Pericardial Tamponade

Transcription

1 Pericardiectomy for Uremic Pericardial Tamponade Harold A. Collins, M.D., Duncan A. Killen, M.D., Walter G. Gobbel, Jr., M.D., and H. Earl Ginn, M.D. T he occurrence of pericarditis has been recognized as an ominous prognostic manifestation of uremia, but only within the last decade has cardiac tamponade been recognized as a lethal complication of uremic pericarditis. The introduction of regular intermittent and increased success in renal homotransplantation have necessitated a change in attitude toward uremic pericarditis. It now can be regarded as another manifestation of uremia which can be expected to improve with adequate therapy. The most hazardous feature of uremic pericarditis is cardiac tamponade, and this too is amenable to appropriate treatment. During the past five years we have encountered at the Vanderbilt University Medical Center 9 uremic patients in whom cardiac tamponade occurred as a result of pericarditis. This is a report of our experience in managing this aspect of renal failure. MATERIAL AND METHODS This report includes only those patients with uremia who developed pericarditis and cardiac tamponade of sufficient severity to warrant pericardiectomy. It does not include those patients with transient pericardial friction rubs or minimal to moderate degrees of pericardial effusion without evidence of tamponade. During the past four years we have encountered 9 patients who fulfilled these criteria. Ages varied from 20 to 54 years. All the patients except one were males. The primary renal lesion was chronic glomerulonephritis in all but one patient, who had renal hypoplasia and hydronephrosis. Similar symptoms occurred in all patients but varied greatly in severity. Dyspnea and precordial discomfort were present in each patient. A few patients noted ascites, swelling of the legs, or unusual weight gain. Cardiac tamponade occurred prior to the initiation of chronic intermittent in 7 of the 9 patients. The episode occurred 5 and 7 months after the beginning of hemo in the other 2 patients. The serum urea nitrogen concentration at the time of tamponade varied from 40 to 240 mg. per 100 ml. From the Departments of Surgery and Medicine, Vanderbilt University Medical Center, and the Veterans Administration Hospital, Nashville, Tenn. Supported in part by US. Public Health Service Grant No. HE and Career Research Development Award KO3 HE Presented at the Sixteenth Annual Meeting of the Southern Thoracic Surgical Association, Washington, D.C., Nov , Address reprint requests to Dr. Collins, Department of Surgery, Vanderbilt University Medical Center, Nashville, Tenn

2 COLLINS, KILLEN, GOBBEL, AND GINN A B FIG. 1. Chest roentgenograms of patient No. 2 (A) one day prior to pericardiectomy for cardiac tamponade due to uremic pericarditis and (B) six months after pericardiectomy. The clinical signs were those classically associated with pericarditis or tamponade. A distinct pericardial rub was audible in 7 of the 9 patients. Several patients who had previously been hypertensive spontaneously became normotensive or hypotensive. The venous pressure was elevated to inspection in all and ranged from 160 to 260 mm. saline in 7 of the 9 patients in whom it was measured. Pulsus paradoxus, varying from 10 to 30 mm. Hg, was present in 8 of the 9 patients. The chest roentgenogram in each patient demonstrated gross enlargement of the cardiac silhouette (Fig. 1A). Contrast angiocardiography. with carbon dioxide demonstrated wide separation between the right atrial wall and the right border of the cardiac shadow in 3 patients (Fig. 2). The electrocardiogram in each patient was abnormal but not diagnostic of pericarditis. Pericardicentesis for either therapeutic or diagnostic purposes was performed in each of the 9 patients (Table). Several patients had pericardicentesis on more than one occasion, the maximum number of times being five. The amount of fluid removed by pericardicentesis varied from 50 to 1,540 ml. and was bloody in every instance. The removal of 200 ml. of fluid usually was required to relieve the hypotension and elevated venous pressure characteristic of tamponade. In 4 patients emergency pericardiectomy became necessary for recurrent tamponade within minutes to hours after pericardicentesis. This extremely rapid, recurrent tamponade occurred despite the fact that the heart had not been punctured during pericardicentesis. The reason for this phenomenon is not clear. Cultures of the pericardial fluid disclosed the presence of gram-negative bacteria in 2 patients. In the other patients no bacterial growth was evident. Initially pericardiectomy was undertaken only as an extreme measure in patients with evidence of severe tamponade. More recently the procedure has been used for those patients with recurrent or continuing signs of tamponade after one pericardicentesis. The contemplated use of hemo with systemic anticoagulation in the presence of a bloody pericardial effusion also has influenced the decision in favor of pericardiectomy. It usually has been possible to 328 THE ANNALS OF THORAClC SURGERY

