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Table of Contents
Year : 2013  |  Volume : 16  |  Issue : 1  |  Page : 58-60
Extradural hematoma following double valve replacement under cardiopulmonary bypass: A rare complication

Department of Anesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Click here for correspondence address and email

Date of Submission26-Jun-2012
Date of Acceptance29-Aug-2012
Date of Web Publication2-Jan-2013


The primary mechanisms responsible for acute neurological deterioration following cardiopulmonary bypass (CPB) include cerebral embolism, cerebral hypoperfusion and/or inflammatory process triggered by CPB. Extradural hematoma (EDH) following CPB is rare but associated with significant mortality and morbidity. We present a case of EDH following double valve replacement in an adolescent boy.

Keywords: Cardiopulmonary bypass, Extradural hematoma, Valve replacement

How to cite this article:
Kumar B, Bhagat H, Raj R, Jayant A. Extradural hematoma following double valve replacement under cardiopulmonary bypass: A rare complication. Ann Card Anaesth 2013;16:58-60

How to cite this URL:
Kumar B, Bhagat H, Raj R, Jayant A. Extradural hematoma following double valve replacement under cardiopulmonary bypass: A rare complication. Ann Card Anaesth [serial online] 2013 [cited 2021 Oct 24];16:58-60. Available from:

   Introduction Top

Acute neurological deterioration following cardiopulmonary bypass (CPB) can be due to stroke or encephalopathy. The primary mechanisms responsible for the neurological deterioration include cerebral embolism, cerebral hypoperfusion, and/or inflammatory process triggered by CPB. Extradural hematoma (EDH) following CPB is rare but associated with significant morbidity and mortality. A few reports describe EDH following cardiac surgery on CPB. [1],[2],[3] We describe our experience of EDH following double valve replacement in an adolescent boy.

   Case Report Top

A 14-year-old boy weighing 29 kg presented with dyspnea on exertion and palpitation since past 4 years. There was no history of orthopnea, paroxysmal nocturnal dyspnea, pedal edema, infective endocarditis, traumatic injury to head, or any neurological symptom. On examination, pulse was regular, the rate was 110/min and the blood pressure was 120/40 mmHg. A pansystolic murmur was heard in mitral area and a diastolic murmur was heard in aortic area. Preoperative hematological and biochemical parameters were unremarkable. The prothrombin time was 15 seconds, activated partial thromboplastin time was 32 seconds with prothrombin time index of 93% (international normalized ratio 1.08), and platelet count was 2,91,000/dl. Preoperative transthoracic echocardiography showed severe regurgitation of aortic and mitral valves. The anterior mitral leaflet tip was flail and prolapsing while posterior mitral leaflet was thickened with decreased mobility. The left atrium and left ventricle were dilated with normal left ventricular systolic function (ejection fraction 70%). The right atrium, right ventricle, and tricuspid valve were normal. Preoperative optimization consisted of oral spironolactone and enalapril without any anticoagulant drugs. Patient underwent double valve replacement (27 mm mitral and 19 mm aortic St. Jude mechanical valve) under CPB. Anticoagulation for CPB was achieved with 3 mg/kg unfractionated heparin. The maximum intraoperative activated clotting time achieved was 639 seconds. The mean perfusion pressure during CPB was maintained between 50 and 70 mmHg. The arterial blood gas during CPB remained within normal range. The total CPB time was 125 min and aortic cross clamp time was 90 min. After the procedure CPB was terminated with the help of adrenaline 0.1 μg/kg/min. Post CPB residual heparin was neutralized with stoichiometrically equal doses of protamine. Following surgery, patient was transferred to the intensive care unit for postoperative mechanical ventilation and stabilization. Hemodynamic and biochemical parameters were within stipulated limits throughout the immediate postoperative period. Nevertheless, the patient failed to regain consciousness even on the next morning following surgery. Detailed neurological examination revealed unequal pupils with right pupil of 4 mm and left pupil of 2 mm, both reacting sluggishly to light. The patient's Glasgow Coma Score (GCS: Eye, Verbal and Motor response) was E-1, V-T (presence of endotracheal tube), M-2. Computerized tomography (CT) scan of head showed 8 × 7 × 3 cm EDH in left parieto-occipital region with left middle cerebral artery (MCA) territory infarct and midline shift [Figure 1]. Coagulation profile revealed prothrombin time 20 seconds, activated partial thromboplastin time 30 seconds, prothrombin time index of 70% (international normalized ratio of 1.6) with normal activated clotting time and platelet counts. An emergency left temporo-parieto occipital craniotomy was done after transfusing four units of fresh frozen plasma and the hematoma was evacuated. Intraoperatively there was diffuse bleeding but no definite bleeder could be identified.
Figure 1: Computerized tomography scan head showing extradural hematoma in left parieto-occipital region with underlying evolving left middle cerebral artery territory infarct and midline shift

