 ~- 56
-99
50 -100
31
99
12
PERICARDIAL
-
.
10 -ix%5.7
-
~~__ ---
-
3s -~~
% -~~
MON.
- FLUID
1.015
1.022 1.020
1.019 1.020
SP. GR.
4.3
4.9
5.0 3.2
4.5
TOTAL PROT. %
g2
Crystals
CHOLES. MG. %
HARRII’LL
.\Sl)
.JOHSSTOS
:
l’lsw~!.\KI)I:\I,
IwI~‘l-sIc)s
IS
MYXEDIh!I.\
511
The protein and cholcsassociated with myxedema have been tabulated. terol contents of the pericardial fluid are less than those of t,hc blood. No adequate explanation has been offered for the occasional prcsenvc of leucocytes, especially polymorphonu~lear lencoeytes, in the fluid. REFEKE;NCES
1. Zondek, 2. Gordon, 20: 3. Report 4.
9. IO. I I. I”. 13. 14.
Das Myxijedemherz, Miinchen. med. Wchnschr. 65: 1180, 1918. H.: Some Clinical Sspects of Hypothyroidism, Canad. M. A. .J. A. H.: 8, 1929. of a Committee of the C-‘linical Society of London, Nominated Deceml)er 19, 1883, to Iurestipate the Snl)jwt of”Myxederm, TV. Clin. Roe. Lend. supp. \‘. “1, ISSY. Taturn, A. L.: Studies in Experimental (‘retinism, With Suggestions as to a Biological Test for Thyroid Secretion, Proc. Am. Physiol. Sot., 1912-13, Boston, p. 23. Goldberg, 8. A.: Changes in Orgxtrs of Thyroirlertomized Sheep and Goats, Quart. J. l:sper. Phpsiol. 17: 13, 3927. Freeman, I<:. H.: (‘hronic Pericardial Eff’usion in Myxetlema: Report of Case, Ann. Int. Mctl. 7: IWO, 1934. Marzullo, E. R., and Frarrco, S.: M~xedema With hfultiple Serous Effusiona and Cardiac* Drvolvement (Myxedema Heart), SK HEART J. 17: 368, 1939. E’eaaby, W. R.: Pericardial YEtFusion in Myxetlema. Report of a Case in Which Intrnpericardial Pressure Was Measured, Ant. HURT J. 19: 749, l!Ml. Merrill, A. J.: ~‘helesterol Pericarditis, Ax. HEART J. 16: 503, 1935. Cams, RI. I,., and Lee, H. J.: Pericardial Effusion in JIyxedema; Report of Case, Wisconsin AI. .J. 35: 33, 1!)36. Lermaq, J., t!larlc, H. J., and Xeans, J. H.: The Heart in Myxedema. Electrecardrograms and Roentgen-Ray Measurements Before and After Therapy, Ann. Int. Bled. 6: lf:?l, 1933. Greene? .r. A.: The (‘oexistence of hlyxetlema and Pellagra in the Same Patrent, Bm. J. M. SC. 195: 618, 1938. (-‘hanev, W. C.: Tendon Reflexes in Myxedenm: A Valualrle Aid in Diagno&, J. A. M. A. 82: 2013, 1924. Daniel, G., and Puder, S.: Perikarditis et Pleuritis Cholesterinea, Virckows Arch. f. path. Anat. 284: 853, 1932.
EFFUSION
IN MYYEl)ERtA
GEORGE T. HARRELL, M.D., WINSTON-SALEM, N. C., ASD CHRISTOPHER JOHXSTOS, M.D., IMzR2q N. C.
