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Splenic abscess following nonoperative management of splenic rupture
Splenic Abscess Following Nonoperative Management of Splenic Rupture By Michael Sands, David Page, and Richard B. Brown Springfield and Boston, Massachusetts 9 A recent case of posttraumatic splenic abscess in a young man following nonoperative management of his splenic rupture is reported. With the recent trend toward nonoperative management of hemodynamicaUy stable splenic rupture, the potential complications of splenic abscess may become more common, In view of the high mortality associated with unrecognized splenic abscess, it is important for the clinician to be aware of this entity. 9 1986 by Grune & Stratton. Inc. INDEX WORDS: Traumatic splenic abscess; abscess; splenic rupture; splenic hematoma.
splenic
PLENIC ABSCESSES are rare clinical entities with significant associated mortality if not recognized. Several comprehensive reviews have summarized the clinical and laboratory findings, therapy, prognosis, and predisposing etiologies, l~ In the largest reviewed series? 17% of splenic abscesses were late sequellae of nonpenetrating abdominal trauma with the majority of the cases from the early literature) In the most recent Mayo Clinic review series of 19 patients, no cases had an underlying history of splenic trauma) The paucity of recent reported cases of posttraumatic splenic abscess may be the result of early splenectomy for traumatic splenic rupture. There is, however, a current surgical trend in both pediatric and adult patients toward the nonoperative management of hemodynamically stable splenic rupture secondary to blunt abdominal trauma in an effort to preserve immunologic splenic function. 6-9 This therapeutic strategy may result in an increase in the number of posttraumatic splenic abscesses.
S
CASE REPORT M.B., a 16-year-old white male, was in good health until February 4, 1984 when he sustained blunt trauma to his left chest while playing football. Persistent left chest and abdominal pain prompted an emergency room visit. Splenic rupture was confirmed by technetium liver/spleen scan. He remained hemodynamica[ly stable, was observed at rest in the hospital for ten days and discharged home on February 16, 1984. On February 20, 1984 he began having fevers to 103 ~ chills,
From the Department of Medicine, Infectious Disease Service, Department of Pathology, Clinical Microbiology, and Division of Surgery, Baystate Medical Center, Springfield, Mass and Tufts University School of Medicine, Boston. Address reprint requests to Michael Sands, MD, Infectious Disease Service, Baystate Medical Center, Springfield, MA O1199. 9 1986 by Grune & Stratton, Inc. 0022-3468/86/2110-0019503.00/0 900
and drenching night sweats associated with increasing left upper quadrant abdominal pain and left shoulder pain exacerbated by coughing. He was readmitted for evaluation, noted to have a WBC of 20,000 with a left shift and stable hemoglobin. A chest x-ray was interpreted as showing a left lower lobe pneumonic process with pleural effusion. He was treated for a "community-acquired pneumonia" with a cephalosporin; however, he continued having night sweats and fevers to 104 ~ Gallium scan and liver/spleen scans were interpreted as consistent with a previous splenic hematoma. Blood cultures were negative. By February 27, 1984, he had lost 17 lb and had continued fever. Pertinent physical findings on examination were limited to percussion dullness and decreased breath sounds at the left chest base posteriorly and left upper quadrant abdominal tenderness with voluntary guarding. On chest x-ray he had an elevated left hemidiaphragm, left lower lobe atelectasis, and a left pleural effusion. He was felt to have a splenic abscess. A C T scan was performed, which demonstrated a hypodense area at the inferior splenic pole containing gas. He received pneumovax and was transferred to Baystate Medical Center for surgery and further management.
