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CC BY 4.0 · J Neuroanaesth Crit Care
DOI: 10.1055/s-0045-1810627
Case Report

A Case of Ischemic Stroke Complicated by Hemorrhagic Transformation in Rheumatic Heart Disease

Kanika Gupta 
1   Department of Anaesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
,
Parvati N. Bankad
1   Department of Anaesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
,
Bishnupriya Mohapatra
1   Department of Anaesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
,
Gaurav Jain
1   Department of Anaesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
› Author Affiliations
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Abstract

We report the case of a 57-year-old male with rheumatic heart disease and chronic hepatitis B, who presented with acute left middle cerebral artery infarct and was thrombolysed with tenecteplase. He subsequently developed hemorrhagic transformation with mass effect. As prothrombin complex concentrate could not be arranged, he was managed with cryoprecipitate, tranexamic acid, and vitamin K. He underwent emergency decompressive craniectomy, followed by hematoma expansion requiring a second surgery. Intraoperatively, he had labile vitals requiring vasopressor support and rate control. Despite transient postoperative improvement, the patient suffered cardiac arrest on day 5. This case highlights the complex interplay of thrombolysis, valvular pathology, and clinical decision-making challenges in the management of hemorrhagic transformation in patients with rheumatic heart disease.


 

Keywords

tenecteplase - ischemic stroke - hemorrhagic transformation - valvular disease

Introduction

Hemorrhagic transformation (HT) is a frequent complication following an ischemic stroke, particularly aggravated by reperfusion strategies such as recombinant tissue plasminogen activator or endovascular interventions. It results from significant disruption of the blood–brain barrier, allowing peripheral blood to leak into brain tissue. The occurrence of HT is associated with increased stroke-related morbidity and mortality, making its prevention crucial.[1] Among the various established causes of ischemic stroke, cardioembolic strokes are typically associated with the most severe clinical outcomes.[2] Patients with cardiac disease and atrial fibrillation (AF) are frequently on anticoagulant therapy, which increases the risk of bleeding and may adversely affect clinical outcomes.[3] Anesthetic management in this subset of patients poses a unique challenge, requiring a delicate balance between maintaining adequate cerebral perfusion, avoiding excessive blood pressure elevation that may exacerbate hemorrhage, and preventing coronary hypoperfusion.


 

Case Report

A 57-year-old male with known rheumatic heart disease (RHD) and chronic hepatitis B infection presented to the cardiology outpatient clinic for follow-up. During the visit (7:30 p.m.), he developed acute dizziness, slurred speech, and right-sided hemiparesis. Magnetic resonance imaging brain revealed an acute left middle cerebral artery (MCA) infarct. At presentation, the National Institutes of Health Stroke Scale (NIHSS) score was 9; blood pressure (BP) 130/90 mm Hg, heart rate (HR) 89/min (AF), SpO2 97% on room air, and Glasgow Coma Scale (GCS) E4V4M6. As he was within the thrombolysis window, intravenous tenecteplase (0.2 mg/kg, to a total of 10 mg) was administered (9:00 p.m.).

RHD had been diagnosed 2 months earlier following episodes of fever and exertional dyspnea. He was started on acitrom 2 mg twice daily, metoprolol 50 mg once daily, and Dytor Plus 10/25 mg once daily. He also had a prior history of transient ischemic attacks, but no formal evaluation was done. On the day of ictus, two-dimensional echocardiography showed severe mitral stenosis (mitral valve area: 0.5 cm2), moderate mitral regurgitation, severe aortic stenosis (aortic valve area: 0.7 cm2, gradient 86/43 mm Hg), moderate tricuspid regurgitation, severe pulmonary hypertension, a grossly dilated left atrium and ventricle, global hypokinesia, and an ejection fraction of 35 to 40%.

He was transferred to the neurology intensive care unit for monitoring. Two hours postthrombolysis, he developed worsening right hemiplegia, dysphasia, anisocoria, and GCS dropped to E3V2M5 ([Fig. 1]). Noncontrast computed tomography (NCCT) head showed HT in the infarcted MCA territory with midline shift and sulcal effacement ([Fig. 2a]). Fibrinogen testing was unavailable, and family did not consent to send samples to an outside laboratory. Laboratory testing showed hemoglobin of 9.1 g/dL, platelet count of 1.1 lac, and prothrombin time/international normalized ratio (INR) 14/1.1. Blood chemistry and remaining investigations were within normal limits.

Zoom
Fig. 1 Timeline of vital parameters, GCS, and NIHSS score. GCS, Glasgow Coma Scale; NIHSS, National Institutes of Health Stroke Scale.
Zoom
Fig. 2 (A) Postthrombolysis NCCT head showing hemorrhagic transformation with perilesional edema. (B) Postoperative NCCT head showing increase in hematoma size and edema. NCCT, noncontrast computed tomography.

