CASE CONFERENCE spleen, rupture
Delayed Splenic Rupture [Petri RW, O'Brien PD, Vukich D J: Delayed splenic rupture. Ann Emerg Med November 1990;19:1302-1305.] INTRODUCTION Today's case concerns a young man who was found to have a ruptured spleen on his second emergency department visit after a fistfight. Paul O'Brien, MID, emergency medicine resident, will discuss the history and ED management. Roland Petri, MD, chief resident in emergency medicine, will discuss the entity of delayed splenic rupture. Additional discussion will be provided by David Vukich, MD, FACEP, chief, emergency medicine. All discussants are from the University of Florida Health Science Center-Jacksonville. CASE PRESENTATION Paul O'Brien, MD: A 24-year-old man presented to the ED with complaint of sudden exacerbation of previously mild epigastric pain. The abdominal pain first developed after the patient was involved in a fistfight with his roommate three days earlier. The patient had been treated in the ED after the fight. Police found the patient, grossly intoxicated, sitting in the street outside his residence suffering facial injuries. Initial ED treatm e n t consisted of repair of a facial laceration and overnight observation due to the patient's intoxicated state. Vital signs at that time were blood pressure of 130/80 m m Hg; pulse, 96; respirations, 20; and temperature, 37 C. Records indicate that the patient's abdominal examination before discharge was unremarkable. The patient felt well, with the exception of persistent mild epigastric pain. Three days later, while at rest, the patient experienced sudden severe exacerbation of the abdominal pain with radiation to the left shoulder. He also noted progressively increasing lightheadedness and weakness, prompting his return to the ED. Vital signs at time of second presentation were blood pressure of 90/60 m m Hg; pulse, 120; respirations, 24; and temperature, 37.2 C orally. Physical examination revealed a thin, ill-appearing young m a n lying on his right side. The head and neck examination was remarkable for right facial ecchymoses and a sutured wound. Auscultation of the chest revealed equal bilateral breath sounds and a rapid heart rate. The abdomen was flat, without scars, without bowel sounds, diffusely tender, with guarding in all quadrants and without palpable masses. Rectal examination was guaiacnegative. The neurologic examination was normal. The patient was unable to sit up when requested due to an increase in lightheadedness. A presumptive diagnosis of delayed splenic rupture was made. IV normal saline, followed by packed RBCs, was infused through multiple large-gauge IV lines. A diagnostic peritoneal lavage was performed. On insertion of the catheter, 10 cm 3 of blood was withdrawn immediately. The on-call surgical service was notified. Preoperative laboratory studies were obtained, with the following results: hematocrit of 16%; hemoglobin, 5.5 g/dL; electrolytes, within normal limits; urinalysis, without RBCs; and chest radiograph, unremarkable. The patient's medical history was unremarkable. He was not taking any medications, and he had no allergies. He was taken to the operating room
19:11 November 1990
Annals of Emergency Medicine
Roland W Petri, MD Paul D O'Brien, MD David J Vukich, MD, FACEP Jacksonville, Florida From the Division of Emergency Medicine, University Hospital of Jacksonville, Jacksonville, Florida. Received for publication March 27, 1989. Revision received March 27, 1990. Accepted for publication June 4, 1990. Address for reprints: David J Vukich, MD, FACER Division of Emergency Medicine, University of Florida Health Science Center-Jacksonville, 655 West Eighth Street, Jacksonville, Florida 32209.
