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CJS, Vol. 39, No. 2, April 1996 151

Although splenic injury is com-mon after blunt abdominaltrauma,1 delayed splenic rup-

ture (DSR), occurring 48 hours ormore after the injury is rare.2,3 DSR isthree times more common in menthan women. Rupture occurs in thefirst 2 weeks after injury in 75% ofcases,4 although in some cases ruptureis reported from 1 month to 11 yearsafter injury.5,6 The death rate is ap-proximately 10%.7 Before the use ofdiagnostic peritoneal lavage (DPL),the reported incidence of DSR amongpatients with blunt abdominal trauma

was approximately 15%, but with theuse of DPL and computed tomogra-phy (CT), its reported frequency hasfallen to 1% to 2%.3,8 Thus, whetherthe condition represents delayedrecognition of splenic rupture ratherthan true DSR is still debated.3,7–9

Thrombolytic therapy for patientswith myocardial infarction becamecommon practice in the late 1980s. Ithas significantly reduced the deathrate from acute myocardial infarctionwhen administered within the first 4to 6 hours after the onset of symp-toms. Such therapy, however, may ac-

tivate bleeding from a number of sites,including organs that have been re-cently traumatized.

CASE REPORT

A 47-year-old woman presentedwith retrosternal chest pain associatedwith diaphoresis, nausea and dyspnea.She had a 1-week history of chest painon exertion but was otherwise well.Six months earlier she had suffered afractured pelvis and right wrist in amotor vehicle accident. At that timethere was no clinical evidence of

Case ReportÉtude de cas

DELAYED RUPTURE OF THE SPLEEN AND STREPTOKINASETHERAPY

Robert Nam, MD;* Michele M. Carr, DDS, MD;† Christopher G. Jamieson, MB BS, FRCSC, FACS

From the Division of General Surgery, Department of Surgery, The Wellesley Hospital, University of Toronto, Toronto, Ont.

*Resident in urology, Department of Surgery, University of Toronto

†Resident in general surgery, Department of Surgery, University of Toronto

Accepted for publication Apr. 5, 1995

Correspondence and reprint requests to: Dr. Christopher G. Jamieson, The Wellesley Hospital, Suite 322, E.K. Jones Building, 160 Wellesley St. E, Toronto ON M4Y 1J3

Delayed rupture of the spleen is a rare but serious complication of blunt abdominal trauma. A 47-year-oldwoman with a history of fractured pelvis from a motor vehicle accident 6 months earlier presented with ev-idence of a myocardial infarction. Subsequent streptokinase administration was complicated by splenic rup-ture, which was managed by evacuation of the clotted blood and splenectomy. The patient made a com-plete recovery. The risk of splenic rupture and bleeding complications resulting from thrombolytic therapyfor myocardial infarction is discussed, as are the controversy over whether delayed splenic rupture is a truediagnosis, the mechanism of rupture and the clues to impending rupture.

Une rupture retardée de la rate constitue une complication rare mais grave d’une contusion de l’abdomen.Une femme de 47 ans qui avait subi une fracture du bassin dans un accident de la circulation 6 mois plustôt se présente avec des signes d’infarctus du myocarde. L’administration subséquente de streptrokinase aété compliquée par une rupture de la rate, qui a été traitée par évacuation du sang coagulé et une splénec-tomie. La patiente s’est rétablie complètement. On discute du risque de rupture de la rate et de complica-tions par saignement à la suite d’une thérapie thrombolytique contre un infarctus du myocarde, de la con-troverse suscitée par la question de savoir si une rupture retardée de la rate constitue un véritable diagnostic,ainsi que du mécanisme de rupture et des signes de rupture imminente.