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Following EDH evacuation the patient's GCS improved to E-1, V-T, M-4 and head CT scan showed left MCA territory infarct with diffuse cerebral edema and no midline shift [Figure 2]. Anticoagulation in the postoperative period was started after 48 hours of EDH evacuation with warfarin and monitored meticulously to keep target international normalized ratio (INR) around 2.5. On the postoperative day (POD) 5, the GCS score remained E-1, V-T, M-4 and head CT scan showed no fresh intracranial hemorrhage (ICH). Patient underwent a tracheostomy on POD 6. Repeat head CT scan showed no new changes but infarct in left middle and posterior cerebral artery territory. He was transferred to ward on POD 25. Subsequently he was discharged from hospital on POD 35 with right sided hemiparesis (Grade 3/5) and GCS of E-1, V-T, M-4.
Figure 2: Post extradural hematoma evacuation computerized tomography scan head showing left middle cerebral artery territory infarct with diffuse cerebral edema and no midline shift

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   Discussion Top

Intracranial EDH is almost always of posttraumatic origin. Spontaneous intracranial EDH is rare and can be caused by adjacent infections, dural vascular malformations, tumors, and disorders of blood coagulation. [4],[5],[6] Among disorders of blood coagulation oral anticoagulant therapy (OAT) has been implicated most often. [7] Higher intensities of anticoagulation clearly increase the risk of ICH, suggesting that OAT may directly cause ICH. [8] Spontaneous EDH following full heparinization during CPB has been reported in the medical literature: In one of those reports, cyanotic congenital heart disease causing coagulation abnormalities was considered as the cause of EDH. [1] Anegawa, et al., reported bifrontal EDH with mass effect in a 12-year-old female following surgery for subaortic stenosis. [3] The causes of space occupying hematoma following CPB could be either full heparinization during surgery and/or associated hypotension during the period of CPB. The latter can cause brain shrinkage and stretching and rupture of the dural bridging veins. [2]

EDH is a neurosurgical emergency that must be recognized and treated immediately. Majority of cases present with nonspecific signs and symptoms like headache or persistent vomiting that may be difficult to elicit in the immediate postoperative period. Altered sensorium is the most common presentation of EDH particularly in children. Other clinical signs such as pupil dilatation, seizures, and hemiparesis occur typically in the presence of associated intradural damage. [9] Radiological changes always occur earlier than clinical changes. Patients undergoing cardiac surgery with CPB are usually kept sedated in the immediate postoperative period and gradually weaned. Therefore, it is important to look for pupillary signs at frequent intervals in the postoperative period to detect any major neurological complication. The CT scan of head should be done immediately in all cases where spontaneous awakening is unusually delayed. It is also essential to check and immediately reverse any coagulation abnormality to minimize the risk of hematoma expansion.

There is no standard protocol for restarting anticoagulation after a neurosurgical procedure in this patient population. In patients who are at high risk for thromboembolism, reinitiating anticoagulation is necessary. Nevertheless ICH occurring secondary to anticoagulant drugs can have devastating consequences. Therefore the decision making process should be individualized by the neurosurgical and cardiothoracic team, in addition to locally prevalent protocols. [10] One of the expert groups suggest that anticoagulation should be resumed after 1 week as the long-term risk of further intracranial bleeding is lower than that of valve thrombosis and thromboembolism. [11] Intravenous heparin (targeted to achieve activated partial thromboplastin time of 1.5-2.0) can be an option.

