BRIEF COMMUNICATIONS
Hemorrhagic Pleural Effusion in Patients Undergoing Chronic Hemodialysis MALCOLM A. GALEN, M.D., STEVEN M. STEINBERG, LCDR, MC, USN, EDMUND G. LOWRIE, M.D., J. MICHAEL LAZARUS, M.D., F.A.C.P., C. L HAMPERS, M.D., and JOHN P. MERRILL, M.D., F.A.C.P., Boston, Massachusetts
Three patients maintained on chronic hemodialysis developed hemorrhagic pleural effusion. The effusions seemed to be solely related to the uremic state, other causes having been excluded. Pulmonary restriction requiring decortication occurred in one patient. We concluded that hemorrhagic pleural effusion may be a complication of uremia in the chronically dialyzed patient and that fibrous pleuritis causing pulmonary restriction may result.
PLEURITIS as a component of the uremic syndrome seems to be well established. The pathologic data of Hoops and Wissler (1) demonstrated fibrinous pleuritis in patients dying of renal failure in the predialysis era. Nidus and associates (2) described 20 episodes of pleural friction rub in 11 azotemic subjects, none of whom had evidence to suggest a cause of pleuritis other than uremia. In four of these, pleural effusion was documented by chest X ray, and in two thoracentesis yielded fluid of high protein content. In four of their patients who died, fibrinous pleuritis was confirmed at autopsy. However, neither of these papers described hemorrhagic pleural fluid, and a review of the literature showed only one other case in which hemorrhagic pleural effusion was described in a uremic patient (3). It was associated with a hemorrhagic pericardial effusion, however. We describe three patients with significant hemorrhagic pleural effusions that seemed to be attributable to the uremic state. Case Histories PATIENT 1
A 52-year-old woman with chronic renal failure secondary to chronic pyelonephritis was transferred to the Peter Bent Brigham Hospital on 6 May 1972. She was azotemic, and physical examination showed findings compatible with a right pleural effusion. Neither a pleural nor a pericardial • From the Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts.
friction rub was audible. Chest X ray confirmed the effusion, and bilateral pleural thickening with pleural calcification on the right was noted. On 16 May 1972 she commenced a program of chronic hemodialysis (6 hours, three times weekly). Diagnostic thoracentesis yielded 50 ml of clear yellow fluid. Data for this and other effusions are shown in Table 1. Complement components 3 and 4 were within normal limits, and testing for antinuclear antibody was negative. Intermediate purified protein derivative and mumps skin tests were both negative. The patient did well until 5 November 1972, when she was hospitalized with a temperature elevation to 38.3 °C [101 °F]. Physical examination was not revealing except for findings consistent with a right pleural effusion. Chest X ray was similar to that procured 6 months earlier. Diagnostic thoracentesis yielded 55 ml of serosanguineous fluid. Two pleural biopsies were obtained, and microscopic examination showed only chronic inflammation. Skin testing with purified protein derivative was again negative, and three sputum cultures and three gastric washings were negative for tubercle bacilli. The patient became afebrile without specific therapy. During the ensuing 8 months she did well. The right pleural effusion persisted despite aggressive hemodialysis that maintained her at the lowest weight at which symptomatic, postural hypotension was avoided. On 10 July 1973 she was rehospitalized for cellulitis of her right leg. Pleural effusion was again noted, and a repeat diagnostic thoracentesis was done. Two hundred millilitres of serosanguineous fluid were aspirated. The cellulitis cleared with conservative management and antibiotic therapy. She remains on chronic hemodialysis with persistent right pleural effusion that continues to vary in size from time to time. PATIENT 2
A 62-year-old man with chronic renal failure of uncertain cause was transferred to the hospital for chronic hemodialysis in May 1971. Blood urea nitrogen (BUN) was 201 mg/100 ml, serum creatinine was 13.5 mg/100 ml, and thrice weekly coil dialysis was begun. A left pleural
Annals of Internal Medicine 82:359-361, 1975
Downloaded From: https://annals.org/ by a Universite Laval Biblioteque User on 08/05/2017
359
Table 1. Blood and Pleural Fluid Values at Each Evaluation*
Patient
Date
Blood f BUN
Creatinine
mg/100 ml 1
2
3
May 1972 November 1972 July 1973 January 1972 November 1972 December 1972 July 1972 November 1972
150 30 45 40 40 50 59 60
12.0 6.5 6.3 9.0 6.3 6.5 7.5 13.5
Pleural Fluid Hematocrit
Leukocytes
%
no./mm3
1 3.0 3.5 2.0 2.0 2.5 4.5 4.0
275 300
Lymphocytes
—
100 404
65| 95
—
— — —
—
Protein
Glucose
LDH
Amylase
g/100 ml
mg/100 ml
15 50
3.5 3.3
116 160
158 86
—
— lit
—
—
—
—
2.9
150
177
38
— — — —
— — — —
— — — —
— — — —
% 15 50
—
100
Polymorphocytes
5
— — —
U/ml 50
* Smears and cultures of the pleural fluid for both pyogenic organisms and tubercle bacillus as well as cytologic examination were done after each thoracentesis. All were negative. BUN = blood urea nitrogen; LDH = lactic dehydrogenase. t Predialysis values. t Plus 24% monocytes.
