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Group a streptococcal peritonitis in a patient undergoing continuous ambulatory peritoneal dialysis
d
;;;;Ll&KINASE
BRIEFCLINICALOBSERVATIONS
ROY S. WIENER, M.D. LING S. ONG, M.D. Strong Memorial Hospital Rochester, New York 14642
AND SPLENIC
Thormbolytic agents are now recognized as important drugs but remain associated with hemorrhagic complications. We report an association between administration of streptokinase and spontaneous splenic rupture. A previously healthy 51-year-old woman presented with chest pain and electrocardiographic changes diagnostic of acute anterior myocardial infarction and received 1.5 million units of streptokinase intravenously followed by a heparin infusion. There was no prior history of trauma or hematologic disease. The patient’s condition improved initially, but on the next day, recurrent chest pain, electrocardiographic changes, and hypotension developed. A right heart catheterization revealed a pulmonary capillary wedge pressure of 3 mm Hg, and large volumes of intravenous fluid were given with improvement. She was then transferred for emergent coronary angiography, which demonstrated total occlusion of a large left anterior descending artery and a minimal disease of the other coronary vessels. At this point, increasing abdominal distension was noted, and the blood sample drawn at the start of catheterization was reported to have a hemoglobin level of 3.8 g/dl. Electromechanical dissociation ensued, and the patient died despite full attempts at resuscitation. At necropsy, there were two liters of unclotted blood in the peritoneal cavity and the splenic capsule was ruptured. The spleen weighed 76 g and was normal by microscopic examination. The heart showed a large anteroseptal myocardial infarction. Spontaneous splenic rupture is rare and usually occurs in the setting of infection or hematologic disease [l]. There is a previous report of spontaneous splenic rupture associated with accidental overdosage of oral warfarin [2], but to our knowledge this is the first reported case in a patient receiving streptokinase. We believe that this diagnosis should be considered when evidence of abdominal catastrophe exists after administration of thrombolytic therapy.
1. Schwartz SI: Spleen, In: Schwartz SI, Shires GT, Spencer FC, Storer EH, eds. Principles of surgery, 4th ed. New York: McGraw-Hill, 1984; 1377. 2. Soyer MT, Merck DE, Aldrete JS: Spontaneous rupture of the spleen. An unusual complication of anticoagulant therapy. Arch Surg 1976; 111: 610. Submitted
November
11, 1988, and accepted November 17, 1988
GROUPA STREPTOCOCCAL PERITONITISIN A PATIENT UNDERGOING CONTINUOUS AMBULATORYPERITONEAL DIALYSIS Peritonitis remains a common complication in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) [l]. Organisms that are commonly associated with CAPD peritonitis include staphylococci, streptococci, Enterobacteriaceae, and Pseudomonas species [l-4]. We report what we believe to be the first reported case of peritonitis caused by a group A streptococcus in a CAPD-treated patient. A 55-year-old white woman with end-stage renal disease secondary to amyloidosis had been undergoing uncomplicated CAPD for 16 months. One week prior to admission, she developed generalized malaise, a non-productive cough, and undocumented fever without chills or sore throat. Shortly thereafter, she developed a fine, macular, pruritic rash on her trunk and abdomen that resolved over the next two to three days and subsequently desquamated. On the day of admission, she awoke with severe epigastric and left upper quadrant pain that worsened through the morning. The peritoneal fluid was cloudy. Her temperature was 38.9”C, with shaking chills, hypotension, and onset of nausea and vomiting. On evaluation she was hypotensive, and her abdomen was firm and distended with generalized tenderness and rebound. The CAPD catheter exit site and tunnel were not erythematous. She had a white blood cell count of 49,800/mm3 with a marked left shift. The cloudy dialysate had a white blood cell count of 59,000/ February
1989