To reverse thrombolysis, prothrombin complex concentrate was considered but could not be arranged due to financial constraints. Six units of cryoprecipitate were urgently transfused. Additionally, tranexamic acid (1 g) and vitamin K (10 mg) were administered. Given the deterioration and imaging findings, he underwent emergency decompressive craniectomy. His last acitrom dose was 10 days prior.

In the operating room, ASA (American Society of Anaesthesiologists) monitors were applied, and a left radial arterial line was secured. Induction was done with fentanyl 200 mcg, etomidate 8 mg, and succinylcholine 75 mg. A right subclavian central line was placed, and norepinephrine started. Anesthesia was maintained with oxygen:air mixture with total intravenous anesthesia (TIVA) using propofol and fentanyl with intermittent doses of atracurium as needed. A defibrillator was kept on standby. In addition, 3% hypertonic saline (100 mL) was administered as an anti-edema measure. Serial arterial blood gas measurements were conducted and PaCO2 was targeted between 30 and 35 mm Hg. Measures were taken to maintain euglycemia and normothermia during all stages of surgery.

Mean arterial pressure (MAP) was maintained at 75 to 90 mm Hg. HR remained 65 to 70/min in AF. Phenylephrine boluses were used as needed. The surgery lasted 3 hours. He received 500 mL crystalloids, 1 unit packed red blood cells (PRBC), and 4 units fresh frozen plasma (FFP). Blood loss was 500 mL; urine output was 600 mL. Postoperatively, the patient was electively ventilated, with stable vitals (GCS of E1VTM3 under sedoanalgesia), and without inotropic support.

A repeat NCCT head after 12 hours showed hematoma expansion with greater midline shift ([Fig. 2b]). After multidisciplinary discussion, emergency hematoma evacuation was planned.

During the second surgery, intraoperatively, HR was 140 to 150/min with AF and fast ventricular rate, and BP was 70/40 mm Hg. Metoprolol (1 mg aliquots) and norepinephrine infusion were used to support hemodynamics. Significant brain bulge was encountered intraoperatively and managed effectively with intravenous furosemide boluses, temporary hyperventilation, and head end elevation. The surgery lasted 4.5 hours. Fluids included 700 mL crystalloids, 2 units PRBC, 2 FFP, and 2 random donor platelets. Blood loss was 700 mL; urine output was 900 mL.

Postoperatively, the patient required high-dose inotropic support. On Day 4, motor response improved to M5, but he suffered cardiogenic shock leading to cardiac arrest.


 

Discussion

HT remains a significant complication following ischemic stroke, with multiple factors contributing to its risk. Advanced age, male sex, coexisting comorbidities such as hypertension and diabetes mellitus, blood pressure fluctuations, severe stroke (NIHSS >22), congestive heart failure with AF, antithrombotic therapy, and a prior history of stroke have all been implicated as predisposing factors.[4] [5] [6]

Patients with valvular heart disease—particularly those with stenotic lesions—pose unique perioperative challenges for neuroanesthesiologists. Sympathetic stimulation at any point during surgery, whether during induction, laryngoscopy, or emergence, can provoke significant hemodynamic disturbances, increasing the risk of perioperative myocardial ischemia, pulmonary hypertension crisis, or heart failure. Hypotension must be avoided, as it can jeopardize both cerebral and coronary perfusion. Additional perioperative factors such as hypoxia, hypercarbia, acidosis, and the use of nitrous oxide may further elevate pulmonary artery pressures and should be carefully mitigated in patients with concurrent pulmonary arterial hypertension (PAH).

Achieving an optimal hemodynamic balance becomes particularly challenging in patients with underlying cardiac disease, where the need to maintain a relatively hypertensive state must be carefully weighed against the risk of hypertensive surges. While excessive elevations in blood pressure may exacerbate hematoma expansion, a relatively hypertensive state is often necessary to maintain adequate coronary perfusion, especially in the presence of severe valvular stenosis. However, there is a notable paucity of evidence in the literature to guide precise hemodynamic targets in this complex clinical setting.

Conditions such as heart failure and valvular heart disease further complicate management by increasing the risk of fluid overload, especially in acute neurological emergencies like traumatic brain injury or subarachnoid hemorrhage, where fluid resuscitation may precipitate cardiac compromise. In such scenarios, the judicious use of opioids during induction can attenuate exaggerated hemodynamic responses to airway manipulation, and the prophylactic administration of vasopressors may help minimize abrupt fluctuations in blood pressure.[7]

This case illustrates the complex interplay between cardioembolic stroke, anticoagulation, thrombolysis-associated HT, and severe RHD. Patients with combined neurovascular and structural cardiac pathology require individualized neuroanesthetic approaches that carefully balance intracranial dynamics and cardiac limitations. In our case, the first surgery was managed with a fentanyl-based induction, TIVA maintenance, and inotropic requirement as deemed necessary, targeting a MAP of 75 to 90 mm Hg and heart rate below 90 bpm. However, the absence of advanced cardiac output monitoring limited dynamic assessment of fluid responsiveness.