E
FFUSION into the pericardium and other YP~‘OLIS cavities is a complication of myxedema on which few data are available. Zondekl first described myxedema heart, disease as a clinical entity, and Gordon’ first proved that pericardial effusion might account for at least part of The occurrence of serous effusions the apparent cardiac enlargement. was noted at autopsy in cases of myxedcma as earl)- as 188K3 Taturn4 and Goldberg5 reproduced pericardial effusion in thyroideetomized sheep and goats. Freeman6 reported the first thoroughly described case of massive pericardial effusion in myxedema. Since his report, other illstances have been recorded.‘, 8 Although the case described by Merrill” resembled myxedema clinically, the basal metabolic rate was elevated. In the case reported by Cams and Lee,l” the presence of pericardial Two patients with untreated fluid was not demonstrated by aspiration. myxedema who came to autopsy at the Massachusetts &neral Hospital had pericardial effusion, although one was small in amount.ll Often the picture is complicated by the development of arteriosclerosis, espcciall) in the coronary arteries, if the myxedema remains untreated for a period of years. The following two cases, in both of which there was underlying artrriosclerotic heart disease, add a few data, including the first quantitative studies on the cholesterol content of the pericardial fluid, and are interesting because of the variation in response to the administ,ration ot’ thyroid substance. CASE 1.--X 5%year-old, white, farm housewife, was admit,ted to Duke Hospital October 1, 1938, complaining of weaknehs, intermittent rwelling of the abdomen, and slight dyspnea, of eighteen months ’ duration. The feet were always cold. The patient was pale, undernourished, breathing quietly, and not orthopneic. Speech was slow and the voice was hoarse. The tongue showed no papillary atrophy. The skin was dry and thickened. The breath sounds at the bases of the lungs were distant. The heart was enlarged, the precaordium quiet, the rate slow, and the sounds distant; the blood pressure was lZO/SO. The abdomen was rounded, shifting dullness was present, and the liver extended 8 cm. below the costal margin. Pitting edema was present over t,he sacrum, but not over the legs. The hemoglobin was 10.9 Gm., the erythrocytes numbered 2,ti00,00(), the color index was 1.3, and the mean corpuscular volume was 140 cubic micra. The urine contained no albumin. Gastric analysis showed 64 degrees of free HCI after the injection of histamine. The total serum protein was 6.4 per cent, with albumin 3.6 per cent, and globulin 2.8 per cent; the cholesterol was 530 mg. per rent. ‘I%? bafial metabolic N.
From the Department C. Received for publication
of Medicine. July
Duke
7, 1942. 505
rniversity
School
of Me(licine,
Durham,
C. pericarclial and small pleural Fig. l.-Case 1. A, Massive B, Complete disappearance of eff,usions on thyroid therapy D,, Improvement effusions after withdrawal of thyroid. therapy, after failure to improve on digitall%
I>. effusion, alone. R second
before therapy. CT Recurrence ?f tnne on thsroltl
HARRELL
AND
JOHNSTON
:
PERICARDIAL
EFFUSION
IN
MYXEDEMA
507
was orthopneic, and had physical and roentgenologic evidence of fluid in all the serous cavities (Fig. 2), peripheral edema, and signs of myxedema. The hemoglobin was 13 Gm., the ergthrocytes numbered 4,4OO,OtlO, the color index was 0.95, the mean corpuscular volume, 97.7 cubic micra the basal metabolic rate, minus 35 per cent, the vital capacity, 600 cc., the venous pressure, 190 mm. of water, and the serum were 5.0 per cent, with albumin 2.7 cholesterol, 270 mg. per cent; the serum proteins time was 19 seconds by the per cent and globulin 2.3 per cent, and the circulation The urine contained no albumin. The pericardial fluitl calcium gluconate method. contained 4.3 per cent of total protein and 94 mg. per cent of cholesterol.
Fig. P.-Case 1. A, Roentgenkymograph when patient was con irregular thyroid, showing absence of pulsations over the lower third of the heart pulsations over the great vessels, in.dicating recurrence of small pericarclial without impairment of ventricular contraction. B, Recurrence of massive and small pleural effusion after complete withdrawal of thyroil therapy; pulsations over the great vessels indicate feeble ventricular contractions.
doses of and good effusion pericardial the small
After rest in bed, restriction of fluids, and complete digitalization produced no response, 64 mg. of thyroid substance were administered daily, with a marked diurcsis of 8,700 cc. on the second day and a weight loss of 3 kg. in two days. On the eleventh and sixteenth days the thyroid dosage was increased, with the result that there was a second and third diuresis, each lasting three days. The edema, serous effusions, mental sluggishness, and coo&ress and thickening of the skin disappeared. CASF > d. 9-A Wyear-old white farmer was admitted to the Duke Hospital September 11, 1939, complaining of orthopnea and edema of one month’s duration. He had been seen in 1932, 1934, and 1937, when he had pellagra, anemia, and hypothyroidism, and had always responded promptly to therapy with desiccated thyroid, iron, and yeast.
The patient presented the classic appearance of myxedema. Signs of fluid were present at the bases of both lungs. The supracardiac dullness was greatly increased (Fig. 3), and the heart sounds were barely audible; the blood pressure was 168/114. The abdomen was distended and tympanitic, and the liver was enlarged. Pitting edema wzds present below the knees. The skin over the hands and feet was rough, dry, red, and scaling. The hemoglobin metabolic rate was
was 9 Gm., minus 39 per
the erythrocytes cent, the serum
numbered 3,100,000, proteins were ti.4 per
the basal cent, with
K. A. Fig. :3.-&w 1. A, Pwical’clial effusion aft.%, partial aspiration of fluid and PCplacement with air, before thyroid a,lministration and after failare of vitamin therapy. B, Small recurrent pleural effusion on right after thyroid therapy was discontinued. an(l clinical signs of myxedema ha<1 retumecl.