effusion was first noted on routine chest X ray in January 1972. This effusion cleared with dialysis-induced dehydration. In November 1972, however, the left pleural effusion reappeared and was refractory to aggressive hemodialysis. He was admitted to the hospital, and physical examination showed only a large left pleural effusion. Neither pericardial nor pleural friction rubs were heard. Chest X ray showed the effusion, and thoracentesis yielded 1600 ml of serosanguineous fluid (Table 1). Repeat thoracentesis with pleural biopsy yielded 1100 ml of serosanguineous fluid. Two further pleural biopsies were subsequently obtained. Microscopic examination of the pleural specimens showed mesothelial cell hyperplasia, cellular fibrosis, and chronic inflammation. Intermediate tuberculin skin test was negative, as was testing for antinuclear antibody. The patient was discharged, but approximately 1 month later he again began to accumulate a left pleural effusion. Outpatient thoracentesis was done, and 1100 ml of serosanguineous fluid were aspirated. Subsequently, accumulation of pleural effusion was less rapid, but marked pleural thickening persisted. The patient remained otherwise clinically well until July 1973, when he died suddenly at home. Postmortem examination was denied. PATIENT 3
A 26-year-old man with chronic renal failure due to chronic pyelonephritis was referred to the hospital in May 1971 with a BUN of 144 mg/100 ml and a creatinine of 13.4 mg/100 ml. On 29 May 1971 thrice weekly, 6-hour hemodialysis was begun. His course was complicated by frequent episodes of dietary indiscretion, with marked fluid overload resulting in congestive heart failure on several occasions. Bilateral pleural effusions were associated with heart failure on at least two occasions. These cleared with aggressive dehydration dialysis, however. On 21 July 1972 he was hospitalized after having gained 5 kg during a 1-week period despite aggressive hemodialysis. Examination showed a pulsus paradoxus of 10 mm Hg, neck vein distention, negative Kussmaul's sign, and bilateral pleural effusions. A three-component pericardial friction rub was audible. Chest X ray showed a large right 360
pleural effusion as well as a smaller left pleural effusion and marked pulmonary vascular engorgement. Echocardiogram suggested a moderate pericardial effusion. Rightsided thoracentesis yielded 800 ml of serosanguineous fluid. Chemical analysis of this fluid was not done because of a laboratory error. Testing for antinuclear antibody and lupus erythematosus cell preparation were negative. Therapy was begun with fluid restriction and daily hemodialysis using regional heparinization. However, during the ensuing 7 days the patient developed signs of pericardial tamponade as well as complete immobility of the right hemithorax and increasing effusion. Pulmonary function studies showed marked decrease in all volumes, including the vital capacity, which was 20% of the predicted volume. Attempts to relieve compression by thoracentesis and pericardiocentesis were unsuccessful, so we believed surgical intervention was indicated. At thoracotomy, the right parietal pleural was markedly thickened, and 1500 ml of organizing clot were removed from the right hemithorax. The visceral pleura was markedly thickened, causing severe compression of the underlying pulmonary tissue. Pleural decortication was done, and pathologic examination showed fibrinous and fibrous pleuritis with acute and chronic inflammation. Culture of the fluid obtained at thoracotomy was sterile. Pericardiectomy was also done, and pathologic changes identical to those noted in the pleura were found. The patient did well until 28 November 1972 when he developed a cough and temperature of 38.9 °C [102 °F]. There was no history of trauma. Physical examination showed findings compatible with a left pleural effusion. Chest X ray confirmed the presence of a large, loculated, left pleural effusion. Thoracentesis was done; however, only 10 ml of serosanguineous fluid with a hematocrit of 4% were obtained. A left thoracotomy was done, and the visceral and parietal pleura were markedly thickened. A large, organized hematoma was removed. Pathologic examination of the tissue showed dense fibrosis, granulation tissue, and organizing hematoma. Postoperatively the patient did well. In January 1974 the patient received a kidney transplant, but he died after the operation. At postmortem examination the thorax showed marked fibrous adhesions. No effusion was present.