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where laparotomy revealed a normal-size spleen, with a stellate-shaped laceration, and several hundred cubic centimeters of free blood in the peritoneal cavity. The spleen could not be repaired, and so splenectomy was performed. The patient recovered without complications. DISCUSSION Roland Petri, MD: The spleen is a vascular organ that essentially functions as the body's largest lymph node. i Its response to antigens includes proliferation of T lymphocytes, antibody-forming B cells, and phagocytic cells. It also clears bacteria; damaged, nucleated, and inclusion body-containing phagocytoses; and other abnormal RBCs. From 30% to 40% of platelets are sequestered in the spleen. The spleen is the m o s t c o m m o n l y injured organ in blunt abdominal trauma. 2 Blunt t r a u m a m a y lead to splenic laceration, contusion, fragmentation, or hilar vessel disruption. Bleeding with immediate evidence of intravascular volume loss most often results. 3 Approximately 5% to 40% (average, 14%) of instances of splenic rupture do not become manifest until the onset of hemodynamic instability in a previously stable patient several hours to five years after the precipitating traumatic event. 4 Baudet, in 1907, was apparently the first to note in the medical literature the phenomenon of delayed hemorrhage after splenic injury. 5 McIndoe published the first review of cases of apparent delayed splenic rupture in 1932. 6 In 1966, a review of all cases of delayed splenic rupture described in the English literature was published by Sizer et al. 7 Two mechanisms postulated to explain delayed splenic rupture are containment of initial hemorrhage by an intact splenic capsule, leading to formation of a traumatic splenic cyst that ruptures at a later time, and containment of hemorrhage, despite initial capsular laceration, by the o m e n t u m and other adjacent structures (also described as occult splenic rupture).S, 9 Question: What is the controversy surrounding the entity of delayed hemorrhage from splenic injury? Dr Petri: Within the past 15 years, some authors have suggested that most cases of delayed splenic rupture actually represent delayed diagnosis of splenic rupture.lO, ll The difference of opinion does not involve disagreement over the incidence of splenic parenchymal injury without immediate loss of capsular integrity but rather disagreement over whether splenic injuries detected two or more days after their p r e c i p i t a t i n g t r a u m a t i c events were truly asymptomatic until just before detection. Question: Does the case described here likely represent delayed hemorrhage or delayed diagnosis of splenic injury? Dr O'Brien: In the present context, this seems to be largely a question of semantics. The patient probably sustained splenic parenchymal injury during the fistfight, with the resultant hemorrhage contained by an intact capsule for two days. The sudden exacerbation of the patient's abdominal pain coupled with the precipitous onset of h e m o d y n a m i c instability two days after the fistfight presumably marked the rupture of the splenic capsule. Question: How may a diagnosis of delayed splenic hemor116/1303
rhage be made? Dr Petri: A diagnosis of delayed splenic rupture should be considered in any patient presenting with abdominal pain or signs of hypovolemia and recent history of blunt abdominal trauma (to include the left lower chest) due to motor vehicle accident, assault, contact sports, fall, and so on. The precipitating traumatic event may seem relatively minor, especially in the presence of a pathologically enlarged spleen. 3 Delayed rupture may occur secondary to a sudden increase in intra-abdominal pressure, as with coughing, but often there is no history of such an antecedent event. Patients with abnormally enlarged spleens are at an increased risk of splenic rupture. Splenomegaly may develop from infectious, inflammatory, infiltrative, or congestive etiologies. It is also found in patients with reti¢uloendothelial hyperplasia. Victims of delayed splenic rupture more often complain of diffuse abdominal pain than left upper quadrant abdominal pain. 3 Seventy-five percent of victims of splenic rupture are said to exhibit Kehr's sign, abdominal pain referred to the left shoulder. 8 Some may complain of nausea. Whether it occurs immediately after the precipitating traumatic event or on a delayed basis, loss of integrity of the splenic capsule is usually marked by the signs of intravascular volume depletion and hemoperitoneum. Physical e x a m i n a t i o n c o m m o n l y reveals orthostatic vital sign changes; abdominal tenderness (left upper quadrant or diffuse), guarding, and rebound; and h y p o a c t i v e bowel sounds. Laboratory examination m a y reveal decreased hematocrit, depending on the time from capsular rupture to ED presentation and the rate and amount of blood loss. Leukocytosis is usually seen. Radiographs of the chest and abdomen may be obtained to look for insensitive and nonspecific signs such as left lower rib fractures or displacement of the gastric bubble or splenic flexure of the colon f r o m the p r o p e r i t o n e a l fat stripe. T h i c k e n e d and edematous gastric folds m a y be visible on plain abdominal film of the abdomen and indicate the severity of trauma that has taken place. The most sensitive indicator of free intraperitoneal b l o o d is d i a g n o s t i c p e r i t o n e a l l a v a g e ( s e n s i t i v i t y , 95 + %).1246 It offers the additional advantages of being rapid and inexpensive, but it does have two drawbacks. First, there is a low incidence of complications, such as wound infection, intestinal perforation, bladder perforation, and vascular injury. 12,17-19 Second, in some instances peritoneal lavage may be too sensitive, detecting bleeding from minor mesenteric and omental lesions or from the procedure itself. 19 Since the recognition of significantly increased risk of sepsis after splenectomy, especially in children, a more complex issue regarding peritoneal lavage has arisen. 20 Namely, positive peritoneal lavage due to splenic injury m a y not mandate splenectomy, and peritoneal lavage is not specific for splenic injury (ie, positive result may be due to liver or other intra-abdominal injury). Within the past five to ten years, m a n y reports demonstrating that computed tomography (CT) can be as sensitive a test as peritoneal ]avage for the evaluation of blunt abdominal trauma have appeared in the radiologic and surgical literature. 21-24 More recently, however, case reports of delayed splenic rupture after initial negative CT scans have appeared in the literature. 25-a7 In m a n y institu-