RESULTS
Operative Findings The abdomen was opened through a left subcostal incision. The left upper quadrant was filled with a mass of omentum wrapped around the lower pole of the spleen, and stuck to the diaphragmatic surface. There were no free planes of dissection between the omenturn, spleen, diaphragm, and stomach. The splenic flexure was adherent to this inflammatory mass inferiorly. The mass was approached circumferentially, dissecting the spleen and omentum as a unit off the diaphragm initially, then opening the lesser sac. After controlling the splenic vessels, including amputating the distal centimeter of the tail of the pancreas, the mass was removed. The remainder of the pancreas, duodenum, liver, stomach, small bowel, and mesentery were normal. There was a moderate amount of old free intra-abdominal blood. Following splenectomy, the area was copiously irrigated with warm saline. A large sump drain was placed in the most dependent portion of the left upper quadrant and exited through a stab wound laterally. The abdomen was closed in layers with running #2 Dexon. The skin was closed with widely spaced staples and intervening single steristrips. Upon opening the specimen, the lower splenic pole was noted to be extremely soft and necrotic and contained a 2 cm circumscribed organized hematoma. The omentum was tightly plastered to this entire mass. Journal of Pediatric Surgery, Vol 21, No 10 (October), 1986: pp 900-901
POST-TRAUMATIC SPLENIC ABCESS
901
Pathologic Findings The spleen weighed 290 g, was covered with hemorrhagic necrotic fibrofatty tissue, and on section contained a 5 x 4 • 2 cm area of hemorrhagic necrosis. Microscopically, there were areas of acute and chronic inflammation and granulation tissue formation. Cultures of the abscess fluid yielded pure growth of Staphylococcus aureus sensitive to oxacillin, cephalothin, clindamycin, and vancomycin; resistant to penicillin G. His postoperative course was unremarkable. He was treated with IV oxacillin 12 g / d and rifampin 300 mg orally every 12 hours for 14 days in the hospital and then with dicloxacillin 1 g four times daily and rifampin 300 mg orally twice daily (achieving a serum cidal capacity of 1:16 against his staphylococcus) for an additional 4 weeks. He has remained afebrile for 6 weeks off antimicrobial therapy, regained 20 lb of body weight and returned to full time employment. DISCUSSION
Splenic abscesses are uncommon in clinical practice, estimated to occur in between 0.14% to 0.70% of autopsy seriesJ Delay or missed diagnosis carries a high mortality.3Predisposing factors to development of splenic abscesses have been classified as follows: (1) pyogenic infections with bacteremic seeding. This includes endocarditis and procedure-related bacteremias and is responsible for the majority of cases; (2) hematologic disorders with associated splenic dysfunc-
tion, eg, hemoglobinopathies; (3) extension and abscess formation from disease in a contiguous structure, ie, colonic or gastric carcinoma with perforation; and (4) traumatic abscesses. Traumatic splenic abscesses result from transient bacteremic seeding of a traumatic splenic hematoma or posttraumatic splenic cyst in the setting of recent or remote blunt abdominal trauma or rarely, infectious mononucleosis. 2 The most frequent clinical finding was fever occurring in 95% to 100% of patients; localizing left upper quadrant abdominal finding occurred in 40%; other signs and symptoms were present less frequently. 1 A high index of suspicion is necessary to make the diagnosis. Roentgenographic findings are nonspecific with left sided chest changes including left pleural effusion, basilar atelectasis, or an elevated left hemidiaphragm occurring in up to 80% of patients. Gallium scan is of limited usefulness because of high uptake by surrounding splenic tissue. Technetium liver/spleen scan with multiple views will demonstrate large abscesses (greater than 2 cm), but may not distinguish abscess from hematoma. Computer tomography is probably the diagnostic procedure of choice providing sensitive definition of abscess with demonstration of gas if present, 3'~~but even CT may demonstrate only a cystic mass and abscess is suspected on clinical grounds. Successful treatment of splenic abscess combines splenectomy and debridement of infected tissue with appropriate antimicrobial therapy for at least 14 days postoperatively. 3
REFERENCES
1. Chun CN, Raft MJ, Contreras L, et al: Splenic abscess. Medicine 59:50-65, 1980 2. Chulay JD, Lankerani MR: Splenic abscess. Am J Med 61:513-522, 1976 3. Linos Da, Nagorney DM, Mcllrath DC: Splenic abscess: The importance of early diagnosis. Mayo Clin Proc 58:261-264. 1983 4. Sarr MG, Zuidsma GD: Splenic abscess: Presentation, diagnosis and treatment. Surgery 92:480-485, 1982 5. Inlow W: Traumatic abscess of the spleen. Ann Surg 85:368 378, 1927 6. Ein S, Shandling B, Simpson JS, et al: Non-operativemanage-
ment of traumatized spleen in children: How and why. J Pediatr Surg 13:117-119, 1978 7. WessonDE, Filler RM, Ein SH, et al: Ruptured spleen: When to operate? J Pediatr Surg 16:324-326, 1981 8. Howman-Giles R, Gilday DL, Venugopal S, et al: Splenic trauma: Non-operative management and longterm follow-up by scintiscan. J Pediatr Surg 13:121-126, 1978 9. Zucker K, Browns K, Rossman D, et al: Non-operative management of splenic trauma. Arch Surg 119:400-404, 1984 10. Grant E, Mertens MA, Mascatello VS: Splenic abscess: Comparison of four imaging methods. AJR 132:465466, 1979
splenic
PLENIC ABSCESSES are rare clinical entities with significant associated mortality if not recognized. Several comprehensive reviews have summarized the clinical and laboratory findings, therapy, prognosis, and predisposing etiologies, l~ In the largest reviewed series? 17% of splenic abscesses were late sequellae of nonpenetrating abdominal trauma with the majority of the cases from the early literature) In the most recent Mayo Clinic review series of 19 patients, no cases had an underlying history of splenic trauma) The paucity of recent reported cases of posttraumatic splenic abscess may be the result of early splenectomy for traumatic splenic rupture. There is, however, a current surgical trend in both pediatric and adult patients toward the nonoperative management of hemodynamically stable splenic rupture secondary to blunt abdominal trauma in an effort to preserve immunologic splenic function. 6-9 This therapeutic strategy may result in an increase in the number of posttraumatic splenic abscesses.