March 1975 • Annals of Internal Medicine • Volume 82 • Number 3
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Discussion
The usual causes of hemorrhagic pleural effusion include pulmonary infarction, malignancy, pneumonitis, tuberculosis, and, in some instances, congestive heart failure. Extensive examination of our patients seems to have ruled these out. Although Patient 3 did manifest congestive heart failure secondary to fluid overload, the magnitude of his effusion seemed to be disproportionate to the degree of heart failure. Also, his second episode of hemothorax was not associated with congestive heart failure. Pericarditis with effusion, pleuritis with effusion, and the more recently described ascites (4, 5) establish polyserositis to be related to the uremic syndrome. Late sequels of uremic pericarditis include a subacute, constrictive pericarditis occurring within several weeks of an acute episode of uremic pericarditis (6-8) as well as chronic constrictive pericarditis (8, 9 ) . Since fibrothorax and pulmonary restriction are a well-recognized complication of hemothorax ( 1 0 ) , it is not surprising that constriction of the lung (analogous to the constriction of the heart found in chronic constrictive pericarditis) could occur as a consequence of uremic, hemorrhagic pleuritis. As with uremic, constrictive pericarditis (11, 12), surgical intervention may be required in some patients with persistent uremic hemothorax if pleural restriction and compromised pulmonary function occur. These three patients showed a rather wide spectrum of severity. Patient 1 had a chronic course of illness with small effusions that were clinically insignificant although distressing to the physicians charged with her care. At the opposite extreme, Patient 3 had a very acute course of illness with restriction of his entire right lung requiring prompt surgical intervention and decortication. Experience with the treatment of uremic pleuritis and pleural effusion indicates that pleuritic pain usually responds promptly to hemodialysis but that effusions may take several weeks to resolve ( 1 3 ) . In these three patients, however, dialysis did not effect significant improvement, although Patients 1 and 2 did achieve stabilization, if not resolution, of their effusions. Pleural effusion persisted even though patients were dialyzed to maintain the minimum weight at which hemodynamic stability was maintained. Why there was blood in the pleural effusions of these patients cannot be ascertained with certainty. However, it is likely that the use of heparin, required for dialysis, in patients with fibrinous uremic pleuritis can lead to bleeding within the pleural space. For example, Patient 1 had a non-
hemorrhagic effusion that subsequently became bloody after she had been on hemodialysis. The observation that virtually all pericardial effusions in dialyzed patients are hemorrhagic in nature (14, 15) supports the contention that heparin may be an important factor in hemorrhagic pleural effusions. Regional heparinization should be considered in patients undergoing hemodialysis in whom uremic pleuritis is established. In addition, one must watch for the development of pulmonary constriction in patients undergoing hemodialysis who have had recurrent hemorrhagic pleuritis. ACKNOWLEDGMENTS: Grant support: grants AM05700-01 and AM05700-02 from the National Institutes of Health. Received 28 June 1974; revision accepted 17 September 1974. • Requests for reprints should be addressed to Edmund G. Lowrie, M.D., Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, MA 02115. References 1. HOOPS HC, WISSLER RW: Uremic pneumonitis. Am J Pathol 31:261-273, 1955 2. NIDUS
BD,
MATALON
R,
CANTACUZINO
D,
et
al:
Uremic
pleuritis—a clinicopathological entity. N Engl J Med 281:255256, 1969 3. MARKETOS S, SARKAS A, MERIKAS G: Haemorrhagic pericardial