Annals of Emergency Medicine
19:11 November 1990
FIGURE. D i f f e r e n t i a l diagnosis. Traumatic Etiology
Medical Etiology
Spleen Liver Small bowel Kidney Bladder Colorectal
Peptic ulcer disease Acute appendicitis Gastritis Pancreatitis Perforated viscus Abdominal aortic aneurysm Ovarian cyst Ectopic pregnancy Hepatoma Infectious mononucleosis Leukemia
tions, CT scan with oral and IV contrast is presently the diagnostic tool of choice in patients for whom lavage is contraindicated to some degree; these patients include young children and those in whom previous abdominal surgery makes adhesions likely. Before the widespread availability of CT, arteriography was popular as a means of evaluating the spleen for injury. 28-3° During the late 1960s and early 1970s, case reports of successful use of arteriography to diagnose delayed splenic rupture appeared in the radiologic literature. 3l Although its use in the detection of splenic rupture has been described since the middle to late 1960s, some disagreement exists over the sensitivity and specificity of radionuclide splenic scanning, a2-34 In particular, questions have arisen regarding the ability of radioisotope splenic scanning to detect small subcapsular injuries and differentiate splenic rupture from other disease processes.35, g6 The radiologic literature contains several case reports describing the use of radioisotope scanning to monitor patients for delayed splenic rupture. 36-39 CT, arteriography, and radioisotope scanning all have the theoretical advantage over peritoneal lavage of being able to localize the site of injury to the spleen. However, arteriography and radioisotope scanning are not as sensitive as peritoneal lavage for the overall evaluation of blunt abdominal trauma.
Question: What is the appropriate management of delayed splenic rupture?
Dr Petri: The patient presenting with signs of hemodynamic instability should be treated with the usual initial attention to maintenance of airway, ventilation and oxygenation, and support of circulation. Initial fluid resuscitation should consist of IV normal saline or lactated Ringer's solution. If more than 2 to 3 L of fluid are required to maintain hemodynamic stability, packed RBCs or whole blood (depending on local availability and transfusion practices) should be infused. Fresh frozen plasma and platelets should be administered only as the need is clearly indicated by abnormalities of platelet count, prothrombin time, or partial thromboplastin time. Splenic trauma was managed nonoperatively before 1900 and carried a mortality of 90% to 100%. 7 Immediate splenectomy therefore became the treatment of choice for 19:11 November 1990
splenic trauma during the early 1900s. 4° Approximately 50 years later, it was recognized that fatal sepsis had a 58fold greater incidence rate in splenectomized children than in the general population. 2o It was subsequently determined that the incidence of sepsis increased after splenectomy in adults also.41,42 The surgical literature since the 1970s has therefore shown support for conservative management of splenic injury. Nonoperative management is reserved for those patients who can be hemodynamically stabilized with less than 40 mL/kg blood and who do not have other injuries that require surgery. 4o Patients selected for nonoperative management are monitored continuously for at least 48 hours with observation for increasing abdominal girth, unstable vital signs, or decreasing hematocrit. In a 1985 report of a series of adult patients initially selected for nonoperative management, almost 75% eventually required operative intervention. 43 Splenorrhaphy may represent a reasonable m a n a g e m e n t compromise, particularly in adults. 44
Question: What entities should be included in the differential diagnosis of a case like the one described here? David Vukich, MD, FACEP: In a patient such as this, with symptoms of several days' duration and a rather nebulous history of trauma clouded by alcohol, the differential diagnosis should initially be quite broad and include both traumatic and medical causes {Figure). Traumatic damage and subsequent hemorrhage of the solid abdominal organs must certainly be high on the list. Statistically, the spleen and liver are the abdominal organs most frequently injured secondary to blunt trauma. Isolated pancreatic injuries are rare in blunt abdominal trauma. Renal injury, with or without subsequent retroperitoneal hematoma, is also to be considered. One must also keep in mind traumatic injuries outside of the abdominal cavity, such as shoulder injury or fractured ribs. Finally, the history of trauma can be a "red herring," serving only to mislead the clinician. Acute appendicitis or other inflammatory conditions of the bowel are quite common in this age group. Given the history of alcohol use, gastritis, peptic ulcer disease, and pancreatitis are also possibilities. Spontaneous rupture of the spleen has been reported but is frequently related to unappreciated trauma. It most often occurs in hematologic disorders such as malaria, infectious mononucleosis, and leukemia. In an older age group, rupture of an abdominal aortic aneurysm should be considered. In the female patient, the differential expands to include ruptured ovarian cyst, ectopic pregnancy, and hepatoma, especially for those with a previous history of contraceptive use.