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splenic rupture, and neither DPL norCT was done.On admission, she had ST-segment

elevation in leads V1 to V3, cardiac en-zyme levels indicative of an acute my-ocardial infarction and a blood hemo-globin level of 143 g/L. A standarddose of streptokinase therapy wasstarted, followed by intravenous he-parin (a bolus of 5000 U and infusionat a rate of 1000 U/h). No contraindi-cations to streptokinase therapy werepresent according to current guide-lines (Table I). A brief episode of hy-potension followed but responded tofluid infusion. Her hemoglobin level2 hours after the initiation of therapywas 76 g/L. Nine hours after admis-sion, she complained of neck pain and

nausea, and her systolic blood pressuredropped to 50 mm Hg. Heparin wasstopped, and she was treated with in-travenous fluids, dobutamine anddopamine. Her systolic pressure, how-ever, remained below 80 mm Hg formore than 3 hours. Her abdomengradually became distended and herhemoglobin level continued to fall.She was thought to have a retroperi-toneal hematoma and was given13 units of packed red blood cells,6 units of fresh frozen plasma and10 units of cryoprecipitate. Thatevening, she suffered respiratory dis-tress requiring intubation and assistedventilation. The chest radiograph wassuggestive of adult respiratory distresssyndrome. Her oxygen requirement

gradually increased, the serum creati-nine and creatine phosphokinase levelsrose and urine output fell. She wassubsequently transferred to a tertiarycare centre.On admission she was hemodynam-

ically stable on dobutamine, with a he-moglobin level of 80 g/L and a nor-mal coagulation profile. However, herabdomen was distended and firm, herlower limbs were grossly edematousand she required ventilation and dialy-sis. Abdominal CT showed intraperi-toneal blood with a fluid–fluid level(suggestive of settled blood compo-nents) and a ruptured spleen (Fig. 1).At operation, a large amount of

clotted blood was evacuated from theabdomen, but there were no sites ofactive bleeding. The anterior spleniccapsule was ruptured, so splenectomywas performed. Blood pressure wasstable and urine output resumed dur-ing the operation.Her oxygen requirements im-

proved immediately after operation.The serum creatinine and urine out-puts had returned to normal by the10th day, and she subsequently madea complete recovery.

DISCUSSION

Thrombolytic therapy is an acceptedtreatment option in the managementof acute myocardial infarction.10 Therisk of severe or life-threatening bleed-ing from combined streptokinase andintravenous heparin therapy is 0.5%.11

However, splenic hemorrhage has notbeen documented as a complication inlarge clinical trials,11,12 rather, intracra-nial, gastrointestinal, retroperitonealand pulmonary sites of bleeding havebeen described.12

Only three cases of spontaneoussplenic rupture after streptokinasetherapy have been reported.13–15 Twoof the reports described the use ofstreptokinase to treat myocardial in-

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152 JCC, Vol. 39, no 2, avril 1996

Table I

High likelihood of left heart thrombus

Genitourinary bleeding within 10 d

Acute pericarditis

Subacute bacterial endocarditis

Hemostatic defects including those secondary to severe hepatic or renal disease

Significant liver dysfunction

Pregnancy or less than 28 days post-partum

Diabetic hemorrhagic retinopathy or other hemorrhagic ophthalmic conditions

Contraindications to Streptokinase Administration (The Wellesley Hospital Protocol, De-partment of Pharmacy, 1994)

Septic thrombophlebitis or occluded arteriovenous cannula at seriously infected site

Streptokinase therapy in the previous 6 mo

Confirmed streptococcal infection

Absolute

Active internal bleeding

History of stroke within 2 mo

Bleeding diathesis

Surgical procedure within 10 d

Intracranial neoplasm, arteriovenous malformation or aneurysm

Severe uncontrolled hypertension (> 200 mm Hg systolic or > 110 mm Hg diastolic)

Recent traumatic cardiopulmonary resuscitation

Relative

Significant gastrointestinal bleeding or active peptic ulcer within 10 d

Evidence of transient ischemic attacks

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farctions,13,14 whereas the third was fordeep venous thrombosis.15 Both pa-tients with myocardial infarctions werepreviously healthy and neither had anyhistory of trauma. In one patient,Gardner-Medwin and associates14 re-ported that pathological examinationof the spleen revealed a single tear onthe posterior surface, an area not usu-ally associated with trauma. No ade-quate explanations were given for thesplenic rupture in these cases.It is unlikely, however, that sponta-

neous rupture occurred in our patient.It is difficult to accept that the spleencan rupture spontaneously fromthrombolytic therapy alone. Morelikely some minor forgotten traumapredisposed the patient to splenic rup-ture. Lesser trauma, such as a fall orfight, often forgotten by the patient,has been implicated as a commoncause of delayed rupture.9 Our patienthad a history of major abdominal

