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CC BY 4.0 · J Neuroanaesth Crit Care 2025; 12(02): 121-123
DOI: 10.1055/s-0044-1801262
Case Report

Anesthetic Management of a Patient with Dilated Cardiomyopathy Undergoing Cerebral Aneurysm Clipping Surgery: A Case Report

Authors

  • Navneh Samagh

    1   Department of Anaesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab, India

  • Sarita Sah

    1   Department of Anaesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab, India

  • Gegal Pruthi

    1   Department of Anaesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab, India

  • Jyoti Sharma

    1   Department of Anaesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab, India
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Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) necessitates prompt neurosurgical intervention. However, patients with associated dilated cardiomyopathy (DCM) face higher cardiovascular instability due to sympathetic surge, stunned myocardium, and tendency to arrhythmias secondary to aSAH. We report a case of DCM and ischemic cardiac disease with a 30% ejection fraction, who presented to us with a severe headache associated with vomiting. Noncontrast computed tomography revealed hematoma in the right fronto-temporoparietal and blood in all the ventricles. Cerebral angiography showed a saccular aneurysm at the right middle cerebral artery bifurcation, thus requiring cerebral aneurysm clipping surgery. Anesthetic agents for induction and maintenance were selected and titrated to minimize cardiac depression and also avoiding systemic hypotension. A bilateral scalp block was administered to blunt sympathetic response to scalp pin application and scalp incision. Hemodynamic monitoring was done perioperatively using pulse index continuous cardiac output monitoring. The patient made an uneventful recovery from the surgery. This case highlights the importance of preoperative planning, accurate interpretation of hemodynamic measurements, and appropriate therapeutic responses to optimize outcomes in cerebral aneurysm surgery associated with DCM.


Keywords

aneurysmal subarachnoid hemorrhage - cardiac output monitoring - cerebral aneurysm clipping - dilated cardiomyopathy - case report

Introduction

Aneurysmal subarachnoid hemorrhage (aSAH) is an acute life-threatening neurosurgical emergency affecting all ages. Dilated cardiomyopathy (DCM), with an incidence of 5 to 8 per 100,000, is characterized by the presence of (1) fractional myocardial shortening less than 25% (>2 standard deviation [SD]) and/or ejection fraction (EF) less than 45% (>2 SD) and (2) left ventricular end-diastolic diameter greater than 117% excluding any known cause of myocardial disease.[1] The cardiovascular changes (sympathetic surge, stunned myocardium, and tendency to arrhythmias) induced by aSAH complicate the management of patients with underlying cardiac condition. Here, we describe a patient with DCM scheduled for cerebral aneurysm clipping surgery (CACS), both of which significantly affect the cardiovascular system. This complicates the perioperative care, requiring advanced monitoring techniques such as transesophageal echocardiography (TEE), pulse index continuous cardiac output (PiCCO), and careful drug administration to avoid cardiac depression and hypotension, thereby maintaining satisfactory myocardial contractility and cerebral perfusion pressure (CPP).


Case report

A 61-year-old woman, weighing 50 kg, presented to us with a history of severe headache associated with nausea and vomiting. She was drowsy and confused, with Glasgow coma scale (GCS) score of 14/15, E4V4M6, heart rate (HR) of 78 beats per minute (bpm), and blood pressure (BP) of 124/74 mm Hg with no neurological deficits. Airway examination revealed modified Mallampati class 4. Noncontrast computed tomography revealed hematoma in the right fronto-temporoparietal and blood in all the ventricles. Cerebral angiography showed a saccular aneurysm measuring 3.1 × 2.6 mm at the right middle cerebral artery bifurcation. Her Hess and Hunt's grade was 3 and Fisher's grade was 4. She was posted for aneurysmal clipping. Her medical records revealed DCM with ischemic heart disease for 8 months, for which she was on ramipril, metoprolol, trimetazidine, atorvastatin, torsemide, and spironolactone. Laboratory investigations were normal except for Pro-brain natriuretic peptide (pro-BNP) of 2,070 pg/mL (normal range: <300 pg/mL). Electrocardiogram (ECG) showed left ventricular hypertrophy. Transthoracic echocardiography revealed moderate left ventricular dysfunction, EF of 30%, severe hypokinesia of the anterior wall, dilated left atrium and left ventricle, and mild mitral regurgitation.