REFERENCES
1. Fefer A: Function of the spleen, in Petersdorf RG, Adams RD, Braunwald E, et al (eds): Principles of Internal Medicine. New York, McGrawHill, 1983, p 301. 2. DiVincenti t~C, Rives JD, LabordeEJ, et al: Blunt abdominal trauma. / Trauma 1968;8:1004-1013. 3. Marx JA: Abdominaltrauma, in Rosen P, BakerFJ, BraenGR, et al {eds): Emergency Medicine." Concepts and Clinical Practice. St Louis, CVMosby, 1983, p 380-408.
Annals of Emergency Medicine
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SPLENIC RUPTURE Petri, O'Brien & Vukich
4. Zabiuski E, Harfins H: Delayed splenic rupture: A clinical syndrome following trauma. Arch Surg 1943;46:186-213.
25. Rose WE), Martyak GG, Brotman S: Changing attitudes toward splenic trauma. A m J Emerg Med 1986;4:170-172.
5. Bandet R: Ruptures de la rate. Med Praet 1907;3:565-581.
26. Pappas D, Mirvis SE, Crepps JT: Splenic trauma: False-negative CT diagnosis in cases of delayed rupture. A m J Radiol 1987;149:727-728.
6. McIndoe AH: Delayed hemorrhage following traumatic rupture of the spleen. Br J Surg 1932;20:249-268. 7. Sizer JS, Wayne ER, Frederick PL: Delayed rupture of the spleen: Review literature and report of six cases. Arch Surg 1966;92:362-366. 8. Clark OH, Lira RC, Margaretten W: Spontaneous delayed splenic rupture. J Trauma 1975;15:245-249. 9. Lorimer WS: Occult rupture of the spleen. Arch Surg 1964;89:434-440. 10. Benjamin CI, Engrav LH, Perry JF: Delayed rupture or delayed diagnosis of rupture of the spleen. Surg Gynecol Obstet 1976;142:171-172. 11. Olsen WR, Polley TZ: A second look at delayed splenic rupture. Arch Surg 1977;112:42~-425. t2. Root HD, Hause CW, McKinley CR, et al: Diagnostic peritoneal lavage. Surgery 1965;57:633-637. 13. Perry JF, DeMeules JE, Root HD: Diagnostic peritoneal lavage in blunt abdominal trauma. Surg Gynecol Obstet 1970;131:742-744. 14. Perry JF, Strate RG: Diagnostic peritoneal lavage in blunt abdominal trauma: Indications. Surgery 1972;71:898-901.
27. Fabian TC, Mangiante EC, white TJ, et al: A prospective study of 91 patients undergoing both computed tomography and peritoneal lavag¢ following blunt abdominal trauma. J Trauma 1986;26:602-607. 28. Aakus T, Enge I: Angiography in traumatic rupture of the spleen. Br J Radiol 1967;40:855-861. 29. Freeark RJ, Love L, Baker RJ: The role of angiography in the management of blunt abdominal trauma. J Trauma 1968;8:557-571. 30. Polin SG, Walklett WD, Sayler OL: Arteriography as an adjunct to the diagnosis of splenic injury. Surgery 1970;67:313-318. 31. Love L, Greenfield GB, Braun TW, et al: Arteriography of splenic trauma. Radiology 1968;91:96-102. 32. Wener L, Boyle CD: Splenic scintiscarming in the preoperative diagnosis of subcapsular hematoma. N Engl ] Med 1967;277:35-37. 33. Gilday DL, Alderson PO: Scintigraphic evaluation of liver and spleen injury. Semin Nucl Med 1974;4:357-370. 34. Nebesar RA, Rabinov K, Potsaid MS: Radionuclide imaging of the spleen in suspected splenic injury. Radiology 1974;110:609-614.