S
CASE REPORT M.B., a 16-year-old white male, was in good health until February 4, 1984 when he sustained blunt trauma to his left chest while playing football. Persistent left chest and abdominal pain prompted an emergency room visit. Splenic rupture was confirmed by technetium liver/spleen scan. He remained hemodynamica[ly stable, was observed at rest in the hospital for ten days and discharged home on February 16, 1984. On February 20, 1984 he began having fevers to 103 ~ chills,
From the Department of Medicine, Infectious Disease Service, Department of Pathology, Clinical Microbiology, and Division of Surgery, Baystate Medical Center, Springfield, Mass and Tufts University School of Medicine, Boston. Address reprint requests to Michael Sands, MD, Infectious Disease Service, Baystate Medical Center, Springfield, MA O1199. 9 1986 by Grune & Stratton, Inc. 0022-3468/86/2110-0019503.00/0 900
and drenching night sweats associated with increasing left upper quadrant abdominal pain and left shoulder pain exacerbated by coughing. He was readmitted for evaluation, noted to have a WBC of 20,000 with a left shift and stable hemoglobin. A chest x-ray was interpreted as showing a left lower lobe pneumonic process with pleural effusion. He was treated for a "community-acquired pneumonia" with a cephalosporin; however, he continued having night sweats and fevers to 104 ~ Gallium scan and liver/spleen scans were interpreted as consistent with a previous splenic hematoma. Blood cultures were negative. By February 27, 1984, he had lost 17 lb and had continued fever. Pertinent physical findings on examination were limited to percussion dullness and decreased breath sounds at the left chest base posteriorly and left upper quadrant abdominal tenderness with voluntary guarding. On chest x-ray he had an elevated left hemidiaphragm, left lower lobe atelectasis, and a left pleural effusion. He was felt to have a splenic abscess. A C T scan was performed, which demonstrated a hypodense area at the inferior splenic pole containing gas. He received pneumovax and was transferred to Baystate Medical Center for surgery and further management.