trauma 6 months before streptokinasetherapy. It would be reasonable to at-tribute her complications to a strep-tokinase-induced DSR.The controversy of whether DSR is

a true diagnosis or merely delayedrecognition of the rupture has beenfuelled by the marked drop in its oc-currence, likely from improved diag-nostic skills. DPL immediately afterabdominal trauma has reduced the in-cidence of DSR from approximately15% to 1%.3,8 Abdominal CT has alsoreduced the incidence of delayed rup-ture, with reported sensitivities andspecificities for acute splenic injury ex-ceeding 96%.16 As a result, some au-thors have expanded their definitionsof DSR to include investigative andclinical considerations. Schlater andOshita17 defined DSR as rupture thatoccurs more than 48 hours after inju -ry and when initial splenic imaging is negative. On the other hand,

Berlatzky and associates7 suggestedthat DSR should be restricted to casesin which there is an asymptomatic in-terval between initial trauma and sec-ondary hemorrhage.Although most DSRs occur within

2 weeks of injury,4 there have been re-ports of intervals ranging from 1 to11 years, with long asymptomatic pe-riods between the time of injury andsecondary splenic hemorrhage.5,6 Thisis consistent with the predominanttheories outlining the mechanism ofDSR. One theory proposes that thesplenic capsule is able to contain theinitial parenchymal hemorrhage withina cystic architecture only to rupturesometime later.1,9,17–20 Subcapsularhematomas would account for the ini-tial unremarkable results of DPL, andif the lesion is small enough, CT scanswould be negative at the time of initialinjury. In contrast, another theory sug-gests that the splenic capsule is directlycompromised from the onset of pri-mary injury with the subsequent hem-orrhage being contained by adjacentstructures such as omentum.1,9,18,21,22 Al-though functionally controlled, theplug would be dependent on intra-abdominal stability because of theweak fibrinous union formed betweenthe two viscera.1

Clues to impending DSR are non-specific. Patients usually complain ofdiffuse abdominal pain1 or fullness andof discomfort in the left upper quad-rant although they may have minimalor no symptoms.6 Taylor and Rosen-field20 found that CT scans, despitetheir accuracy, could not identify all in-trasplenic lacerations at the time of ini-tial injury. Also, Gruenberg and Ho-ran23 reported a case of DSR 25 daysafter trauma in which initial investiga-tions of DPL and visceral angiographyall gave negative results. Although ourpatient did not undergo CT or DPL atthe time of abdominal trauma, therewere no signs or symptoms of splenic

DELAYED SPLENIC RUPTURE AND STREPTOKINASE

CJS, Vol. 39, No. 2, April 1996 153

FIG. 1. Computed tomography scan (coronal slice) with intravenous contrast enhancement showslarge amount of intraperitoneal fluid (white arrow), suggestive of settled blood components or activebleeding with extravasation of contrast. Liver (open arrow) is displaced by this fluid. There is multilay-ered hematoma surrounding enlarged spleen (black arrow) suggestive of splenic rupture.

⇒

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injury. Thus, it would be easy to missDSR. Also, because the incidence of ableeding event after streptokinasetreatment has been reported12 to beapproximately 30% within the first96 hours, hypotensive episodes are notinfrequent. These are usually treatedconservatively with fluids or bloodtransfusions as needed. Hence, as oc-curred in our patient, unless specificclinical indications of a splenic rupturearise, streptokinase-induced hemor-rhage is unlikely to be suspected.Splenic hemorrhage is a potential

abdominal catastrophe. Signs of hypo-volemia accompanied by abdominaldistension and tenderness, and hy-poactive bowel sounds may be present.Left upper quadrant pain and tender-ness, Kehr’s sign (left shoulder paindue to irritation of the left hemidi-aphragm) and Ballance’s sign (dullnessaround the splenic area signifyinghematoma formation combined withshifting dullness in the right flank fromfree blood), however, are felt to bemore specific of a splenic injury.1,4,8,9 Al-though a mild leukocytosis and lowhemoglobin and hematocrit levels areconsistent with splenic hemorrhage,they are nonspecific and can be mis-leading.4,9 Definitive diagnosis can usu-ally be made by DPL and CT (Fig. 1).In view of the wide range of latent