15. Thal ER, Shires GT: Peritoneal lavage in blunt abdominal trauma. A m J Surg 1973;125:64-67.
35. Washburn ME, Balk MW, Mazat BA, et al: Experimental subcapsular hematoma of the spleen. Ann Surg 1978;187:407-410.
16. Parvin S, Smith DE, Asher WM, et al: Effectiveness of peritoneal lavage in blunt abdominal trauma. Ann Surg 1975;181:255-261.
36. Flickinger FW, Jackson GL: Radionuclide scan findings in delayed splenic rupture. Radiology 1978;129:763-764.
17. Engrav LH, Benjamin CI, Strate RG, et al: Diagnostic peritoneal lavage in blunt trauma. J Trauma 1975;15:854-859. 18. Caffee HH, Benfield JR: Is peritioneal lavage for the diagnosis of hemoperitoneum safe? Arch Surg 1971;103:4-7. 19. Olsen W, Hillbrith D: Abdominal paracentesis or peritoneal lavage in blunt abdominal trauma. J Trauma 1971;11:824-829.
37. Solheim K, Neadrum HJ: Scintigraphic follow-up of splenic rupture. Clin Nucl Med 1985;10:851-854. 38. sziklas JJ, Spencer RP/ Rosenberg RJ: Delayed splenic rupture: A suggestion for predictive monitoring. J Nucl Med 1985;26:609-611. 39. Slavin JD, Minehan TF, Spencer RP: Scan demonstration of delayed splenic rupture. J Nucl Med 1974;15:632-633.
20. Singer DB: Postsplenectomy sepsis, in Rosenberg HS, Bolande RP (eds): Perspectives in Pediatric Pathology. Chicago, Year Book, vol 1, 1973, p 285-311.
40. Filler RM: Experience with the management of splenic injuries. Aust N Z J Surg 1984;54:443-445.
21. Jeffery RB, Laing FC, Federle MP, et al: Computed tomography of splenic trauma. Radiology 1981;14l:729-732.
41. Dickerman JD: Traumatic asplenia in adults: A defined hazard? Arch Surg 1981;116:361-363.
22. Wing VW, Federle MP, Morris JA, et al: The clinical impact of CT for blunt abdominal trauma. A m [ Radiol 1985;145:1191-1194.
42. O'Neal BJ, McDonald JC: The risk of sepsis in the asplenic adult. Ann Surg 1981;194:775-778.
23. Nelson EW, Holliman CJ, Jueli BE, et al: Computerized tomography in the evaluation of blunt abdominal trauma. Am J Surg 1983;146:751-754.
43. Mahon PA, Sutton JE: Nonoperative management of adult splenic injury due to blunt trauma: A warning. A m J Surg 1985;149:716-721.
24. Trunkey DD: Abdominal trauma, in Trunkey DD, Lewis RF (eds): Current Therapy of Trauma. St Louis, CV Mosby, 1984, p 93-100.
44. Barrett J, Sheaff C, Abuabana S, et al: Splenic preservation in adults after blunt and penetrating trauma. Am f Surg 1983;145:313-317.