and pleural effusion in chronic uraemia. Med J Aust 1:637-639, 1964 4. SINGH S, MITRA S, BERMAN L: Ascites in patients on mainten-
ance hemodialysis. Nephron 12:114-120, 1974 5. MAHONEY
J, PINGGERA W, HOLMES
J, et al: Ascites during
maintenance hemodialysis, in Abstracts, Fifth International Congress of Nephrology, vol. 5. Basel, S. Karger AG, 1972, p. 64 6. SPAULDING WB: Subacute constrictive uremic pericarditis. Arch Intern Med 119:644-647, 1967 7. REYMAN TA: Subacute constrictive uremic pericarditis. Am J Med 46:972-975, 1969 8. COMTY CM, COHEN SL, SHAPIRO FL: Pericarditis in chronic
uremia and its sequels. Ann Intern Med 75:173-183, 1971 9. LINDSAY J JR, CRAWLEY IS, CALLAWAY GM JR: Chronic con-
strictive pericarditis following uremic hemopericardium. Am Heart J 79:390-395, 1970 10. DRAPANAS T, LITWIN MS: Trauma: management of the acutely injured patient, in Textbook of Surgery, edited by SABISTON DC. Philadelphia, W. B. Saunders Co., 1972, p. 369 11. ESMOND WG, LEE YC, HERNANDEZ F: Successful pericardectomy
in chronic constrictive uremic pericarditis. South Med J 64:533536,1971 12. NICKEY WA, CHINITZ JL, FLYNN JJ, et al: Surgical correction
of uremic constrictive pericarditis. Ann Intern Med 75:227-229, 1971 13. HAMPERS CL, SCHUPAK E, LOWRIE EG, et al (editors): Long-
Term Hemodialysis: The Management of the Patient with Chronic Renal Failure, 2nd ed. New York, Grune & Stratton, 1973, p. 83 14. BEAUDRY C, NAKAMOTO S, KOLFF WJ: Uremic pericarditis and
cardiac tamponade in chronic renal failure. Ann Intern Med 64:990-995, 1966 15. HAGER EB: Clinical observations on five patients with uremic pericardia. N Engl J Med 273:304-308, 1965
Galen et al. • Pleural Effusion in Hemodialysis
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361
Hemorrhagic Pleural Effusion in Patients Undergoing Chronic Hemodialysis MALCOLM A. GALEN, M.D., STEVEN M. STEINBERG, LCDR, MC, USN, EDMUND G. LOWRIE, M.D., J. MICHAEL LAZARUS, M.D., F.A.C.P., C. L HAMPERS, M.D., and JOHN P. MERRILL, M.D., F.A.C.P., Boston, Massachusetts
Three patients maintained on chronic hemodialysis developed hemorrhagic pleural effusion. The effusions seemed to be solely related to the uremic state, other causes having been excluded. Pulmonary restriction requiring decortication occurred in one patient. We concluded that hemorrhagic pleural effusion may be a complication of uremia in the chronically dialyzed patient and that fibrous pleuritis causing pulmonary restriction may result.
PLEURITIS as a component of the uremic syndrome seems to be well established. The pathologic data of Hoops and Wissler (1) demonstrated fibrinous pleuritis in patients dying of renal failure in the predialysis era. Nidus and associates (2) described 20 episodes of pleural friction rub in 11 azotemic subjects, none of whom had evidence to suggest a cause of pleuritis other than uremia. In four of these, pleural effusion was documented by chest X ray, and in two thoracentesis yielded fluid of high protein content. In four of their patients who died, fibrinous pleuritis was confirmed at autopsy. However, neither of these papers described hemorrhagic pleural fluid, and a review of the literature showed only one other case in which hemorrhagic pleural effusion was described in a uremic patient (3). It was associated with a hemorrhagic pericardial effusion, however. We describe three patients with significant hemorrhagic pleural effusions that seemed to be attributable to the uremic state. Case Histories PATIENT 1
A 52-year-old woman with chronic renal failure secondary to chronic pyelonephritis was transferred to the Peter Bent Brigham Hospital on 6 May 1972. She was azotemic, and physical examination showed findings compatible with a right pleural effusion. Neither a pleural nor a pericardial • From the Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts.
