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Ann Thorac Surg 2007;83:1172-1174
© 2007 The Society of Thoracic Surgeons


Case Reports

Unusual Complication of Heparin-Induced Thrombocytopenia After Mitral Valve Surgery: Spontaneous Rupture of Spleen

Christina Mitchell, MDa, Catherine A. Riley, MDb, Bobbak Vahid, MDb,*

a Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania
b Department of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania

Accepted for publication August 28, 2006.


Abbreviations and Acronyms CT = Computed Tomography; ED = Emergency Department; FFP = fresh frozen plasma; HIT = Heparin-Induced Thrombocytopenia; ICU = Intensive Care Unit; INR = International Normalized Ratio; MTHFR = Methyl-tetra-hydro-folate Reductase; PTT = Partial Thromboplastin Time


* Address correspondence to Dr Vahid, 834 Walnut St, Suite 650, Philadelphia, PA 19107 (Email: bobbak.vahid{at}mail.tju.edu).


    Abstract
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 Abstract
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A 64-year-old man presented with cardiac tamponade 2 weeks after mitral valve surgery. The patient was anticoagulated for persistent atrial fibrillation after cardiac surgery. A pericardial catheter was placed. Five days after presentation the patient was started on intravenous heparin infusion. The patient had abdominal pain and hypotension develop. A splenic hematoma was diagnosed and a splenectomy was performed. Pathology showed multiple fibrin thrombi in the spleen. The heparin-associated antibodies were detected. Heparin-induced thrombocytopenia is a potentially fatal condition in patients requiring heparin after cardiac surgery. Evaluation for heparin-associated antibodies in these patients may be warranted before heparin therapy.


    Introduction
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Heparin is a common agent used for systemic anticoagulation. Approximately 1% to 3% of patients exposed to unfractionated heparin may develop an antibody-mediated thrombocytopenia. This condition is known as heparin-induced thrombocytopenia type II (HIT) [1]. The HIT carries an increased risk for both venous and arterial thrombosis. The HIT-associated antibodies are commonly detected after cardiac surgery [2]. Thrombotic complications and high mortality have been reported after cardiotomy [3]. In this report we describe a case of atraumatic rupture of spleen due to HIT and splenic infarction. We believe that this is the first case of HIT presenting as splenic rupture after cardiac surgery.

A 64-year-old man presented to the emergency department with palpitation and worsening dyspnea for 1 day. Two weeks before presentation the patient underwent mitral valve annuloplasty for severe mitral valve regurgitation secondary to mitral valve prolapse with posterior flail leaflet. Postoperatively the patient had persistent atrial fibrillation develop that required anticoagulation. The anticoagulation with heparin infusion and warfarin was initiated. Eight days before presentation the patient was discharged home after mitral valve surgery on warfarin. On presentation he was in mild respiratory distress. On physical examination he showed a temperature of 37.6°C, a blood pressure of 83/42 mm Hg, an elevated jugular venous pulse, an irregular heart rhythm, and clear chest auscultation. An electrocardiogram showed atrial fibrillation with a ventricular rate of 130 beats/min. A chest roentgenogram showed clear lung fields and enlarged cardiac shadow size. Urgent echocardiography in the emergency room revealed pericardial effusion with tamponade physiology. The patient was admitted to the intensive care unit. Laboratory findings on admission showed a white blood cell count of 6.4 x 103/mL, a hemoglobin of 10 g/dL, a normal platelet count, a normal serum chemistry, a prothrombin time of 43.5 seconds, an international normalized ratio of 4.2, and a partial thromboplastin time of 55 seconds. Fresh frozen plasma and intravenous vitamin K were given to correct the coagulopathy. A percutaneous pericardial catheter was placed. A bloody effusion of 220 mL was drained. The patient’s heart rate and blood pressure were normalized after drainage of the fluid. The prothrombin time and partial thromboplastin time were normalized after fresh frozen plasma and vitamin K therapy. The pericardial catheter was removed after 3 days. The pericardial fluid cultures and cytology were unremarkable.

Anticoagulation was re-started. Heparin infusion was started 5 days after admission. Six days after admission the patient had sudden and sharp abdominal pain in the left upper quadrant develop. Physical examination revealed a blood pressure of 65/40 mm Hg, a heart rate of 140 beats/mins, and diffuse abdominal tenderness. Laboratory findings included normal prothrombin time, partial thromboplastin time of 88 seconds (normal, 25 to 32 secs), and hemoglobin of 7.8 g/dL. A computed tomographic scan of the abdomen and pelvis revealed a markedly enlarged and heterogeneous spleen consistent with acute splenic hemorrhage with a large amount of hemoperitoneum (Fig 1). The patient underwent emergent exploratory laparotomy and splenectomy. A splenectomy was performed and approximately 4 L of blood was evacuated from the abdominal cavity. The patient was transfused with 9 units of packed red blood cells in the perioperative period. Pathology of the spleen revealed marked presence of arterial platelet-fibrin thrombi with parenchymal infarction and hemorrhage. Figure 2 shows the change in platelet count during hospitalization. The decline in platelet count after heparin infusion is characteristic of heparin-induced thrombocytopenia. The serotonin release assay and heparin-platelet factor 4 solid phase immunoassay confirmed the presence of HIT-associated antibodies in the patient’s serum. A compression ultrasonography of the upper and lower extremities revealed the presence of right great saphenous vein thrombosis with extension into the right common femoral vein.