RESULTS
Operative Findings The abdomen was opened through a left subcostal incision. The left upper quadrant was filled with a mass of omentum wrapped around the lower pole of the spleen, and stuck to the diaphragmatic surface. There were no free planes of dissection between the omenturn, spleen, diaphragm, and stomach. The splenic flexure was adherent to this inflammatory mass inferiorly. The mass was approached circumferentially, dissecting the spleen and omentum as a unit off the diaphragm initially, then opening the lesser sac. After controlling the splenic vessels, including amputating the distal centimeter of the tail of the pancreas, the mass was removed. The remainder of the pancreas, duodenum, liver, stomach, small bowel, and mesentery were normal. There was a moderate amount of old free intra-abdominal blood. Following splenectomy, the area was copiously irrigated with warm saline. A large sump drain was placed in the most dependent portion of the left upper quadrant and exited through a stab wound laterally. The abdomen was closed in layers with running #2 Dexon. The skin was closed with widely spaced staples and intervening single steristrips. Upon opening the specimen, the lower splenic pole was noted to be extremely soft and necrotic and contained a 2 cm circumscribed organized hematoma. The omentum was tightly plastered to this entire mass. Journal of Pediatric Surgery, Vol 21, No 10 (October), 1986: pp 900-901
POST-TRAUMATIC SPLENIC ABCESS
901
Pathologic Findings The spleen weighed 290 g, was covered with hemorrhagic necrotic fibrofatty tissue, and on section contained a 5 x 4 • 2 cm area of hemorrhagic necrosis. Microscopically, there were areas of acute and chronic inflammation and granulation tissue formation. Cultures of the abscess fluid yielded pure growth of Staphylococcus aureus sensitive to oxacillin, cephalothin, clindamycin, and vancomycin; resistant to penicillin G. His postoperative course was unremarkable. He was treated with IV oxacillin 12 g / d and rifampin 300 mg orally every 12 hours for 14 days in the hospital and then with dicloxacillin 1 g four times daily and rifampin 300 mg orally twice daily (achieving a serum cidal capacity of 1:16 against his staphylococcus) for an additional 4 weeks. He has remained afebrile for 6 weeks off antimicrobial therapy, regained 20 lb of body weight and returned to full time employment. DISCUSSION
Splenic abscesses are uncommon in clinical practice, estimated to occur in between 0.14% to 0.70% of autopsy seriesJ Delay or missed diagnosis carries a high mortality.3Predisposing factors to development of splenic abscesses have been classified as follows: (1) pyogenic infections with bacteremic seeding. This includes endocarditis and procedure-related bacteremias and is responsible for the majority of cases; (2) hematologic disorders with associated splenic dysfunc-
tion, eg, hemoglobinopathies; (3) extension and abscess formation from disease in a contiguous structure, ie, colonic or gastric carcinoma with perforation; and (4) traumatic abscesses. Traumatic splenic abscesses result from transient bacteremic seeding of a traumatic splenic hematoma or posttraumatic splenic cyst in the setting of recent or remote blunt abdominal trauma or rarely, infectious mononucleosis. 2 The most frequent clinical finding was fever occurring in 95% to 100% of patients; localizing left upper quadrant abdominal finding occurred in 40%; other signs and symptoms were present less frequently. 1 A high index of suspicion is necessary to make the diagnosis. Roentgenographic findings are nonspecific with left sided chest changes including left pleural effusion, basilar atelectasis, or an elevated left hemidiaphragm occurring in up to 80% of patients. Gallium scan is of limited usefulness because of high uptake by surrounding splenic tissue. Technetium liver/spleen scan with multiple views will demonstrate large abscesses (greater than 2 cm), but may not distinguish abscess from hematoma. Computer tomography is probably the diagnostic procedure of choice providing sensitive definition of abscess with demonstration of gas if present, 3'~~but even CT may demonstrate only a cystic mass and abscess is suspected on clinical grounds. Successful treatment of splenic abscess combines splenectomy and debridement of infected tissue with appropriate antimicrobial therapy for at least 14 days postoperatively. 3
REFERENCES
1. Chun CN, Raft MJ, Contreras L, et al: Splenic abscess. Medicine 59:50-65, 1980 2. Chulay JD, Lankerani MR: Splenic abscess. Am J Med 61:513-522, 1976 3. Linos Da, Nagorney DM, Mcllrath DC: Splenic abscess: The importance of early diagnosis. Mayo Clin Proc 58:261-264. 1983 4. Sarr MG, Zuidsma GD: Splenic abscess: Presentation, diagnosis and treatment. Surgery 92:480-485, 1982 5. Inlow W: Traumatic abscess of the spleen. Ann Surg 85:368 378, 1927 6. Ein S, Shandling B, Simpson JS, et al: Non-operativemanage-
ment of traumatized spleen in children: How and why. J Pediatr Surg 13:117-119, 1978 7. WessonDE, Filler RM, Ein SH, et al: Ruptured spleen: When to operate? J Pediatr Surg 16:324-326, 1981 8. Howman-Giles R, Gilday DL, Venugopal S, et al: Splenic trauma: Non-operative management and longterm follow-up by scintiscan. J Pediatr Surg 13:121-126, 1978 9. Zucker K, Browns K, Rossman D, et al: Non-operative management of splenic trauma. Arch Surg 119:400-404, 1984 10. Grant E, Mertens MA, Mascatello VS: Splenic abscess: Comparison of four imaging methods. AJR 132:465466, 1979