Interact CardioVasc Thorac Surg 2007;6:514-516. doi:10.1510/icvts.2006.147405
© 2007 European Association of Cardio-Thoracic Surgery
Negative results - Cardiopulmonary bypass |
Cerebral vein thrombosis after coronary artery bypass surgery
Dimitrios Zervakisa,*,
Panagiotis Angelidakisb,
Panagiotis Dedeiliasc and
Antonia Koutsoukoua
a Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos General Hospital, 45-47, Ipsilandou Street, Athens, GR-10676 Greece
b Department of Neurology, Evangelismos General Hospital, Athens, Greece
c 1st Cardiosurgery Department, Evangelismos General Hospital, Athens, Greece
Received 24 October 2006;
received in revised form 16 April 2007;
accepted 17 April 2007
*Corresponding author. Tel.: +30-210-7201913; fax: +30-210-7244941.
E-mail address: dzervakis{at}hotmail.com (D. Zervakis).
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Abstract
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A case of cerebral vein thrombosis after cardiac artery bypass grafting is presented in a patient with coronary artery disease and prolonged angina. Postoperatively he failed the weaning trials because of brain dysfunction characterized by confusion, agitation and hyperpnea. He was initially considered to represent a typical case of post cardiac surgery brain underperfusion, but as he later developed persistent signs of endocranial hypertension, imaging of the brain vessels was carried out revealing obstruction of the left transverse and the frontal half of the oblique sinus. The patient was treated with anticoagulation and cerebrospinal fluid drainage through a lumbo-peritoneal shunt. He was discharged from the ICU in good condition after 102 days of hospitalization. As magnetic resonance imaging of the brain is generally recommended in cases with post cardiac surgery brain dysfunction with normal computed tomography scan, adding magnetic resonance phlebography to the examination protocol seems rational.
Key Words: Cerebrovascular disease; Extracorporeal circulation; Intracranial hypertension
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1. Case description
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A 56-year-old male was admitted in the general intensive care unit (ICU) ten days after coronary artery bypass surgery, because of weaning failure due to brain dysfunction. The patient was referred to the cardiac surgeon because of unstable angina, due to two-vessel disease, proven by coronary angiography and underwent triple venous graft placement in the course of left anterior descending and left circumflex artery branches. Ischemia and bypass time were 45 and 95 min, respectively, while no intraoperative major events were recorded. Postoperatively he was admitted to the cardiosurgical ICU. On the second postoperative day, sedation withdrawal revealed moderate brain dysfunction with confusion, irritability and disorientation predominating in the picture. During the subsequent days he developed a fever of 38–39 oC, hypotension and gradual kidney function worsening. After a second failed trial of awakening, he was transferred to the general ICU for further treatment.
On admission, the patient presented hypotension, oliguria, fever and new onset atrial fibrillation. First neurological examination after discontinuing sedation revealed confusion, irritability, tachypnea with hypocapnea without hypoxemia and no focal neurologic signs. Transesophageal echocardiogram and ultrasonogram of carotids and vertebral arteries were normal. He was considered to represent a typical case of anoxic encephalopathy due to diminished tissue perfusion even though overall systolic cardiac performance was preserved and no intraoperative major events were recorded. He was supported with fluids, inotropes, sedation, full anticoagulation and infection control maneuvers for the following 40 days.
Brain parenchyma was found normal in terms of three sequential computed tomography (CT) scans (2nd, 6th and 21st day), as well as magnetic resonance imaging (MRI) (21st day). Repeated neurologic examinations gradually revealed typical signs of intracranial hypertension, namely central hyperventilation, bilateral 6th cranial nerve palsy and generalized muscle rigidity with inward flexion posture. An elevated intracranial pressure (33 cm H2O), disclosed during a lumbar puncture on the 33rd day led to the conduction of MR angiography (MRA) of the brain with special attention to venous brain drainage (35th day). Although brain tissue appeared normal on the MRA, there was suspicion regarding the integrity of the frontal half of the oblique sinus, as well as the left transverse sinus (Fig. 1). Interventional angiography (43rd day) failed to image the oblique sinus frontal half and furthermore revealed a flow impediment to the left transverse sinus as well the left internal jugular vein from its origin.
After diagnosing cerebral vein thrombosis, he was put under even more intensified heparin therapy and sequential attempts of cerebrospinal fluid drainage were undertaken, initially by external lumbar drain and later by the placement of a lumboperitoneal shunt. The patient's situation gradually improved and withdrawal of sedation and inotropes were allowed. He was discharged on the 102nd postoperative day from the ICU in a good condition. Forty-five days later, he was discharged from hospital.