The choice of optimum INR for OAT should take into account patient risk factors and the thrombogenicity of the individual prosthesis. [12] However, the outcome of the bleeding events may be more severe than the outcome of the thromboembolic events. In order to avoid risk of bleeding we started warfarin 48 hours after EDH evacuation and maintained INR meticulously near about 2.5 since the risk of embolism rises sharply below an INR of 2.5. [13] We ruled out re-bleed by repeating head CT scan on POD 5 and 10 and gradually increased INR to 3 after ruling out any re-bleed on further head CT scan 2 weeks after surgery.

   Conclusion Top

Subtle neurological complications are not uncommon following CPB. However, spontaneous EDH is a very rare entity. Close vigilance should be maintained to detect any neurological complication in the postoperative period. Delay in detection worsen the outcome in this group of patients.

   References Top

1.Ahmad FU, Pandey P, Mahapatra AK. Spontaneous posterior fossa extradural hematoma- A rare complication following cardiac surgery. Pediatr Neurosurg 2005;41:49-51.  Back to cited text no. 1
2.Hoffman HJ, Mustard WT. Spontaneous intracranial extradural hematoma occurring during open heart surgery. Can J Surg 1973;16:130-1.  Back to cited text no. 2
3.Anegawa S, Hayashi T, Furukawa Y, Nagashima T, Kumate M. Spontaneous epidural hematoma after open heart surgery: Case report. No Shinkei Geka 1999;27:1023-6.  Back to cited text no. 3
4.Chaiyasate S, Halewyck S, van Rompaey K, Clement P. Spontaneous extradural hematoma as a presentation of sinusitis: Case report and literature review. Int J Pediatr Otorhinolaryngol 2007;71:827-30.  Back to cited text no. 4
5.Shahlaie K, Fox A, Butani L, Boggan JE. Spontaneous epidural hemorrhage in chronic renal failure: A case report and review. Pediatr Nephrol 2004;19:1168-72.  Back to cited text no. 5
6.Wani AA, Ramzan AU, Kirmani AR, Bhatt AR, Hamdani N, Zargar J. Intradiploic epidermoid causing spontaneous extradural hematoma: Case report. Neurosurgery 2008;62:E971.  Back to cited text no. 6
7.Hylek EM, Singer DE. Risk factors for intracranial hemorrhage in outpatients taking warfarin. Ann Intern Med 1994;120:891-902.  Back to cited text no. 7
8.Rosand J, Eckman MH, Knudsen KA, Singer DE, Greenberg SM. The effect of warfarin and intensity of anticoagulation on outcome of intracerebral hemorrhage. Arch Intern Med 2004;164:880-4.  Back to cited text no. 8
9.Jamjoom A, Cummins B, Jamjoom ZA. Clinical characteristics of traumatic extradural haematoma: A comparison between children and adults. Neurosurg Rev 1994;17:277-81.  Back to cited text no. 9
10.Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, et al. American Heart Association; American Stroke Association Stroke Council; High Blood Pressure Research Council; Quality of Care and Outcomes in Research Interdisciplinary Working Group. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: A guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007;38:2001-23.  Back to cited text no. 10
11.Butchart EG, Gohlke-Bärwolf C, Antunes MJ, Tornos P, De Caterina R, Cormier B, et al. Working Groups on Valvular Heart Disease, Thrombosis, and Cardiac Rehabilitation and Exercise Physiology, European Society of Cardiology. Recommendations for the management of patients after heart valve surgery. Eur Heart J 2005;26:2463-71.  Back to cited text no. 11
12.Butchart EG. Prosthesis-specific and patient-specific anticoagulation. In: Butchart EG, Bodnar E, editors. Current Issues in Heart Valve Disease: Thrombosis, Embolism and Bleeding. London: ICR Publishers; 1992. p. 293-317.  Back to cited text no. 12
13.Cannegieter SC, Rosendaal FR, Wintzen AR, van den meer FJ, Vandenbroucke JP, Briet E. Optimal oral anticoagulant therapy in patients with mechanical heart valves. N Engl J Med 1995;333:11-7.  Back to cited text no. 13

Correspondence Address:
Bhupesh Kumar
Department of Anesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.105373

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  [Figure 1], [Figure 2]