Informed high-risk written consent was taken. Standard American Society of Anesthesiologists (ASA) monitors were attached, and difficult airway cart, including fiberoptic bronchoscope and video laryngoscope, was kept ready. The right radial artery was cannulated under local anesthesia to monitor continuous invasive BP (IBP). Baseline vitals were HR 78 bpm, saturation 99%, and IBP 124/74 mm Hg. Anesthesia was induced with morphine 6 mg, etomidate 10 mg, and vecuronium 6 mg, which were administrated to facilitate tracheal intubation with video laryngoscope. One minute prior to laryngoscopy, 60 mg of 2% lignocaine was administered to blunt hypertensive response to laryngoscopy and intubation. Both adrenaline and norepinephrine infusions were preconnected to separate intravenous cannulas for hemodynamic instability during induction. Her postintubation IBP was 110/68 mm Hg. Ultrasound-guided right internal jugular vein was catheterized to monitor central venous pressure (CVP). The PiCCO monitor was connected, and cardiac output (CO), stroke volume (SV), stroke volume variation (SVV), and systemic vascular resistance (SVR) were continuously monitored ([Fig. 1]). Bilateral scalp block was administered with 30 mL of 0.25% bupivacaine. Anesthesia was maintained with 50% oxygen in the air, and infusion of propofol was targeted to maintain a bispectral index between 40 and 60. She was given paracetamol 1 g and levetiracetam 500 mg intraoperatively. Mechanical ventilation was instituted to target EtCO2 of 30 to 35 mm Hg. Goal-directed fluid therapy was initiated using normal saline. Infusions of adrenaline and dobutamine were titrated to maintain SV, SVV, CO, and SVR within the target range of 60 to 100 mL, less than 12%, 3.5 to 5.5 L/min, 800 to 1,200 dynes/s/cm5, respectively. Volume expansion was performed (250 mL of normal saline over 10 minute) if SVV was greater than 12%. The patient had a blood loss of 500 mL, and her urine output was 350 mL during 180 minutes of surgery. She received 2,000 mL of crystalloids. We did not infuse mannitol as it increases intravascular volume and may cause significant short-term changes in SV, CO, and SVR.[2] The same was discussed with the surgeon and adequate brain relaxation was achieved with the use of propofol infusion intraoperatively. In the operating room, after reversing the vecuronium effect, her trachea was extubated when she followed the commands. She was then transferred to the intensive care unit, where PiCCO monitoring was continued for 48 hours. She was started on nimodipine 60 mg orally 4 hourly and transferred to the ward after the 8th day and discharged from the hospital on the 10th day without any neurologic deficit and stable hemodynamics with an EF of 28%. Her Glasgow Outcome Scale, Extended (GOSE) at 3 and 6 months was 8.

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Fig. 1 Cardiac output monitor displaying various hemodynamic parameters.

Discussion

Management of a patient undergoing CACS with associated DCM is a challenge for neuroanesthesiologists. Aneurysmal SAH results in sympathetic hyperactivity, stunned myocardium, and cardiac arrhythmias. Diverse types of ECG changes are observed in 27 to 100% following aSAH. Impaired left ventricular function, manifesting as regional wall motion abnormalities or globally impaired contractility on echocardiography, occurs in 13 to 18% of cases.[3] This myocardial dysfunction is often reversible once the acute neurological event is managed.[4] On the other hand, DCM is characterized by decreased myocardial and systolic function of one or both ventricles, resulting in reduced ventricular contractility and elevated filling pressure.

DCM patients are usually treated with angiotensin-converting enzyme inhibitors, β-blockers, and cardiotonic drugs to decrease afterload, slow ventricular remodeling, and enhance CO, and these drugs must be continued.[5] Baseline ECG focused on DCM and aSAH-related arrhythmias must be done. Echocardiography must be performed to evaluate ventricular and valvular function.[6]

The goals of anesthetic management in such cases are to maintain sinus rhythm, avoid tachycardia, avoid fluid overload, avoid increase in afterload, preserve adequate myocardial contractility, CO, prevent thromboembolic events, and ensure smooth emergence to facilitate early neurological examination. Minimizing myocardial oxygen demand while stabilizing hemodynamic parameters is essential to preserve both myocardial and cerebral perfusion. Early extubation and precise fluid management prevent exacerbation of DCM and allow for better neurological recovery.[5] Advanced CO monitoring guides fluid therapy maintaining CO. This is as per the recommendations of high-risk cardiac patients undergoing noncardiac surgeries.[7] Postoperatively, continued monitoring for arrhythmias, heart failure, or fluid imbalance is crucial for any delayed cardiac complications.

Anesthetic management in patients with DCM with left ventricular dysfunction should focus on minimizing myocardial depression. To proactively manage the risk of induction hypotension, both adrenaline and norepinephrine infusions were preconnected to separate intravenous cannulas, ready for rapid administration if needed. Adrenaline was prepared to counteract any sudden, profound hypotensive episodes due to further decreased contractility, while norepinephrine was available to provide controlled vasopressor support, maintaining SVR without significantly increasing the HR.

Traditional measures for guiding fluid therapy include HR, mean arterial pressure, urine output, CVP, and lactic acid levels. Noninvasive methods like transthoracic echocardiography and bioimpedance are easy to install and allow continuous monitoring but may face operator-dependent challenges and noise interference. Invasive techniques such as pulmonary artery catheters and TEE provide direct measurements but carry higher risks.[8] Monitoring various cardiac parameters is conveniently accomplished with PiCCO. Although SV monitoring can also be executed safely with TEE, being less invasive, we used PiCCO. Intraoperatively, adrenaline was started at a dose of 0.01 to 0.05 µg/kg/min and dobutamine at 2.5 to 5 µg/kg/min to enhance myocardial contractility and improve CO during episodes of hypotension. Norepinephrine and other vasoconstrictors were not required, as the PiCCO monitor showed that the CO was low during hypotensive episodes, with an elevated SVR. Additionally, the HR remained stable at 60 to 70 bpm intraoperatively, which allowed us to proceed with adrenaline to maintain BP and myocardial perfusion without significantly increasing myocardial oxygen demand.

In conclusion, this case higlights the importance of individualized approach, using a cardio-stable induction agent, bilateral scalp block as a part of multimodal analgesia, PiCCO monitoring for fluid monitoring and hemodynamic management perioperatively, and judicious use of inotropes in optimizing outcome of a patients with DCM undergoing cerebral aneurysmal surgery.



Conflict of Interest

None declared.


Address for correspondence

Gegal Pruthi, DM
Department of Anaesthesiology, All India Institute of Medical Sciences
Bathinda 151001, Punjab
India   

Publication History

Article published online:
20 January 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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Fig. 1 Cardiac output monitor displaying various hemodynamic parameters.