During the second procedure, undertaken due to neurological deterioration, the patient demonstrated a significantly diminished hemodynamic reserve. Norepinephrine infusion was required to maintain MAP, and transient hypotension occurred following dural opening, suggestive of preload intolerance. Despite aiming for similar targets, the patient showed poor response to fluids and inotropes, likely due to worsening of heart dysfunction and PAH. Lack of intraoperative echocardiography further limited real-time cardiovascular evaluation. These factors contributed to postoperative pulmonary edema and heart failure, ultimately leading to mortality.

Globally, stroke affects approximately 15 million individuals annually, accounting for 5.7 million deaths. In low- and middle-income countries, RHD contributes to 3 to 7.5% of all strokes. Wang et al noted a higher mortality rate among patients with ischemic stroke due to RHD compared with other etiologies.[8] However, data on the safety and outcomes of thrombolysis in this population remain limited. In patients with an INR <1.7 and no recent anticoagulant intake, current guidelines support the use of intravenous thrombolysis, though clinical decision-making remains nuanced in the presence of structural heart disease and PAH.

Clinical Implications and Learning Points

  • Confirm anticoagulation status before thrombolysis (INR <1.7 acceptable per guidelines).

  • Ensure early imaging and close monitoring postthrombolysis.

  • Coordinate care across neurology, anesthesiology, cardiology, and critical care.

  • Avoid fluid overload; use goal-directed therapy with vasopressors and preload monitoring.

  • Utilize point-of-care testing to support thrombolytic decisions in high-risk patients.

Conversely, initiating thrombolysis without confirming coagulation parameters, delaying intervention for neurological deterioration, or underestimating the cardiac implications during neurosurgical planning can all contribute to poor outcomes ([Fig. 3]).[9] [10] [11] [12]

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Fig. 3 Balancing cerebral and cardiac goals in patients with RHD undergoing neurosurgery. The left (pink) highlights cardiac goals such as maintaining preload, avoiding tachycardia, and ensuring normoxia and normocapnia to prevent right ventricular strain and pulmonary hypertension. The right (green) emphasizes cerebral protection—maintaining autoregulation, reducing cerebral metabolic demand (CMRO2), preventing raised intracranial pressure (ICP), and preserving cerebral perfusion pressure (CPP). The seesaw metaphor underscores the delicate balance anesthesiologists must achieve between optimizing cardiac stability and ensuring neuroprotection. RHD, rheumatic heart disease.

 

 

Conclusion

This case highlights the need for careful anesthetic and medical management in patients with ischemic stroke, recent thrombolysis, and severe valvular disease. In resource-limited settings, protocol-driven strategies and early multidisciplinary planning are vital to balance neuroprotection with cardiovascular stability.


 

 

Conflict of Interest

None declared.

Acknowledgement

We acknowledge Dr. Pooja Chandran, Senior Resident – Cardiac Anaesthesiology, AIIMS Rishikesh, for her valuable suggestion.


Address for correspondence

Gaurav Jain, MBBS, MD, PDCC
Department of Anaesthesiology, Critical Care and Pain Medicine, Level 6, All India Institute of Medical Sciences
Rishikesh 249203, Uttarakhand
India   

Publication History

Article published online:
22 August 2025

© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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Zoom
Fig. 1 Timeline of vital parameters, GCS, and NIHSS score. GCS, Glasgow Coma Scale; NIHSS, National Institutes of Health Stroke Scale.
Zoom
Fig. 2 (A) Postthrombolysis NCCT head showing hemorrhagic transformation with perilesional edema. (B) Postoperative NCCT head showing increase in hematoma size and edema. NCCT, noncontrast computed tomography.
Zoom
Fig. 3 Balancing cerebral and cardiac goals in patients with RHD undergoing neurosurgery. The left (pink) highlights cardiac goals such as maintaining preload, avoiding tachycardia, and ensuring normoxia and normocapnia to prevent right ventricular strain and pulmonary hypertension. The right (green) emphasizes cerebral protection—maintaining autoregulation, reducing cerebral metabolic demand (CMRO2), preventing raised intracranial pressure (ICP), and preserving cerebral perfusion pressure (CPP). The seesaw metaphor underscores the delicate balance anesthesiologists must achieve between optimizing cardiac stability and ensuring neuroprotection. RHD, rheumatic heart disease.