mm3 with 9’7 percent neutrophils. The dialysate was concentrated by centrifugation. Gram stain of the sediment revealed many neutrophils and many gram-positive cocci suggestive of streptococci. Culture grew many mucoid beta-hemolytic group A streptococci identified by standard techniques. The patient was treated with vancomycin intraperitoneally. She showed clinical improvement, but had some residual abdominal tenderness. Repeat analysis of her peritoneal fluid on the sixth hospital day revealed a white blood cell count of 1,150/mm3 with 71 percent neutrophils and a negative culture result. She was discharged to complete a course of intraperitoneal vancomycin on an outpatient basis. Analysis of the group A streptococcus revealed that it produced large amounts of streptococcal pyrogenic exotoxin type C and hyaluranic acid and was M type 18. Serologic analysis revealed that the patient’s acute and convalescent antibody titers against streptococcal pyrogenic exotoxin type C were less than or equal to 1:lO and 1:20, respectively. These analyses were performed as previously described [VI. This is the first reported case of definitive group A streptococcal peritonitis in a patient undergoing CAPD. Other studies have reported that “Streptococcus species” are causes of peritonitis in CAPDtreated patients but none mention group A streptococcus as a specific etiology [4,7]. An interesting aspect of this case was the appearance of a desquamating rash of unclear pathogenesis, which occurred shortly before the onset of peritonitis. It is possible that our patient may have had a syndrome similar to toxic shock or scarlet fever prior to the development of frank peritonitis. Toxic shock syndrome with a desquamating rash has been described in a patient undergoing CAPD who had peritonitis caused by Staphylococcus aureus [8]. Group A streptococci that produce streptococcal pyrogenie exotoxin can cause scarlet fever and a toxic shock-like syndrome [9], one symptom of which is the development of a desquamating rash.
The American
Journal
of Medicine
Volume
86
249
BRIEF CLINICAL OBSERVATIONS
Analysis of the group A streptococcus from our patient revealed that it was a high producer of streptococcal pyrogenic exotoxin type C and hyaluronic acid and was M type 18. Other strains of group A streptococci that have been isolated from recent scarlet fever or rheumatic fever outbreaks have shown a similar pattern [9]. In addition, serologic analysis of acute and convalescent sera from our patient, although inconclusive, suggested a weak antibody response to streptococcal pyrogenic exotoxin type C and possible in uiuo production of the toxin. A possible scenario is that the patient became infected with group A streptococci one week prior to admission. This infection did not produce pharyngitis but was significant enough to result in fever, malaise, and a cough. During this illness, it is possible that sufficient streptococcal pyrogenic exotoxin may have been produCed to cause a mild form of scarlet fever or toxic shock with resultant desquamating rash. A transient bacteremia may have occurred with seeding of the peritoneal cavity, resulting in peritonitis. This hypothesis is supported by the clinical findings of skin rash and desquamation, as well as the microbiologic findings that the group A streptococcus was a streptococcal pyrogenie exotoxin producer, M type 18, and a hyperproducer of hyaluranic acid, and that the toxin may have been produced in vivo as evidenced by a rise in the patient’s antibody titer. SEPHENJ. CAVALIERI,~~.D. Creighton University School of Medicine and St. Joseph Hospital Omaha, Nebraska JEANM. ALLAIS,M.D. Creighton University School of Medicine Omaha, Nebraska PATRICKM.SCHLIEVERT,P~.D. University of Minnesota Medical School Minneapolis, Minnesota DAVIDL. DWORZACK,M.D. Creighton University School of Medicine Omaha, Nebraska RICHARDB. CLARK,P~.D. Creighton University School of
Medicine and
St. Joseph Hospital Omaha, Nebraska 1. Grefbera N. Danielson BG. Nilsson P: Peritonitis in patients on continuous ambulatory peritoneal dialysis. A changing scene. Stand J infect Dis 1984; 16:
250
February
1989
The American
Journal