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Annals of Emergency Medicine
19:11 November 1990
Delayed Splenic Rupture [Petri RW, O'Brien PD, Vukich D J: Delayed splenic rupture. Ann Emerg Med November 1990;19:1302-1305.] INTRODUCTION Today's case concerns a young man who was found to have a ruptured spleen on his second emergency department visit after a fistfight. Paul O'Brien, MID, emergency medicine resident, will discuss the history and ED management. Roland Petri, MD, chief resident in emergency medicine, will discuss the entity of delayed splenic rupture. Additional discussion will be provided by David Vukich, MD, FACEP, chief, emergency medicine. All discussants are from the University of Florida Health Science Center-Jacksonville. CASE PRESENTATION Paul O'Brien, MD: A 24-year-old man presented to the ED with complaint of sudden exacerbation of previously mild epigastric pain. The abdominal pain first developed after the patient was involved in a fistfight with his roommate three days earlier. The patient had been treated in the ED after the fight. Police found the patient, grossly intoxicated, sitting in the street outside his residence suffering facial injuries. Initial ED treatm e n t consisted of repair of a facial laceration and overnight observation due to the patient's intoxicated state. Vital signs at that time were blood pressure of 130/80 m m Hg; pulse, 96; respirations, 20; and temperature, 37 C. Records indicate that the patient's abdominal examination before discharge was unremarkable. The patient felt well, with the exception of persistent mild epigastric pain. Three days later, while at rest, the patient experienced sudden severe exacerbation of the abdominal pain with radiation to the left shoulder. He also noted progressively increasing lightheadedness and weakness, prompting his return to the ED. Vital signs at time of second presentation were blood pressure of 90/60 m m Hg; pulse, 120; respirations, 24; and temperature, 37.2 C orally. Physical examination revealed a thin, ill-appearing young m a n lying on his right side. The head and neck examination was remarkable for right facial ecchymoses and a sutured wound. Auscultation of the chest revealed equal bilateral breath sounds and a rapid heart rate. The abdomen was flat, without scars, without bowel sounds, diffusely tender, with guarding in all quadrants and without palpable masses. Rectal examination was guaiacnegative. The neurologic examination was normal. The patient was unable to sit up when requested due to an increase in lightheadedness. A presumptive diagnosis of delayed splenic rupture was made. IV normal saline, followed by packed RBCs, was infused through multiple large-gauge IV lines. A diagnostic peritoneal lavage was performed. On insertion of the catheter, 10 cm 3 of blood was withdrawn immediately. The on-call surgical service was notified. Preoperative laboratory studies were obtained, with the following results: hematocrit of 16%; hemoglobin, 5.5 g/dL; electrolytes, within normal limits; urinalysis, without RBCs; and chest radiograph, unremarkable. The patient's medical history was unremarkable. He was not taking any medications, and he had no allergies. He was taken to the operating room
19:11 November 1990
Annals of Emergency Medicine
Roland W Petri, MD Paul D O'Brien, MD David J Vukich, MD, FACEP Jacksonville, Florida From the Division of Emergency Medicine, University Hospital of Jacksonville, Jacksonville, Florida. Received for publication March 27, 1989. Revision received March 27, 1990. Accepted for publication June 4, 1990. Address for reprints: David J Vukich, MD, FACER Division of Emergency Medicine, University of Florida Health Science Center-Jacksonville, 655 West Eighth Street, Jacksonville, Florida 32209.
1302/115
SPLENIC RUPTURE Petri, O'Brien & Vukich
where laparotomy revealed a normal-size spleen, with a stellate-shaped laceration, and several hundred cubic centimeters of free blood in the peritoneal cavity. The spleen could not be repaired, and so splenectomy was performed. The patient recovered without complications. DISCUSSION Roland Petri, MD: The spleen is a vascular organ that essentially functions as the body's largest lymph node. i Its response to antigens includes proliferation of T lymphocytes, antibody-forming B cells, and phagocytic cells. It also clears bacteria; damaged, nucleated, and inclusion body-containing phagocytoses; and other abnormal RBCs. From 30% to 40% of platelets are sequestered in the spleen. The spleen is the m o s t c o m m o n l y injured organ in blunt abdominal trauma. 2 Blunt t r a u m a m a y lead to splenic laceration, contusion, fragmentation, or hilar vessel disruption. Bleeding with immediate evidence of intravascular volume loss most often results. 3 Approximately 5% to 40% (average, 14%) of instances of splenic rupture do not become manifest until the onset of hemodynamic instability in a previously stable patient several hours to five years after the precipitating traumatic event. 4 Baudet, in 1907, was apparently the first to note in the medical literature the phenomenon of delayed hemorrhage after splenic injury. 5 McIndoe published the first review of cases of apparent delayed splenic rupture in 1932. 