3 Pericardiectomy for Uremic Tamponade FIG. 2. Chest roentgenogyam of patient No. 1 obtained with patient in left lateral decubitus position after the intravenous injection of 100 ml. of CO,. Filling of the superior vena cava, right atrium, inferior vena cava, and hepatic veins is present. The wide separation between the lateral border of the right atrium and the right lung is evident. accomplish an extensive pericardiectomy through a left anterolateral thoracotomy performed with the patient under general anesthesia. An attempt was made to remove the anterior pericardium from one phrenic nerve to the other. The fluid in every instance was bloody and frequently was loculated because of thick fibrinous deposition. In the 2 patients with superimposed bacterial infection, the pericardium was drained externally. RESULTS Each patient survived operation, and without exception immediate, striking improvement in the hemodynamic status occurred. Following pericardiectomy, the patients have survived for periods ranging from 6 weeks to 18 months. Evidence of tamponade disappeared in each patient, and the chest roentgenogram usually showed a striking reduction in the size of the cardiac shadow (Fig. 1B). Pericardial tamponade did not recur, and in no instance was death due to cardiac impairment. The usual cause of death was some additional complication of uremia or its treatment. COMMENT Pericarditis is a frequent complication of chronic renal failure and is currently observed in 40 to 50% of such cases [l, 13, 171. Previously, the onset of pericarditis with uremia signified the likelihood of death within two to three weeks [3, 131. With modern methods of treatment, uremic pericarditis is often reversed and prolonged survival is possible.

4 COLLINS, KILLEN, GOBBEL, AND GINN SUMMARY OF TREATMENT IN NINE PATIENTS WITH UREMIC CARDIAC TAMPONADE Length of Survival Time after of Occur- Fluid (ml.) Cardiac rence of Tam- Patient Tam- Pericar- Pericar- ponade No. ponade dicentesis diectomy (mo.) Outcome 'Still living. 7 mo. after 5 mo. after 4 times; 1,540 2 times; 1, times: times; times; , ,100 1,000 1, , ' - Died following aspiration of vomitus Died after 2 unsuccessful cadaver transplants Died of sepsis 5 mo. after successful cadaver transplant Chronic program; died of pneumonia Not acceptable for program Treatment withdrawn Continues on program Not acceptable for program Continues on program In the past the occurrence of cardiac tamponade was considered to be a rare complication of chronic renal failure. The significance of cardiac tamponade as a cause of death in 2 patients with chronic renal failure was first reported by Goodner and Brown in 1956 [6]. Since that time several other reports have appeared [4, It is now clear that the presence of cardiac tamponade is not as infrequent as previously was assumed and that it is probably a progressive form of uremic pericar- 330 THE ANNALS OF THORACIC SURGERY