Figure 1
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Fig 1. A computed tomographic scan of abdomen showing splenic hematoma (arrow) and intraabdominal fluid.

 

Figure 2
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Fig 2. Platelet (PLT) counts during hospitalization. Arrow indicates the initiation of heparin infusion.

 
We believe our case report describes an unusual complication of heparin-induced thrombocytopenia thrombosis after mitral valve surgery and cardiopulmonary bypass. The patient had thrombocytopenia develop quickly after re-exposure to heparin. The microthrombi formation in the spleen resulted in infarctions and eventually splenic rupture. The presence of lower extremity venous thrombosis could also be another manifestation of HIT in our patient. Complete thrombophilic workup was unremarkable for other hypercoagulable conditions. The patient was started on direct thrombin inhibitor agent (argatroban). Figure 2 also shows recovery of his platelet count. He was started on warfarin therapy for long-term anticoagulation.


    Comment
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 Abstract
 Introduction
 Comment
 References
 
Unfractionated heparin is routinely used during cardiopulmonary bypass. Heparin-associated antibodies are detectable in 25% to 50% of patients during the first 10 days after cardiac surgery. If these antibodies activate platelets and coagulation, heparin-induced thrombocytopenia develops. The HIT can present as a sudden drop in platelet count while on heparin therapy, especially within 3 months after cardiac surgery. The HIT is a prothrombotic condition and 38% to 81% of the patients have thrombosis develop. Although HIT is generally associated with predominance of venous versus arterial thrombosis, in postcardiac surgery arterial thrombosis predominates. Major complications of arterial thrombosis are limb ischemia, thrombotic cerebrovascular infarction, and myocardial infarction. Arterial thrombi are rarely seen in the mesenteric, renal, or spinal arteries. The HIT-associated mortality in cardiac surgery patients is as high as 28% [4–7].

Splenic rupture is extremely rare after cardiac surgery [7]. There are rare cases of spontaneous splenic rupture associated with heparin treatment reported in recent literature. In these reports the splenic rupture was associated with either subcutaneous or intravenous heparin therapy. The presence of platelet-fibrin thrombi, splenic infarction, or decline in platelet count during heparin therapy was not reported in any of these cases [8–10]. Although HIT and thrombotic complications of HIT are more common after cardiac surgery, the splenic infarction and spontaneous rupture of the spleen has not been reported in the past.

Rapid decline in platelet count while on heparin therapy, especially within 3 months after cardiac surgery should alert the clinicians to the possibility of HIT. Spontaneous rupture of the spleen should be considered as a rare complication of HIT after cardiac surgery. Arterial or venous thrombi in other organs are other potential complications of heparin-induced thrombocytopenia. Evaluation for heparin-associated antibodies may be warranted in these patients before heparin therapy.


    References
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 Abstract
 Introduction
 Comment
 References
 

  1. Menajovsky BL. Heparin-induced thrombocytopenia: clinical manifestations and management strategies Am J Med 2005;118:21S-30S.
  2. Bauer TL, Arepally G, Konkle BA, et al. Prevalence of heparin-associated antibodies without thrombosis in patients undergoing cardiopulmonary bypass surgery Circulation 1997;95:1242-1246.[Abstract/Free Full Text]
  3. Wan C, Warner M, DeVarennes B, et al. Clinical presentation, temporal relationship, and outcome in thirty-three patients with type 2 heparin-induced thrombocytopenia after cardiotomy Ann Thorc Surg 2006;82:21-27.[Abstract/Free Full Text]
  4. Warkentin TE, Greinacher A. Heparin-induced thrombocytopenia and cardiac surgery An Thorac Surg 2003;76:2121-2131.
  5. Lubenow N, Kempf R, Eichner A, et al. Heparin-induced thrombocytopenia: temporal pattern of thrombocytopenia in relation to initial use or reexposure to heparin Chest 2002;122:37-42.[Medline]
  6. Warkentin TE, Kelton JG. Temporal aspects of heparin-induced thrombocytopenia N Engl J Med 2001;344:1286-1292.[Abstract/Free Full Text]
  7. Pilkey RM, Lawrence, MD, Wolfson Al, et al. Splenic rupture resulting from acute pancreatitis after cardiac surgery with intra-aortic balloon pumping: case report Can J Surg 1994;37:428-429.[Medline]
  8. Weiss SJ, Smith T, Laurin E, et al. Spontaneous splenic rupture due to subcutaneous heparin therapy J Emer Med 2000;18:421-426.
  9. Burg MD, Dallara JJ. Rupture of a previously normal spleen in association with enoxaparin: an unusual cause of shock J Emerg Med 2001;20:349-352.[Medline]
  10. Ghobrial MW, Karim M, Mannam S. Spontaneous splenic rupture following the administration of intravenous heparin: case report and retrospective case review Am J Hematol 2002;71:314-317.[Medline]




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