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| CASE REPORT |
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| Year : 2020 | Volume
: 10
| Issue : 6 | Page : 297-299 |
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Post-operative ischaemic stroke after transpulmonary embolism: A diagnostic challenge
Sagarika Panda, Gaurav Jain, Sonu Sama, Vamshi Krishna
Department of Anaesthesiology and Critical Care, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
| Date of Submission | 12-Nov-2020 |
| Date of Acceptance | 17-Nov-2020 |
| Date of Web Publication | 24-Dec-2020 |
Correspondence Address:
Dr. Gaurav Jain
Department of Anaesthesiology and Critical Care, All India Institute of Medical Sciences, Virbhadra Marg, Rishikesh - 249 203, Uttarakhand
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/cmrp.cmrp_58_20
Fixing a femoral neck fracture in elderly patients restores their independent mobility, and decreases the associated mortality and morbidity. Perioperative stroke is the most undesired complication in such patients, having a miserable outcome. We report a similar case where the patient developed ischaemic stroke in the immediate post-operative period, where a diagnostic workup revealed the presence of a new-onset pulmonary arterial hypertension with suspected embolism, in the absence of cardiopulmonary shunt, visible thrombus or embolus of cardiac origin. This case highlights the diagnostic dilemma in evaluating the cause of post-operative stroke and emphasises the need for a multimodal approach to investigate the suspected acute pulmonary embolism and to identify the possible sites for the origin of an embolus.
Keywords: Angiography, deep-vein thrombosis, ischaemic stroke, pulmonary embolism
How to cite this article:
Panda S, Jain G, Sama S, Krishna V. Post-operative ischaemic stroke after transpulmonary embolism: A diagnostic challenge. Curr Med Res Pract 2020;10:297-9 |
How to cite this URL:
Panda S, Jain G, Sama S, Krishna V. Post-operative ischaemic stroke after transpulmonary embolism: A diagnostic challenge. Curr Med Res Pract [serial online] 2020 [cited 2021 Jan 25];10:297-9. Available from: http://www.cmrp.org/text.asp?2020/10/6/297/304829 |
| Introduction | |  |
Post-operative stroke is a life-threatening complication, having a reported incidence of 0.2%–0.3% in orthopaedic surgeries. The literature is sparse on an association of post-operative ischaemic stroke with a new-onset pulmonary arterial hypertension (PAH) secondary to a suspected embolic phenomenon, in the absence of cardiopulmonary shunt, visible thrombus or embolus of cardiac origin.
| Case Report | | |
A 67-year-old female with no comorbidities presented to the emergency department with the chief complaints of pain in the left hip and inability to bear weight, after sustaining an injury due to fall from height. She had excruciating pain on attempting the log roll test. The radiological work-up classified it as Garden III femoral neck fracture. The other laboratory investigations, chest radiograph, electrocardiogram and echocardiogram were unremarkable.
She underwent a left hip bipolar cemented hemiarthroplasty, under combined spinal-epidural anaesthesia. The intraoperative period (duration 2 h) remained uneventful, with an estimated blood loss of 200 ml. After the 1st post-operative hour, she developed a sudden onset of respiratory distress, chest discomfort, tachypnoea, tachycardia, hypotension (blood pressure: 82/50 mmHg), restlessness, generalised weakness and oxygen desaturation to 82%. The motor power was grade 2/5 in the upper extremity (UE) and grade 1/5 in the lower extremity (LE), bilaterally. The deep tendon reflexes (UE normal and LE non-assessable) and the sensory functions were normal. There were no signs of intracranial hypertension, cerebellar dysfunction or cranial nerve palsy, and she was afebrile. We initiated her on oxygen therapy (6 L/min) through facemask and rehydration with Ringer lactate (500 ml intravenously) over 20 min. Arterial blood analysis revealed Type 1 respiratory failure (PO2: 44 mmHg, PaCO2: 33.6 mmHg, pH: 7.46 and HCO3: 23.2 mEq/L). In view of the persistent symptoms, we transferred her to the intensive care unit and initiated invasive mechanical ventilation (assisted controlled mode) and vasopressor infusion (noradrenaline: 0.2 μg/kg/min). Electrocardiogram revealed an inverted T-wave in the chest lead V4 and V5, and D-dimer was 5.5 mg/ml. Echocardiogram showed a moderately dilated right ventricle (RV), an interventricular septal shift towards the left chamber and PAH, but no cardiac thrombus or shunts [Figure 1]. Chest radiograph and the LE Doppler were normal, although pelvic veins could not be assessed. In view of the clinical presentation, she was graded under moderate-to-high clinical probability (modified Geneva score: 9; Well's score: 9) for pulmonary embolism (PE), and initiated on low-molecular-weight heparin (60 mg subcutaneously twice a day). | Figure 1: Echocardiogram showing a moderately dilated right ventricle, an interventricular septal shift towards the left chamber