friction rub was audible. Chest X ray confirmed the effusion, and bilateral pleural thickening with pleural calcification on the right was noted. On 16 May 1972 she commenced a program of chronic hemodialysis (6 hours, three times weekly). Diagnostic thoracentesis yielded 50 ml of clear yellow fluid. Data for this and other effusions are shown in Table 1. Complement components 3 and 4 were within normal limits, and testing for antinuclear antibody was negative. Intermediate purified protein derivative and mumps skin tests were both negative. The patient did well until 5 November 1972, when she was hospitalized with a temperature elevation to 38.3 °C [101 °F]. Physical examination was not revealing except for findings consistent with a right pleural effusion. Chest X ray was similar to that procured 6 months earlier. Diagnostic thoracentesis yielded 55 ml of serosanguineous fluid. Two pleural biopsies were obtained, and microscopic examination showed only chronic inflammation. Skin testing with purified protein derivative was again negative, and three sputum cultures and three gastric washings were negative for tubercle bacilli. The patient became afebrile without specific therapy. During the ensuing 8 months she did well. The right pleural effusion persisted despite aggressive hemodialysis that maintained her at the lowest weight at which symptomatic, postural hypotension was avoided. On 10 July 1973 she was rehospitalized for cellulitis of her right leg. Pleural effusion was again noted, and a repeat diagnostic thoracentesis was done. Two hundred millilitres of serosanguineous fluid were aspirated. The cellulitis cleared with conservative management and antibiotic therapy. She remains on chronic hemodialysis with persistent right pleural effusion that continues to vary in size from time to time. PATIENT 2
A 62-year-old man with chronic renal failure of uncertain cause was transferred to the hospital for chronic hemodialysis in May 1971. Blood urea nitrogen (BUN) was 201 mg/100 ml, serum creatinine was 13.5 mg/100 ml, and thrice weekly coil dialysis was begun. A left pleural
Annals of Internal Medicine 82:359-361, 1975
Downloaded From: https://annals.org/ by a Universite Laval Biblioteque User on 08/05/2017
359
Table 1. Blood and Pleural Fluid Values at Each Evaluation*
Patient
Date
Blood f BUN
Creatinine
mg/100 ml 1
2
3
May 1972 November 1972 July 1973 January 1972 November 1972 December 1972 July 1972 November 1972
150 30 45 40 40 50 59 60
12.0 6.5 6.3 9.0 6.3 6.5 7.5 13.5
Pleural Fluid Hematocrit
Leukocytes
%
no./mm3
1 3.0 3.5 2.0 2.0 2.5 4.5 4.0
275 300
Lymphocytes
—
100 404
65| 95
—
— — —
—
Protein
Glucose
LDH
Amylase
g/100 ml
mg/100 ml
15 50
3.5 3.3
116 160
158 86
—
— lit
—
—
—
—
2.9
150
177
38
— — — —
— — — —
— — — —
— — — —
% 15 50
—
100
Polymorphocytes
5
— — —
U/ml 50
* Smears and cultures of the pleural fluid for both pyogenic organisms and tubercle bacillus as well as cytologic examination were done after each thoracentesis. All were negative. BUN = blood urea nitrogen; LDH = lactic dehydrogenase. t Predialysis values. t Plus 24% monocytes.