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2. Discussion
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Brain dysfunction after cardiac surgery is quite common (17–61% for all types) and generally carries guarded prognosis in severe cases [1]. Prolonged duration of operation, age, previous morbidity and use of pump are major contributing factors [1]. Common mechanisms include brain tissue underperfusion, posterior circulation or large hemispheric stroke, medications used, massive microembolism during the native circulation reconstitution due to microthrombi, small lipid and gas emboli, and activation of the inflammatory cascade throughout the body [1]. Coma, confusion and agitation with only subtle focal deficits predominate in the clinical picture in the most severe cases. Brain CT scan is often negative [1, 2] but MRI reveals pathologic signal lesions in many patients [3]. Intracranial pressure has been mentioned to increase during cardiopulmonary bypass due to cerebral edema [4], but the appearance of characteristic signs of intracranial hypertension is virtually not mentioned. Cerebral vein thrombosis is a well-recognized clinical entity, characterized by symptoms and signs of intracranial hypertension, fever, elevated erythrocyte sedimentation rate and the appearance of hemorrhagically transformed ischemic lesions in certain regions of brain parenchyma [5]. Although in its severest form it causes global brain dysfunction, milder cases with headaches, focal seizures and fever have been increasingly recognized. Elevated intracranial pressure is the only manifestation in 25–33% of patients [5]. Major predisposing factors are pregnancy, hypotensive states, massive cerebrospinal fluid leak, cranial trauma and hypercoagulable states. Prognosis depends mainly on initial clinical presentation [6]. Diagnosis is suspected through detailed CT scan with intravenous contrast and confirmed with either MR phlebography of the brain or interventional angiography, the latter remaining the most reliable method [5, 7]. Current therapy consists of aggressive anticoagulation with heparin during the acute phase, combined with lowering intracranial pressure maneuvers [8].
The only predisposing factors found in our patient were perioperative hypotension and routine aprotinin use. All known hypercoagulable states were excluded by laboratory methods. After the coronary artery bypass surgery, he developed global brain dysfunction, which later evolved to intracranial hypertension clinical syndrome. In the absence of angiographic findings, this could represent a pseudotumor cerebri case [9]. He was finally diagnosed to have cerebral vein thrombosis on the basis of undoubted radiological findings but he also had elevated erythrocyte sedimentation rate, fever and fluctuating hemodynamic instability, all typically described in the context of the sinus vein thrombosis syndrome. Elevated intracranial pressure in terms of clinical examination and objective measurement triggered the investigation process. Throughout the clinical course, the brain parenchyma remained free of local and generalized findings. Additionally, full anticoagulation because of paroxysmal atrial fibrillation in the early postoperative period might have offered some protection. Although cerebral vein thrombosis is mentioned to result from a number of clinical conditions characterized by low tissue perfusion, to our knowledge relationship with cardiac surgery has never been published before, with the exception of a case with known antiphospholipid syndrome [10]. We propose that such a diagnosis could offer an explanation in some cases with discrete perioperative episodes of hypotension and postoperative brain insufficiency, especially when elevated intracranial pressure seems to predominate in the clinical syndrome.
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References
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- Arrowsmith JE, Grocott HP, Reves JG, Newman MF. Central nervous complications of cardiac surgery. Br J Anaesth 2000; 84:378–393.[Abstract/Free Full Text]
- Hedberg M, Boivie P, Edstrom C, Engstrom K. Cerebrovasular accidents after cardiac surgery: an analysis of C-T scans in relation to clinical symptoms. Scand Cardiovasc J 2005; 39:99–305.
- Perez-Vela J, Ramos-Gonzalez A, Lopez-Almodovar L, Renes-Gareno E, Escriba-Barcena A, Rubio-Regidor M, Ballenilla F, Perales-Rodriguez N, Rufilanchas-Sanchez J. Neurologic complications in the immediate postoperative period after cardiac surgery. Role of magnetic resonance imaging. Rev Esp Cardiol 2005; 58:1014–1021.[CrossRef][Medline]
- Smith P. Cerebral dysfunction after cardiac surgery: closing address. Ann Thorac Surg 1995; 59:1359–1362.[Free Full Text]
- Stam J. Thrombosis of the cerebral veins and sinuses. N Eng J Med 2005; 352:1791–1798.[Free Full Text]
- Ferro JM, Canhao P, Stam J, Bousser M-G, Barinagarrementeria F. Prognosis of cerebral vein and dural sinus thrombosis: results of the international study on cerebral vein and dural thrombosis (ISCVT). Stroke 2004; 35:664–670.[Abstract/Free Full Text]
- Ehtisham A, Stern B. Cerebral vein thrombosis: a review. Neurologist 2006; 12:32–38.[CrossRef][Medline]
- Einhaupl K, Bousser M-G, de Bruijn SFTM, Ferro JM, Martinelli M, Masuhr F, Stam J. EFNS guideline on the treatment of cerebral venous and sinus thrombosis. Eur J Neurol 2006; 13:553–559.[CrossRef][Medline]
- Higgins JN, Gillard JH, Owler BK, Harkness K, Pickard JD. MR venography in idiopathic intracranial hypertension: unappreciated and misunderstood. J Neurol Neurosurg Psych 2004; 75:621–625.[Abstract/Free Full Text]
- Emir M, Ozisic K, Cagli K, Bakuy V, Ozisic P, Sener E. Dural sinus thrombosis after cardiopulmonary bypass. Perfusion 2004; 19:133–135.[Abstract/Free Full Text]
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Abstract
1. Case description