187-193. 2. Rubin J, Wallace WA, Taylor HM, et al: Peritonitis during continuous ambulatory peritoneal dialysis. Ann Intern Med 1980; 92: 7-13. 3. Rubin SJ: Continuous ambulatory peritoneal dialysis: dialysate fluid cultures. Clin Microbial Newslett 1984; 6: 3-5. 4. Vas SI: Microbiologic aspects of chronic ambulatory peritoneal dialysis. Kidney Int 1983; 23: 83-92. 5. Blomster-Hautomaa DA, Novick RP, Schlievert PM: Localization of biologic functions of toxic shock syndrome toxin-l by use of monoclonal antibodies and cyanogen bromide-generated toxin fragments. J lmmunol 1986; 137: 3572-3576. 6. Schlievert PM, Bettin KM, Watson DW: Purification and characterization of group A streptococcal pyrogenie exotoxin type C. Infect lmmun 1977; 16: 673679. 7. Gokal R, Ramos JM, Francis DMA, et al: Peritonitis in continuous ambulatory peritoneal dialysis. Laboratory and clinical studies. Lancet 1982; II: 1388-1391. 8. Gregory MC, Duffy DP: Toxic shockfollowingstaphylococcal peritonitis. Clin Nephrol 1983; 20: lOl104. 9. Cone LA, Woodard DR, Schlievert PM, Tomory GM: Clinical and bacteriolonic observations of a toxic shock-like syndrome &e to Sfrepfococcus pyogenes. N Engl J Med 1987; 317: 146-149. Submitted January 22,1988,
and accepted in revised form December 9, 1988
UNILATERALHYPERLUCENT LUNGDUETO INTERSTITIAL PULMONARYHEMORRHAGE FROMAORTICDISSECTION Timely recognition of aortic dissection is essential because appropriately instituted medical and surgical therapy will improve the prognosis. Severe chest pain is usually the initial clue to this diagnosis. Chest radiography is a sensitive diagnostic test for aortic dissection [l]. Radiographic abnormalities, e.g., widened mediastinum, shift of mediastinal structures, aortic dilatation, displacement of aortic intima1 calcifications, blurring of the aortic knob, and pleural effusion, are found in a very high percentage of cases. However, aortic dissection may cause atypical radiographic findings that, unfortunately, can divert attention from this diagnosis. We recently encountered a patient with aortic dissection who had a unilateral hyperlucent lung on chest radiography. Obstruction of the right pulmonary artery has been rarely described in aortic dissection from mediastinal hemorrhage [2,3]. In our patient, the left lung was involved and mediastinal abnormalities did not account for the pulmonary vascular obstruction. Instead, hemorrhage tracked along the bronchovascular interstitium and diffusely compressed the pulmonary circulation within the left lung. This type of presentation of Medicine
Volume
86
has not, to our knowledge, been previously described and demonstrates important physiologicradiologic principles. A 75-year-old white male smoker presented with intense, transient, non-radiating substernal chest pain and diaphoresis, He had no history of similar previous chest pain, cardiac disease, hypertension, or diabetes. His pulse was 88 beats/minute, blood pressure was 140/88 mm Hg, and results of cardiac and peripheral vascular examinations were unremarkable. There were bilateral end-expiratory wheezes, but no splinting or chest tenderness. Electrocardiographic findings and cardiac enzyme levels were unremarkable. Chest radiography showed no infiltrates, pleural fluid, or mediastinal abnormalities, but suggested reduced left lung vascularity (Figure 1). Ventilation-perfusion lung scanning (Figure 2) confirmed decreased left lung perfusion without focal defects and also revealed delayed 133xenon left lung washout. Following admission, fatal cardiopulmonary arrest occurred with electromechanical dissociation. At autopsy, a thoracic aortic dissection 3 cm above the aortic valve was seen. Medial dissection occurred over only a short area; hemorrhage primarily ruptured into the adventitia near the point of intimal tearing. Adventitial hemorrhage caused complete dehiscence of a normal aortic valve and fatal hemopericardium. Hemorrhage also tracked anteriorly into the common adventitia shared by the aorta and pulmonary artery. Bleeding spread along the adventitia of the peripheral pulmonary arteries nearly to the pleura in the left lung (Figure 3). Hemorrhage into the perivascular-bronchial bundle space compressed both the pulmonary arteries and bronchi, explaining both the decreased perfusion and air trapping seen on the ventilation-perfusion scan. There was no evidence of bronchiolitis, pulmonary emboli, intrabronchial tumor, or other pulmonary vascular abnormalities. In this case, recognition of a proximal aortic dissection was hampered by the unusual initial radiographic presentation of unilateral hyperlucent lung. Mediastinal hemorrhage from dissection has been described as compressing the pulmonary artery and causing.