5 Pericardiectomy for Uremic Tamponade ditis. It is equally clear that uremic patients should not die from this complication. The fact that prolonged survival is possible if cardiac tamponade is treated aggressively is emphasized by our experience and by that of others [l, 4, 81. The involvement of the pericardium as well as other serous membranes in uremia has been recognized for many years. Richard Bright in 1836 [5] tabulated six instances of old adhesion, eight of recent inflammation, and twenty-three of serous accumulation in the pericardium of 100 patients with uremia. More recent studies [l, 3, 141 have amply confirmed Bright s original observations but have done little to elucidate the pathogenesis of uremic pericarditis or tamponade. The various theories advanced to explain the causes of this complication include infectious [3], chemical, hematological [ 121, metabolic [3], myocardial [7], and uremic toxin [ 11. Unfortunately, none of these theories satisfactorily explains all cases of uremic pericarditis. The relationship of hemo to pericarditis and cardiac tamponade is of interest. In most instances uremic pericarditis has regressed with the use of effective hemo. In others, however, clinical evidence of pericarditis first appeared after the institution of intermittent hemo [l, 41. The use of total systemic heparinization for hemo in patients with pericardial effusion poses the threat of additional intrapericardial bleeding and augmented compression of the heart. For this reason most observers favor the use of regional heparinization 11, 4, 121. The diagnosis of uremic pericardial tamponade is not particularly difficult if it is suspected in patients with chronic renal failure. Occasionally, rapid deterioration of renal function in a previously stable patient is the result of tamponade [9]. More commonly, the classic findings of elevated venous pressure, diminished pulse pressure, and distant heart sounds are evident. These observations are frequently ascribed to fluid overload, myocardiopathy [2], or a failing heart, and the presence of tamponade is not suspected. In every instance of tamponade in our experience, the chest roentgenogram has demonstrated striking enlargement of the cardiac shadow. The electrocardiogram is usually abnormal, but it has not provided specific evidence for pericarditis or tamponade. Rarely have we seen the concave ST-segment elevation characteristic of acute pericarditis. The usual electrocardiographic findings in our patients were nonspecific ST-T wave changes and low-voltage QRS complexes. The most helpful diagnostic measures have been pericardicentesis or specialized roentgenographic exposures. In every patient, even those with thick fibrinous effusion, it has been possible to remove varying quantities of abnormal fluid by pericardicentesis. This finding clearly establishes the diagnosis in addition to providing therapeutic benefit. A chest film with the patient in a left lateral decubitus position

6 COLLINS, KILLEN, GOBBEL, AND GINN during the intravenous injection of carbon dioxide or other contrast media will ordinarily demonstrate a significant separation between the right atrial chamber and the lateral border of the cardiac shadow when pericardial effusion is present. This finding is virtually diagnostic of pericardial effusion. Echocardiography is another suitable technique for documenting the presence of pericardial effusion. The presence of uremic pericarditis is probably an indication for if it appears that the patient is an acceptable candidate for the procedure. With intensive hemo, Bailey and associates [ 13 have reported that the pericarditis can be expected to resolve in 72% of patients. The presence of cardiac tamponade, however, poses a life-threatening situation for the patient. It is our impression that at least one pericardicentesis is desirable in each patient. Immediate and dramatic clinical improvement usually follows. Several groups of investigators have reported the successful management of uremic cardiac tamponade by pericardicentesis and alone [l, 4, 9, 101. Such an approach certainly seems warranted initially. In our experience, however, the relief was usually temporary, and recurrent tamponade frequently necessitated repeated pericardicentesis. One of the difficulties with pericardicentesis is the character of the intrapericardial fluid. It is commonly bloody with large fibrin clots and may be densely loculated. In this situation it is possible to remove only a small portion by pericardicentesis. The need for pericardiectomy thus becomes compelling. Aside from recurrent or continuing tamponade, other considerations may indicate the desirability of pericardiectomy. The possibility of increased intrapericardial bleeding during systemic heparinization for hemo has been described previously. In addition, cannot be depended upon to prevent or alleviate cardiac tamponade. In the experience of Beaudry and associates [4], 14 of 15 patients developed cardiac tamponade after the institution of effective hemo. It is also possible that cardiac tamponade can be accentuated by. Hager [9] has described this occurrence in a patient following peritoneal for which heparinization was not necessary. During fluid can be removed from the vascular compartment more rapidly than it can be mobilized from extravascular compartments. This may further accentuate defects in the ventricular diastolic filling gradient. Another consideration is the possible late sequela of cardiac tamponade after its spontaneous resolution. Although not common, chronic constrictive pericarditis has been reported with increasing frequency in these circumstances [9, 15, 161. These considerations lead us to believe that pericardiectomy for cardiac tamponade should be accomplished if an initial pericardicentesis does not give immediate and lasting relief. If hemo with systemic heparinization is to be used, pericardiectomy appears even 332 THE ANNALS OF THORACIC SURGERY