periods reported for DSR (48 hoursto 11 years), it is possible that our pa-tient had sustained splenic trauma thatremained clinically silent. It is unlikelythat her cardiac ischemia was due toDSR before presentation since her he-moglobin level was normal, and sig-nificant blood loss would be necessaryto prompt cardiac dysfunction in anotherwise healthy person. This degreeof splenic hemorrhage would in-evitably be associated with abdominalsigns and symptoms, which were ab-sent initially. The administration ofstreptokinase, however, would un-doubtedly precipitate a splenic hem-

orrhage. To our knowledge, therehave been no reports in the literatureof DSR after streptokinase therapy.Although early thrombolytic ther-

apy is an accepted treatment for my-ocardial infarction, an active inquiryinto any history of blunt abdominaltrauma is reasonable. The danger ofDSR is that it can be clinically silent.Initial investigations at the time of ab-dominal trauma may be negative, andtherefore DSR may not be consideredin a patient with subsequent intra-abdominal bleeding. The effects ofthrombolytic agents should be closelyfollowed when DSR is possible.Prompt recognition of abdominalbleeding from DSR could prevent un-necessary morbidity and mortality.

References

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2. McIndoe AH: Delayed haemorrhagefollowing traumatic rupture of thespleen. Br J Surg 1932; 20: 249–268

3. Benjamin CI, Engrav LH, Perry JF:Delayed rupture or delayed diagnosisof rupture of the spleen. Surg GynecolObstet 1976; 142: 171–172

4. Sizer JS, Wayne ER, Frederick PL:Delayed rupture of the spleen. ArchSurg 1966; 92: 362–366

5. Zabinski E, Harfins H: Delayedsplenic rupture: a clinical syndromefollowing trauma. AMA Arch Surg1943; 46: 186–213

6. Dahiya SL, Phillips E, Neufeld P etal: Delayed rupture of the spleen. IntSurg 1976; 61: 295–296

7. Berlatzky Y, Shiloni E, Anner H et al:Delayed rupture of the spleen or de-layed diagnosis of the splenic injury?Isr J Med Sci 1980; 16: 659–664

8. Olsen WR, Polley TZ: A second lookat delayed splenic rupture. Arch Surg1977; 112: 422–425

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10. Effectiveness of intravenous throm-bolytic treatment in acute myocardialinfarction. Gruppo Italiano per loStudio della Streptochinasi nell’In-farto Miocardico (GISSI). Lancet1986; 1: 397–402

11. An international randomized trialcomparing four thrombolytic strate-gies for acute myocardial infarction.The GUSTO investigators. N Engl JMed 1993; 329: 673–682

12. McLeod DC, Coln WG, Thayer CF et al: Pharmacoepidemiology of bleeding events after use of r-alteplase or streptokinase in acutemyocardial infarction. Ann Pharma-cother 1993; 27: 956–962

13. Weiner RS, Ong LS: Streptokinaseand splenic rupture. [letter] Am JMed 1989; 86: 249

14. Gardner-Medwin J, Sayer J, MahidaYR et al: Spontaneous rupture ofspleen following streptokinase ther-apy. [letter] Lancet 1989; 2: 1398

15. Eklof B, Gjores JE, Lohi A et al:Spontaneous rupture of liver andspleen with severe intra-abdominalbleeding during streptokinase treat-ment of deep venous thrombosis. JVasc Dis 1977; 6: 369–371

16. Jeffrey RB, Laing FC, Federle MP etal: Computed tomography of splenictrauma. Radiology 1981; 141:729–732

17. Schlater DC, Oshita BH: Delayedrupture of the spleen. Ann EmergMed 1990; 19: 399–403

18. Petri RW, O’Brien PD, Vukich DJ:Delayed splenic rupture. Ann EmergMed 1990; 10: 1302–1305

19. Clark OH, Lim RC, Margaretten W:Spontaneous delayed splenic rupture.J Trauma 1975; 15: 245–249

20. Taylor CR, Rosenfield AT: Limita-tions of computed tomography in therecognition of delayed splenic rup-ture. J Comput Assist Tomogr 1984;8: 1205–1207

21. Johnson AE: A case of long-delayedrupture of the spleen followingtrauma. Br J Surg 1962; 50: 231–232

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