;;;;Ll&KINASE
BRIEFCLINICALOBSERVATIONS
ROY S. WIENER, M.D. LING S. ONG, M.D. Strong Memorial Hospital Rochester, New York 14642
AND SPLENIC
Thormbolytic agents are now recognized as important drugs but remain associated with hemorrhagic complications. We report an association between administration of streptokinase and spontaneous splenic rupture. A previously healthy 51-year-old woman presented with chest pain and electrocardiographic changes diagnostic of acute anterior myocardial infarction and received 1.5 million units of streptokinase intravenously followed by a heparin infusion. There was no prior history of trauma or hematologic disease. The patient’s condition improved initially, but on the next day, recurrent chest pain, electrocardiographic changes, and hypotension developed. A right heart catheterization revealed a pulmonary capillary wedge pressure of 3 mm Hg, and large volumes of intravenous fluid were given with improvement. She was then transferred for emergent coronary angiography, which demonstrated total occlusion of a large left anterior descending artery and a minimal disease of the other coronary vessels. At this point, increasing abdominal distension was noted, and the blood sample drawn at the start of catheterization was reported to have a hemoglobin level of 3.8 g/dl. Electromechanical dissociation ensued, and the patient died despite full attempts at resuscitation. At necropsy, there were two liters of unclotted blood in the peritoneal cavity and the splenic capsule was ruptured. The spleen weighed 76 g and was normal by microscopic examination. The heart showed a large anteroseptal myocardial infarction. Spontaneous splenic rupture is rare and usually occurs in the setting of infection or hematologic disease [l]. There is a previous report of spontaneous splenic rupture associated with accidental overdosage of oral warfarin [2], but to our knowledge this is the first reported case in a patient receiving streptokinase. We believe that this diagnosis should be considered when evidence of abdominal catastrophe exists after administration of thrombolytic therapy.
1. Schwartz SI: Spleen, In: Schwartz SI, Shires GT, Spencer FC, Storer EH, eds. Principles of surgery, 4th ed. New York: McGraw-Hill, 1984; 1377. 2. Soyer MT, Merck DE, Aldrete JS: Spontaneous rupture of the spleen. An unusual complication of anticoagulant therapy. Arch Surg 1976; 111: 610. Submitted
November
11, 1988, and accepted November 17, 1988
GROUPA STREPTOCOCCAL PERITONITISIN A PATIENT UNDERGOING CONTINUOUS AMBULATORYPERITONEAL DIALYSIS Peritonitis remains a common complication in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) [l]. Organisms that are commonly associated with CAPD peritonitis include staphylococci, streptococci, Enterobacteriaceae, and Pseudomonas species [l-4]. We report what we believe to be the first reported case of peritonitis caused by a group A streptococcus in a CAPD-treated patient. A 55-year-old white woman with end-stage renal disease secondary to amyloidosis had been undergoing uncomplicated CAPD for 16 months. One week prior to admission, she developed generalized malaise, a non-productive cough, and undocumented fever without chills or sore throat. Shortly thereafter, she developed a fine, macular, pruritic rash on her trunk and abdomen that resolved over the next two to three days and subsequently desquamated. On the day of admission, she awoke with severe epigastric and left upper quadrant pain that worsened through the morning. The peritoneal fluid was cloudy. Her temperature was 38.9”C, with shaking chills, hypotension, and onset of nausea and vomiting. On evaluation she was hypotensive, and her abdomen was firm and distended with generalized tenderness and rebound. The CAPD catheter exit site and tunnel were not erythematous. She had a white blood cell count of 49,800/mm3 with a marked left shift. The cloudy dialysate had a white blood cell count of 59,000/ February
1989