6 In 1966, a review of all cases of delayed splenic rupture described in the English literature was published by Sizer et al. 7 Two mechanisms postulated to explain delayed splenic rupture are containment of initial hemorrhage by an intact splenic capsule, leading to formation of a traumatic splenic cyst that ruptures at a later time, and containment of hemorrhage, despite initial capsular laceration, by the o m e n t u m and other adjacent structures (also described as occult splenic rupture).S, 9 Question: What is the controversy surrounding the entity of delayed hemorrhage from splenic injury? Dr Petri: Within the past 15 years, some authors have suggested that most cases of delayed splenic rupture actually represent delayed diagnosis of splenic rupture.lO, ll The difference of opinion does not involve disagreement over the incidence of splenic parenchymal injury without immediate loss of capsular integrity but rather disagreement over whether splenic injuries detected two or more days after their p r e c i p i t a t i n g t r a u m a t i c events were truly asymptomatic until just before detection. Question: Does the case described here likely represent delayed hemorrhage or delayed diagnosis of splenic injury? Dr O'Brien: In the present context, this seems to be largely a question of semantics. The patient probably sustained splenic parenchymal injury during the fistfight, with the resultant hemorrhage contained by an intact capsule for two days. The sudden exacerbation of the patient's abdominal pain coupled with the precipitous onset of h e m o d y n a m i c instability two days after the fistfight presumably marked the rupture of the splenic capsule. Question: How may a diagnosis of delayed splenic hemor116/1303
rhage be made? Dr Petri: A diagnosis of delayed splenic rupture should be considered in any patient presenting with abdominal pain or signs of hypovolemia and recent history of blunt abdominal trauma (to include the left lower chest) due to motor vehicle accident, assault, contact sports, fall, and so on. The precipitating traumatic event may seem relatively minor, especially in the presence of a pathologically enlarged spleen. 3 Delayed rupture may occur secondary to a sudden increase in intra-abdominal pressure, as with coughing, but often there is no history of such an antecedent event. Patients with abnormally enlarged spleens are at an increased risk of splenic rupture. Splenomegaly may develop from infectious, inflammatory, infiltrative, or congestive etiologies. It is also found in patients with reti¢uloendothelial hyperplasia. Victims of delayed splenic rupture more often complain of diffuse abdominal pain than left upper quadrant abdominal pain. 3 Seventy-five percent of victims of splenic rupture are said to exhibit Kehr's sign, abdominal pain referred to the left shoulder. 8 Some may complain of nausea. Whether it occurs immediately after the precipitating traumatic event or on a delayed basis, loss of integrity of the splenic capsule is usually marked by the signs of intravascular volume depletion and hemoperitoneum. Physical e x a m i n a t i o n c o m m o n l y reveals orthostatic vital sign changes; abdominal tenderness (left upper quadrant or diffuse), guarding, and rebound; and h y p o a c t i v e bowel sounds. Laboratory examination m a y reveal decreased hematocrit, depending on the time from capsular rupture to ED presentation and the rate and amount of blood loss. Leukocytosis is usually seen. Radiographs of the chest and abdomen may be obtained to look for insensitive and nonspecific signs such as left lower rib fractures or displacement of the gastric bubble or splenic flexure of the colon f r o m the p r o p e r i t o n e a l fat stripe. T h i c k e n e d and edematous gastric folds m a y be visible on plain abdominal film of the abdomen and indicate the severity of trauma that has taken place. The most sensitive indicator of free intraperitoneal b l o o d is d i a g n o s t i c p e r i t o n e a l l a v a g e ( s e n s i t i v i t y , 95 + %).1246 It offers the additional advantages of being rapid and inexpensive, but it does have two drawbacks. First, there is a low incidence of complications, such as wound infection, intestinal perforation, bladder perforation, and vascular injury. 12,17-19 Second, in some instances peritoneal lavage may be too sensitive, detecting bleeding from minor mesenteric and omental lesions or from the procedure itself. 19 Since the recognition of significantly increased risk of sepsis after splenectomy, especially in children, a more complex issue regarding peritoneal lavage has arisen. 20 Namely, positive peritoneal lavage due to splenic injury m a y not mandate splenectomy, and peritoneal lavage is not specific for splenic injury (ie, positive result may be due to liver or other intra-abdominal injury). Within the past five to ten years, m a n y reports demonstrating that computed tomography (CT) can be as sensitive a test as peritoneal ]avage for the evaluation of blunt abdominal trauma have appeared in the radiologic and surgical literature. 21-24 More recently, however, case reports of delayed splenic rupture after initial negative CT scans have appeared in the literature. 25-a7 In m a n y institu-
Annals of Emergency Medicine
19:11 November 1990
FIGURE. D i f f e r e n t i a l diagnosis. Traumatic Etiology
Medical Etiology