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In suspicion of PE, we performed computed tomography (CT) pulmonary angiography on the 2nd post-operative day, which confirmed the RV dilatation, and PAH (main pulmonary trunk: 34 mm) [Figure 2]. However, any focal filling defect in the pulmonary vessels was not evident. To rule out the suspected stroke, we performed a CT scan brain, which revealed ill-defined hypodensity in the right corona radiata and centrum semi-ovale, and few lacunar infarcts in the bilateral ganglio-capsular region and pons [Figure 3] and [Figure 4]. The subsequent CT brain angiography confirmed the presence of acute infarct in the left insular cortex and right centrum semi-ovale. Based on clinical presentation and the radiological work-up, we made a diagnosis of post-operative stroke, possibly due to embolisation, and managed her conservatively. Gradually, her clinical condition stabilised, and we tapered off the noradrenaline infusion on the 4th post-operative day. Repeat echocardiography showed normalised parameters, and she was extubated on the 10th post-operative day. After extubation, she was lethargic, was non-communicative and had persistent motor weakness (bilateral UE: grade 3/5, bilateral LE: grade 2/5). It improved gradually over a period of 2 weeks (motor power bilateral UE and LE: 4/5 grade), and she was discharged to a step-down facility with no other complications. | Figure 2: Pulmonary computed tomography angiography showing right ventricular dilatation, with dilated main pulmonary trunk
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 | Figure 3: Computed tomography scan brain showing an ill-defined hypodensity in the right corona radiata and centrum semi-ovale
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 | Figure 4: Computed tomography scan brain showing lacunar infarcts in the bilateral ganglio-capsular region and pons
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| Discussion | | |
Orthopaedic patients are at a significant risk of thromboembolic complications such as deep-vein thrombosis, cardiovascular dysfunction, PE and ischaemic stroke. The underlying pathophysiology involves the embolisation of cement material, fat globules, air or marrow particles from the surgery site. It passes through the blood circulation to the heart and lungs or in the case of paradoxical embolism to the brain.[1] The site of emboli impaction is usually the main pulmonary trunk and pulmonary or segmental arteries, with an inverse correlation between the size and terminal location of an embolus.[2] The micro-emboli, especially air and fat globules, owing to deformability, can even traverse unaffected through the pulmonary capillaries and may enter the systemic circulation.[3] Hence, such emboli may remain undetected even on pulmonary angiography. An animal study by Byrick et al.[3] also concluded it to occur within 3 h after orthopaedic surgery. Thus, cerebral embolisation with consequent infarction is a possibility even in the absence of a cardiac shunt or pulmonary arteriovenous fistula.[3] The CT angiography is a standard imaging modality to rule out the thrombus or embolus in the blood vessels. However, as a lone modality, it may be inefficient to exclude the acute PE in high clinical probability patients, thus requiring other complementary tests.[3] Contrast-enhanced trans-oesophageal echocardiography could aid in the diagnosis of transpulmonary embolism by looking for cardiac shunts, especially where transthoracic echocardiography (TE) is inconclusive. We could not utilise this modality due to availability issues. However, there was no evidence of any thrombus, air or fat globules in pulmonary or cerebral circulation on CT angiography, performed on the 2nd day after the onset of symptoms. There was also no doubt about the possibility of any cardiac shunt on TE. The D-dimer was strongly positive, however pelvic veins were inaccessible, to rule out the deep-vein thrombosis. The critical condition of this patient precluded the possibility of an early diagnostic scan, and, thus, we presume that any evident emboli might have resolved by the time we performed the angiography scan. Suri et al.[4] observed similar resolution of air emboli with evolving cerebral infarct at 12 h after the onset of hemiplegia.[4]
Apart from mechanical blockade, the emboli also initiate an acute and complex cascade of pro-inflammatory mediators, which may lead to profound pulmonary vasoconstriction, impaired myocardial contractility, right heart failure, systemic hypotension and altered coagulation.[5] We observed similar complications in this patient, which potentiated a high suspicion for the possibility of PE in the immediate post-operative period.
| Conclusion | | |
This case highlights the challenges and controversies in investigating the cause of post-operative ischaemic stroke and emphasises the need for a broader clinical and diagnostic approach in investigating a suspected acute PE, and the possible sites for its origin.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Parvizi J, Holiday AD, Ereth MH, Lewallen DG. Sudden death during primary hip arthroplasty. Clin Orthop Relat Res 1999;369:39-48.  |
| 2. | Belzile D, Jacquet S, Bertoletti L, Lacasse Y, Lambert C, Lega JC, et al. Outcomes following a negative computed tomography pulmonary angiography according to pulmonary embolism prevalence: A meta-analysis of the management outcome studies. J Thromb Haemost 2018;16:1107-20. |
| 3. | Byrick RJ, Mullen JB, Mazer CD, Guest CB. Transpulmonary systemic fat embolism. Studies in mongrel dogs after cemented arthroplasty. Am J Respir Crit Care Med 1994;150:1416-22. |
| 4. | Suri V, Gupta R, Sharma G, Suri K. An unusual cause of ischemic stroke Cerebral air embolism. Ann Indian Acad Neurol 2014;17:89-91. [ PUBMED] [Full text] |
| 5. | Kotyra M, Houltz E, Ricksten SE. Pulmonary haemodynamics and right ventricular function during cemented hemiarthroplasty for femoral neck fracture. Acta Anaesthesiol Scand 2010;54:1210-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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