7 Pericardiectomy for Uremic Tamponade more desirable. With careful control of anesthesia, metabolism, and fluids, even patients in the terminal stages of chronic renal failure tolerate a thoracotomy surprisingly well, and usually can be initiated or resumed within a few days postoperatively. It is our impression that an extensive pericardial resection is desirable when it is performed for uremic cardiac tamponade. This, it is hoped, would diminish the possibility of the subsequent development of chronic constrictive pericarditis. In our opinion the occurrence of uremic pericarditis or cardiac tamponade need not be regarded as an ominous prognostic sign but as a signal for aggressive treatment of the tamponade and the chronic renal failure. By using this approach, a significant prolongation of life can result. SUMMARY Uremic pericarditis was once considered a sign of imminent death. With the introduction of regular intermittent hemo and success in renal homotransplantation, the occurrence of pericarditis now can be regarded as a manifestation of uremia which can be improved with appropriate therapy. The most ominous feature of uremic pericarditis is the occurrence of tamponade, which can be a severe life-threatening emergency. During the past four years we have encountered 9 uremic patients for whom emergency pericardiectomy was necessary because of tamponade. The majority of these patients developed uremic pericarditis and tamponade prior to the initiation of maintenance hemo. The other manifestations of uremia frequently obscured the presence of tamponade. Diagnosis is usually possible by classic clinical findings and can be confirmed by radiological techniques and diagnostic pericardicentesis. In our experience pericardicentesis has seldom produced more than temporary relief from tamponade. Despite the obvious risks in this critically ill group, all patients survived pericardiectomy and had significant improvement in their cardiovascular status. While the precise cause of uremic pericarditis with tamponade is unknown, pericardiectomy does appear to have a significant role in prolonging the life of afflicted individuals. REFERENCES 1. Bailey, C. L., Hampers, C. L., Hager, E. B., and Merrill, J. P. Uremic pericarditis. Circulation 38:582, Bailey, G. L., Hampers, C. L., and Merrill, J. P. Reversible cardiomyopathy in uremia. Trans. Amer. SOC. Artif. Intern. Organs 13:263, Barach, A. L. Pericarditis in chronic nephritis. Amer. J. Med. Sci. 163:44, VOL. 9, NO. 4, APRIL,

8 COLLINS, KILLEN, GOBBEL, AND GINN 4. Beaudry, C., Nakamoto, S., and Kolff, W. J. Uremic pericarditis and cardiac tamponade in chronic renal failure. Ann. Intern. Med. 64:990, Bright, R. Tabular view of the morbid appearances in 100 cases connected with albuminous urine. Guy. Hosp. Rep. 1:380, Goodner, C. J., and Brown, H. Report of two cases of cardiac tamponade in uremic pericarditis. J.A.M.A. 162: 1459, Gouley, B. A. Myocardial degeneration associated with uremia in advanced hypertensive disease and chronic glomerular nephritis. Amer. J. Med. Sci. 200:39, Guild, W. R., Bray, G., and Merrill, J. P. Hemopericardium with cardiac tamponade in chronic uremia. New Eng. J. Med. 257:230, Hager, E. B. Clinical observations of five patients with uremic pericardial tamponade. New Eng. J. Med. 273:304, Merikas, G., Marketos, S., and Konstantopoulos, E. Uremic pericardial tamponade. Canad. Med. Ass. J. 95:119, Merikas, G., Samartzis, M., and Marketos, S. Massive cardiac tamponade in uremic pericarditis with complete recovery. New Eng. J. Med. 266:1089, Nakamoto, S., and Kolff, W. J. Hemorrhagic diathesis in uremia and the avoidance of bleeding problem during. Ann. N.Y. Acad. Sci. 115:348, Richter, A. B., and O Hare, J. P. The heart in chronic glomerular nephritis. New Eng. J. Med. 214:824, Sokol, A., Gral, T., Edelbaum, D. N., Rosen, V., and Rubini, M. E. Correlation of autopsy findings and clinical experience in chronically dialyzed patients. Trans. Amer. SOC. Artif. Intern. Organs 13:51, Spaulding, W. B. Subacute constrictive uremic pericarditis. Arch. Intern. Med. (Chicago) 119:644, Tsaltas, T. T. Comparison of various methods of : Subjective experiences and laboratory data. Trans. Amer. SOC. Artif. Intern. Organs 13:29, Wacker, W., and Merrill, J. P. Uremic pericarditis in acute and chronic renal failure. J.A.M.A. 156:764, THE ANNALS OF THORACIC SURGERY