Of these two instances of pc~ricardial effusion in association with myxedrma, the first was nndouhtedl;v caused bg the myxedema itself, for the fluid disappeared undo thyroid replacement therapy, recurred after complete withdrawal of thyroid, did not disappear under digitalis therapy, and did respond a. second time to thyroid administration. The effusion in the second case did not respond to thyroid substance alone, on withdrawal of thyroid but also required digitalis, and did not recnr and digitalis. In each of these cases there was evidence of underlying arteriosclerotic heart disease. The more severely damaged heart (Case 2) did not respond to thyroid substance alone, and the second responsein
M
F----
*Guinea
F
SES
--z5410 -s--F
--i3F--E396-a--E'54s
AGE
pig
3 mo. 16 yr. 4 yr. J yr. 8 yr. inoculation.
s yr. 3 yr.
DURATION
-31 -35 -39 -3-i
-42 -45 t19
B. M. R. v0
A
Neg. Neg. lt Neg.
Trace Trace
URINE ALBUMIN
6.4 6.5
-___-50::
. .-l_.--_-~
6.4
__--
-. 2L--_.-~ -_--
TEIN
TOThI, PRO-
36 217 3.3 2.4
3.8
7.
ALB.
2.8 2.3 xi--4.1
---il--pp-
-236: -227
r---
--------p-p-~~___
BLOOD
319 270 156 292
357
278
I
Neg.
Neg.
Neg. Neg. Neg. Contam-Neg. inated Neg. Neg. Neg. Neg. p-p-Neg. -----
I
TABLE
72 109
4w 2600
75
-100 ~- 56
-99
50 -100
31
99
12
PERICARDIAL
-
.
10 -ix%5.7
-
~~__ ---
-
3s -~~
% -~~
MON.
- FLUID
1.015
1.022 1.020
1.019 1.020
SP. GR.
4.3
4.9
5.0 3.2
4.5
TOTAL PROT. %
g2
Crystals
CHOLES. MG. %
HARRII’LL
.\Sl)
.JOHSSTOS
:
l’lsw~!.\KI)I:\I,
IwI~‘l-sIc)s
IS
MYXEDIh!I.\
511
The protein and cholcsassociated with myxedema have been tabulated. terol contents of the pericardial fluid are less than those of t,hc blood. No adequate explanation has been offered for the occasional prcsenvc of leucocytes, especially polymorphonu~lear lencoeytes, in the fluid. REFEKE;NCES
1. Zondek, 2. Gordon, 20: 3. Report 4.
9. IO. I I. I”. 13. 14.
Das Myxijedemherz, Miinchen. med. Wchnschr. 65: 1180, 1918. H.: Some Clinical Sspects of Hypothyroidism, Canad. M. A. .J. A. H.: 8, 1929. of a Committee of the C-‘linical Society of London, Nominated Deceml)er 19, 1883, to Iurestipate the Snl)jwt of”Myxederm, TV. Clin. Roe. Lend. supp. \‘. “1, ISSY. Taturn, A. L.: Studies in Experimental (‘retinism, With Suggestions as to a Biological Test for Thyroid Secretion, Proc. Am. Physiol. Sot., 1912-13, Boston, p. 23. Goldberg, 8. A.: Changes in Orgxtrs of Thyroirlertomized Sheep and Goats, Quart. J. l:sper. Phpsiol. 17: 13, 3927. Freeman, I<:. H.: (‘hronic Pericardial Eff’usion in Myxetlema: Report of Case, Ann. Int. Mctl. 7: IWO, 1934. Marzullo, E. R., and Frarrco, S.: M~xedema With hfultiple Serous Effusiona and Cardiac* Drvolvement (Myxedema Heart), SK HEART J. 17: 368, 1939. E’eaaby, W. R.: Pericardial YEtFusion in Myxetlema. Report of a Case in Which Intrnpericardial Pressure Was Measured, Ant. HURT J. 19: 749, l!Ml. Merrill, A. J.: ~‘helesterol Pericarditis, Ax. HEART J. 16: 503, 1935. Cams, RI. I,., and Lee, H. J.: Pericardial Effusion in JIyxedema; Report of Case, Wisconsin AI. .J. 35: 33, 1!)36. Lermaq, J., t!larlc, H. J., and Xeans, J. H.: The Heart in Myxedema. Electrecardrograms and Roentgen-Ray Measurements Before and After Therapy, Ann. Int. Bled. 6: lf:?l, 1933. Greene? .r. A.: The (‘oexistence of hlyxetlema and Pellagra in the Same Patrent, Bm. J. M. SC. 195: 618, 1938. (-‘hanev, W. C.: Tendon Reflexes in Myxedenm: A Valualrle Aid in Diagno&, J. A. M. A. 82: 2013, 1924. Daniel, G., and Puder, S.: Perikarditis et Pleuritis Cholesterinea, Virckows Arch. f. path. Anat. 284: 853, 1932.