effusion was first noted on routine chest X ray in January 1972. This effusion cleared with dialysis-induced dehydration. In November 1972, however, the left pleural effusion reappeared and was refractory to aggressive hemodialysis. He was admitted to the hospital, and physical examination showed only a large left pleural effusion. Neither pericardial nor pleural friction rubs were heard. Chest X ray showed the effusion, and thoracentesis yielded 1600 ml of serosanguineous fluid (Table 1). Repeat thoracentesis with pleural biopsy yielded 1100 ml of serosanguineous fluid. Two further pleural biopsies were subsequently obtained. Microscopic examination of the pleural specimens showed mesothelial cell hyperplasia, cellular fibrosis, and chronic inflammation. Intermediate tuberculin skin test was negative, as was testing for antinuclear antibody. The patient was discharged, but approximately 1 month later he again began to accumulate a left pleural effusion. Outpatient thoracentesis was done, and 1100 ml of serosanguineous fluid were aspirated. Subsequently, accumulation of pleural effusion was less rapid, but marked pleural thickening persisted. The patient remained otherwise clinically well until July 1973, when he died suddenly at home. Postmortem examination was denied. PATIENT 3
A 26-year-old man with chronic renal failure due to chronic pyelonephritis was referred to the hospital in May 1971 with a BUN of 144 mg/100 ml and a creatinine of 13.4 mg/100 ml. On 29 May 1971 thrice weekly, 6-hour hemodialysis was begun. His course was complicated by frequent episodes of dietary indiscretion, with marked fluid overload resulting in congestive heart failure on several occasions. Bilateral pleural effusions were associated with heart failure on at least two occasions. These cleared with aggressive dehydration dialysis, however. On 21 July 1972 he was hospitalized after having gained 5 kg during a 1-week period despite aggressive hemodialysis. Examination showed a pulsus paradoxus of 10 mm Hg, neck vein distention, negative Kussmaul's sign, and bilateral pleural effusions. A three-component pericardial friction rub was audible. Chest X ray showed a large right 360
pleural effusion as well as a smaller left pleural effusion and marked pulmonary vascular engorgement. Echocardiogram suggested a moderate pericardial effusion. Rightsided thoracentesis yielded 800 ml of serosanguineous fluid. Chemical analysis of this fluid was not done because of a laboratory error. Testing for antinuclear antibody and lupus erythematosus cell preparation were negative. Therapy was begun with fluid restriction and daily hemodialysis using regional heparinization. However, during the ensuing 7 days the patient developed signs of pericardial tamponade as well as complete immobility of the right hemithorax and increasing effusion. Pulmonary function studies showed marked decrease in all volumes, including the vital capacity, which was 20% of the predicted volume. Attempts to relieve compression by thoracentesis and pericardiocentesis were unsuccessful, so we believed surgical intervention was indicated. At thoracotomy, the right parietal pleural was markedly thickened, and 1500 ml of organizing clot were removed from the right hemithorax. The visceral pleura was markedly thickened, causing severe compression of the underlying pulmonary tissue. Pleural decortication was done, and pathologic examination showed fibrinous and fibrous pleuritis with acute and chronic inflammation. Culture of the fluid obtained at thoracotomy was sterile. Pericardiectomy was also done, and pathologic changes identical to those noted in the pleura were found. The patient did well until 28 November 1972 when he developed a cough and temperature of 38.9 °C [102 °F]. There was no history of trauma. Physical examination showed findings compatible with a left pleural effusion. Chest X ray confirmed the presence of a large, loculated, left pleural effusion. Thoracentesis was done; however, only 10 ml of serosanguineous fluid with a hematocrit of 4% were obtained. A left thoracotomy was done, and the visceral and parietal pleura were markedly thickened. A large, organized hematoma was removed. Pathologic examination of the tissue showed dense fibrosis, granulation tissue, and organizing hematoma. Postoperatively the patient did well. In January 1974 the patient received a kidney transplant, but he died after the operation. At postmortem examination the thorax showed marked fibrous adhesions. No effusion was present.
March 1975 • Annals of Internal Medicine • Volume 82 • Number 3
Downloaded From: https://annals.org/ by a Universite Laval Biblioteque User on 08/05/2017
Discussion