Spleen Liver Small bowel Kidney Bladder Colorectal
Peptic ulcer disease Acute appendicitis Gastritis Pancreatitis Perforated viscus Abdominal aortic aneurysm Ovarian cyst Ectopic pregnancy Hepatoma Infectious mononucleosis Leukemia
tions, CT scan with oral and IV contrast is presently the diagnostic tool of choice in patients for whom lavage is contraindicated to some degree; these patients include young children and those in whom previous abdominal surgery makes adhesions likely. Before the widespread availability of CT, arteriography was popular as a means of evaluating the spleen for injury. 28-3° During the late 1960s and early 1970s, case reports of successful use of arteriography to diagnose delayed splenic rupture appeared in the radiologic literature. 3l Although its use in the detection of splenic rupture has been described since the middle to late 1960s, some disagreement exists over the sensitivity and specificity of radionuclide splenic scanning, a2-34 In particular, questions have arisen regarding the ability of radioisotope splenic scanning to detect small subcapsular injuries and differentiate splenic rupture from other disease processes.35, g6 The radiologic literature contains several case reports describing the use of radioisotope scanning to monitor patients for delayed splenic rupture. 36-39 CT, arteriography, and radioisotope scanning all have the theoretical advantage over peritoneal lavage of being able to localize the site of injury to the spleen. However, arteriography and radioisotope scanning are not as sensitive as peritoneal lavage for the overall evaluation of blunt abdominal trauma.
Question: What is the appropriate management of delayed splenic rupture?
Dr Petri: The patient presenting with signs of hemodynamic instability should be treated with the usual initial attention to maintenance of airway, ventilation and oxygenation, and support of circulation. Initial fluid resuscitation should consist of IV normal saline or lactated Ringer's solution. If more than 2 to 3 L of fluid are required to maintain hemodynamic stability, packed RBCs or whole blood (depending on local availability and transfusion practices) should be infused. Fresh frozen plasma and platelets should be administered only as the need is clearly indicated by abnormalities of platelet count, prothrombin time, or partial thromboplastin time. Splenic trauma was managed nonoperatively before 1900 and carried a mortality of 90% to 100%. 7 Immediate splenectomy therefore became the treatment of choice for 19:11 November 1990
splenic trauma during the early 1900s. 4° Approximately 50 years later, it was recognized that fatal sepsis had a 58fold greater incidence rate in splenectomized children than in the general population. 2o It was subsequently determined that the incidence of sepsis increased after splenectomy in adults also.41,42 The surgical literature since the 1970s has therefore shown support for conservative management of splenic injury. Nonoperative management is reserved for those patients who can be hemodynamically stabilized with less than 40 mL/kg blood and who do not have other injuries that require surgery. 4o Patients selected for nonoperative management are monitored continuously for at least 48 hours with observation for increasing abdominal girth, unstable vital signs, or decreasing hematocrit. In a 1985 report of a series of adult patients initially selected for nonoperative management, almost 75% eventually required operative intervention. 43 Splenorrhaphy may represent a reasonable m a n a g e m e n t compromise, particularly in adults. 44
Question: What entities should be included in the differential diagnosis of a case like the one described here? David Vukich, MD, FACEP: In a patient such as this, with symptoms of several days' duration and a rather nebulous history of trauma clouded by alcohol, the differential diagnosis should initially be quite broad and include both traumatic and medical causes {Figure). Traumatic damage and subsequent hemorrhage of the solid abdominal organs must certainly be high on the list. Statistically, the spleen and liver are the abdominal organs most frequently injured secondary to blunt trauma. Isolated pancreatic injuries are rare in blunt abdominal trauma. Renal injury, with or without subsequent retroperitoneal hematoma, is also to be considered. One must also keep in mind traumatic injuries outside of the abdominal cavity, such as shoulder injury or fractured ribs. Finally, the history of trauma can be a "red herring," serving only to mislead the clinician. Acute appendicitis or other inflammatory conditions of the bowel are quite common in this age group. Given the history of alcohol use, gastritis, peptic ulcer disease, and pancreatitis are also possibilities. Spontaneous rupture of the spleen has been reported but is frequently related to unappreciated trauma. It most often occurs in hematologic disorders such as malaria, infectious mononucleosis, and leukemia. In an older age group, rupture of an abdominal aortic aneurysm should be considered. In the female patient, the differential expands to include ruptured ovarian cyst, ectopic pregnancy, and hepatoma, especially for those with a previous history of contraceptive use.
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