mm3 with 9’7 percent neutrophils. The dialysate was concentrated by centrifugation. Gram stain of the sediment revealed many neutrophils and many gram-positive cocci suggestive of streptococci. Culture grew many mucoid beta-hemolytic group A streptococci identified by standard techniques. The patient was treated with vancomycin intraperitoneally. She showed clinical improvement, but had some residual abdominal tenderness. Repeat analysis of her peritoneal fluid on the sixth hospital day revealed a white blood cell count of 1,150/mm3 with 71 percent neutrophils and a negative culture result. She was discharged to complete a course of intraperitoneal vancomycin on an outpatient basis. Analysis of the group A streptococcus revealed that it produced large amounts of streptococcal pyrogenic exotoxin type C and hyaluranic acid and was M type 18. Serologic analysis revealed that the patient’s acute and convalescent antibody titers against streptococcal pyrogenic exotoxin type C were less than or equal to 1:lO and 1:20, respectively. These analyses were performed as previously described [VI. This is the first reported case of definitive group A streptococcal peritonitis in a patient undergoing CAPD. Other studies have reported that “Streptococcus species” are causes of peritonitis in CAPDtreated patients but none mention group A streptococcus as a specific etiology [4,7]. An interesting aspect of this case was the appearance of a desquamating rash of unclear pathogenesis, which occurred shortly before the onset of peritonitis. It is possible that our patient may have had a syndrome similar to toxic shock or scarlet fever prior to the development of frank peritonitis. Toxic shock syndrome with a desquamating rash has been described in a patient undergoing CAPD who had peritonitis caused by Staphylococcus aureus [8]. Group A streptococci that produce streptococcal pyrogenie exotoxin can cause scarlet fever and a toxic shock-like syndrome [9], one symptom of which is the development of a desquamating rash.
The American
Journal
of Medicine
Volume
86
249
BRIEF CLINICAL OBSERVATIONS
Analysis of the group A streptococcus from our patient revealed that it was a high producer of streptococcal pyrogenic exotoxin type C and hyaluronic acid and was M type 18. Other strains of group A streptococci that have been isolated from recent scarlet fever or rheumatic fever outbreaks have shown a similar pattern [9]. In addition, serologic analysis of acute and convalescent sera from our patient, although inconclusive, suggested a weak antibody response to streptococcal pyrogenic exotoxin type C and possible in uiuo production of the toxin. A possible scenario is that the patient became infected with group A streptococci one week prior to admission. This infection did not produce pharyngitis but was significant enough to result in fever, malaise, and a cough. During this illness, it is possible that sufficient streptococcal pyrogenic exotoxin may have been produCed to cause a mild form of scarlet fever or toxic shock with resultant desquamating rash. A transient bacteremia may have occurred with seeding of the peritoneal cavity, resulting in peritonitis. This hypothesis is supported by the clinical findings of skin rash and desquamation, as well as the microbiologic findings that the group A streptococcus was a streptococcal pyrogenie exotoxin producer, M type 18, and a hyperproducer of hyaluranic acid, and that the toxin may have been produced in vivo as evidenced by a rise in the patient’s antibody titer. SEPHENJ. CAVALIERI,~~.D. Creighton University School of Medicine and St. Joseph Hospital Omaha, Nebraska JEANM. ALLAIS,M.D. Creighton University School of Medicine Omaha, Nebraska PATRICKM.SCHLIEVERT,P~.D. University of Minnesota Medical School Minneapolis, Minnesota DAVIDL. DWORZACK,M.D. Creighton University School of Medicine Omaha, Nebraska RICHARDB. CLARK,P~.D. Creighton University School of
Medicine and
St. Joseph Hospital Omaha, Nebraska 1. Grefbera N. Danielson BG. Nilsson P: Peritonitis in patients on continuous ambulatory peritoneal dialysis. A changing scene. Stand J infect Dis 1984; 16:
250
February
1989
The American
Journal