The usual causes of hemorrhagic pleural effusion include pulmonary infarction, malignancy, pneumonitis, tuberculosis, and, in some instances, congestive heart failure. Extensive examination of our patients seems to have ruled these out. Although Patient 3 did manifest congestive heart failure secondary to fluid overload, the magnitude of his effusion seemed to be disproportionate to the degree of heart failure. Also, his second episode of hemothorax was not associated with congestive heart failure. Pericarditis with effusion, pleuritis with effusion, and the more recently described ascites (4, 5) establish polyserositis to be related to the uremic syndrome. Late sequels of uremic pericarditis include a subacute, constrictive pericarditis occurring within several weeks of an acute episode of uremic pericarditis (6-8) as well as chronic constrictive pericarditis (8, 9 ) . Since fibrothorax and pulmonary restriction are a well-recognized complication of hemothorax ( 1 0 ) , it is not surprising that constriction of the lung (analogous to the constriction of the heart found in chronic constrictive pericarditis) could occur as a consequence of uremic, hemorrhagic pleuritis. As with uremic, constrictive pericarditis (11, 12), surgical intervention may be required in some patients with persistent uremic hemothorax if pleural restriction and compromised pulmonary function occur. These three patients showed a rather wide spectrum of severity. Patient 1 had a chronic course of illness with small effusions that were clinically insignificant although distressing to the physicians charged with her care. At the opposite extreme, Patient 3 had a very acute course of illness with restriction of his entire right lung requiring prompt surgical intervention and decortication. Experience with the treatment of uremic pleuritis and pleural effusion indicates that pleuritic pain usually responds promptly to hemodialysis but that effusions may take several weeks to resolve ( 1 3 ) . In these three patients, however, dialysis did not effect significant improvement, although Patients 1 and 2 did achieve stabilization, if not resolution, of their effusions. Pleural effusion persisted even though patients were dialyzed to maintain the minimum weight at which hemodynamic stability was maintained. Why there was blood in the pleural effusions of these patients cannot be ascertained with certainty. However, it is likely that the use of heparin, required for dialysis, in patients with fibrinous uremic pleuritis can lead to bleeding within the pleural space. For example, Patient 1 had a non-
hemorrhagic effusion that subsequently became bloody after she had been on hemodialysis. The observation that virtually all pericardial effusions in dialyzed patients are hemorrhagic in nature (14, 15) supports the contention that heparin may be an important factor in hemorrhagic pleural effusions. Regional heparinization should be considered in patients undergoing hemodialysis in whom uremic pleuritis is established. In addition, one must watch for the development of pulmonary constriction in patients undergoing hemodialysis who have had recurrent hemorrhagic pleuritis. ACKNOWLEDGMENTS: Grant support: grants AM05700-01 and AM05700-02 from the National Institutes of Health. Received 28 June 1974; revision accepted 17 September 1974. • Requests for reprints should be addressed to Edmund G. Lowrie, M.D., Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, MA 02115. References 1. HOOPS HC, WISSLER RW: Uremic pneumonitis. Am J Pathol 31:261-273, 1955 2. NIDUS
BD,
MATALON
R,
CANTACUZINO
D,
et
al:
Uremic
pleuritis—a clinicopathological entity. N Engl J Med 281:255256, 1969 3. MARKETOS S, SARKAS A, MERIKAS G: Haemorrhagic pericardial
and pleural effusion in chronic uraemia. Med J Aust 1:637-639, 1964 4. SINGH S, MITRA S, BERMAN L: Ascites in patients on mainten-
ance hemodialysis. Nephron 12:114-120, 1974 5. MAHONEY
J, PINGGERA W, HOLMES
J, et al: Ascites during
maintenance hemodialysis, in Abstracts, Fifth International Congress of Nephrology, vol. 5. Basel, S. Karger AG, 1972, p. 64 6. SPAULDING WB: Subacute constrictive uremic pericarditis. Arch Intern Med 119:644-647, 1967 7. REYMAN TA: Subacute constrictive uremic pericarditis. Am J Med 46:972-975, 1969 8. COMTY CM, COHEN SL, SHAPIRO FL: Pericarditis in chronic
uremia and its sequels. Ann Intern Med 75:173-183, 1971 9. LINDSAY J JR, CRAWLEY IS, CALLAWAY GM JR: Chronic con-
strictive pericarditis following uremic hemopericardium. Am Heart J 79:390-395, 1970 10. DRAPANAS T, LITWIN MS: Trauma: management of the acutely injured patient, in Textbook of Surgery, edited by SABISTON DC. Philadelphia, W. B. Saunders Co., 1972, p. 369 11. ESMOND WG, LEE YC, HERNANDEZ F: Successful pericardectomy
in chronic constrictive uremic pericarditis. South Med J 64:533536,1971 12. NICKEY WA, CHINITZ JL, FLYNN JJ, et al: Surgical correction
of uremic constrictive pericarditis. Ann Intern Med 75:227-229, 1971 13. HAMPERS CL, SCHUPAK E, LOWRIE EG, et al (editors): Long-
Term Hemodialysis: The Management of the Patient with Chronic Renal Failure, 2nd ed. New York, Grune & Stratton, 1973, p. 83 14. BEAUDRY C, NAKAMOTO S, KOLFF WJ: Uremic pericarditis and
cardiac tamponade in chronic renal failure. Ann Intern Med 64:990-995, 1966 15. HAGER EB: Clinical observations on five patients with uremic pericardia. N Engl J Med 273:304-308, 1965
Galen et al. • Pleural Effusion in Hemodialysis
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361