187-193. 2. Rubin J, Wallace WA, Taylor HM, et al: Peritonitis during continuous ambulatory peritoneal dialysis. Ann Intern Med 1980; 92: 7-13. 3. Rubin SJ: Continuous ambulatory peritoneal dialysis: dialysate fluid cultures. Clin Microbial Newslett 1984; 6: 3-5. 4. Vas SI: Microbiologic aspects of chronic ambulatory peritoneal dialysis. Kidney Int 1983; 23: 83-92. 5. Blomster-Hautomaa DA, Novick RP, Schlievert PM: Localization of biologic functions of toxic shock syndrome toxin-l by use of monoclonal antibodies and cyanogen bromide-generated toxin fragments. J lmmunol 1986; 137: 3572-3576. 6. Schlievert PM, Bettin KM, Watson DW: Purification and characterization of group A streptococcal pyrogenie exotoxin type C. Infect lmmun 1977; 16: 673679. 7. Gokal R, Ramos JM, Francis DMA, et al: Peritonitis in continuous ambulatory peritoneal dialysis. Laboratory and clinical studies. Lancet 1982; II: 1388-1391. 8. Gregory MC, Duffy DP: Toxic shockfollowingstaphylococcal peritonitis. Clin Nephrol 1983; 20: lOl104. 9. Cone LA, Woodard DR, Schlievert PM, Tomory GM: Clinical and bacteriolonic observations of a toxic shock-like syndrome &e to Sfrepfococcus pyogenes. N Engl J Med 1987; 317: 146-149. Submitted January 22,1988,
and accepted in revised form December 9, 1988
UNILATERALHYPERLUCENT LUNGDUETO INTERSTITIAL PULMONARYHEMORRHAGE FROMAORTICDISSECTION Timely recognition of aortic dissection is essential because appropriately instituted medical and surgical therapy will improve the prognosis. Severe chest pain is usually the initial clue to this diagnosis. Chest radiography is a sensitive diagnostic test for aortic dissection [l]. Radiographic abnormalities, e.g., widened mediastinum, shift of mediastinal structures, aortic dilatation, displacement of aortic intima1 calcifications, blurring of the aortic knob, and pleural effusion, are found in a very high percentage of cases. However, aortic dissection may cause atypical radiographic findings that, unfortunately, can divert attention from this diagnosis. We recently encountered a patient with aortic dissection who had a unilateral hyperlucent lung on chest radiography. Obstruction of the right pulmonary artery has been rarely described in aortic dissection from mediastinal hemorrhage [2,3]. In our patient, the left lung was involved and mediastinal abnormalities did not account for the pulmonary vascular obstruction. Instead, hemorrhage tracked along the bronchovascular interstitium and diffusely compressed the pulmonary circulation within the left lung. This type of presentation of Medicine
Volume
86
has not, to our knowledge, been previously described and demonstrates important physiologicradiologic principles. A 75-year-old white male smoker presented with intense, transient, non-radiating substernal chest pain and diaphoresis, He had no history of similar previous chest pain, cardiac disease, hypertension, or diabetes. His pulse was 88 beats/minute, blood pressure was 140/88 mm Hg, and results of cardiac and peripheral vascular examinations were unremarkable. There were bilateral end-expiratory wheezes, but no splinting or chest tenderness. Electrocardiographic findings and cardiac enzyme levels were unremarkable. Chest radiography showed no infiltrates, pleural fluid, or mediastinal abnormalities, but suggested reduced left lung vascularity (Figure 1). Ventilation-perfusion lung scanning (Figure 2) confirmed decreased left lung perfusion without focal defects and also revealed delayed 133xenon left lung washout. Following admission, fatal cardiopulmonary arrest occurred with electromechanical dissociation. At autopsy, a thoracic aortic dissection 3 cm above the aortic valve was seen. Medial dissection occurred over only a short area; hemorrhage primarily ruptured into the adventitia near the point of intimal tearing. Adventitial hemorrhage caused complete dehiscence of a normal aortic valve and fatal hemopericardium. Hemorrhage also tracked anteriorly into the common adventitia shared by the aorta and pulmonary artery. Bleeding spread along the adventitia of the peripheral pulmonary arteries nearly to the pleura in the left lung (Figure 3). Hemorrhage into the perivascular-bronchial bundle space compressed both the pulmonary arteries and bronchi, explaining both the decreased perfusion and air trapping seen on the ventilation-perfusion scan. There was no evidence of bronchiolitis, pulmonary emboli, intrabronchial tumor, or other pulmonary vascular abnormalities. In this case, recognition of a proximal aortic dissection was hampered by the unusual initial radiographic presentation of unilateral hyperlucent lung. Mediastinal hemorrhage from dissection has been described as compressing the pulmonary artery and causing.