Anaesthetic management of a case of dilated cardiomyopathy for breast surgery with supraglottic airway device

 

Nayana Kulkarni^1*, Rajnish Nagarkar^1#, RavindraTandale², Shital Patil³, Shirish Deo⁴

 

 

Abstract               Background: Dilated cardiomyopathy (DCM) is defined as a myocardial disease characterised by left ventricle (LV) or biventricular dilatation, normal LV wall thickness, and systolic dysfunction. DCM is defined by two key factors: (a) Left ventricular ejection fraction (LVEF) less than 45% and/or fractional myocardial shortening less than 25% (b) Left Ventricular End Diastolic Diameter (LVEDD) greater than 117% by excluding presence or known cause of myocardial disease. DCM s considered as the most common form of non-ischemic cardiomyopathy. It is also the third common cause of heart failure. An EF of 20% and severe ventricular dysfunction is a predictor of sudden death in such patients. There are very few cases of perioperative management of patients with DCM. Each case showed a novel approach to management Case Report: We report a case of a 52-year-old Asian female with DCM who underwent breast cancer surgery. The patient had documented an EF of 20% while the adenosine scanning revealed no signs of stress-induced ischemia or arrhythmias. The patient was managed successfully with no intraoperative invasive monitoring using supraglotic airway device. The anaesthetic management of a patient with DCM is a challenge for the anaesthetist. Meticulous perioperative planning of patients with DCM is required for a safe and uneventful anaesthesia. The possibility of antipsychotic-induced DCM as a causative factor need to be investigated.

Key Words: Dilated cardiomyopathy, Supraglottic airway device, Antipsychotics.

 

INTRODUCTION

Dilated cardiomyopathy (DCM) is defined as a left ventricular dilation attributed with systolic dysfunction. Impaired ventricular function, as well as diastolic dysfunction, could also develop. Individuals with DCM are at high risk of developing right or left ventricular failure or even both. Patients presenting with DCM may have heart failure (HF) symptoms either due to exercise or at rest. In most cases, patients are asymptomatic. Some of the life-threatening risks of DCM include syncope, ventricular arrhythmias, atrioventricular block, and sudden death¹. As per current evidence, different etiologiessuch as infectious, inherited, and inflammatory diseases have been attributed to cause DMC. However, the actual cause of DCM remains unexplained in most of the cases even after a thorough review for secondary cause². The reported incidence of DCM varies due to the diagnostic criteria used. The annual incidence varies from five to eight cases per 100,000 individuals³. Patients with DCM are always a challenge to the anesthesiologist as they are high-risk patients with several complications including progressive cardiac failure³. We report a case of an Asian female with DCM who underwent breast cancer surgery with no intraoperative invasive monitoring using supraglotic airway device (SGAD).

 

 

 

CASE PRESENTATION

A 52-year-old Asian female weighing 62 kilograms and a height of 158 cm presented to our hospital for breast disease. The patient presented with watery discharge from the nipple and was admitted for a wide local excision (WLE) or breast conserving surgery. The patient was being treated with digoxin (0.25 mg), torsemide (10 mg), spironolactone (50 mg), carvedilol (6.25 mg) and rosuvastatin/aspirin (10/75 mg) for four years. Her metabolic equivalents (METS) was less than four. She was fairly healthy and performed daily activities without any assistance. Her tolerance was limited. She was on antipsychotic medications, i.e. sodium valproate, olanzapine, and ziprasidone for 17 years. Her heart rate was regular (72/min) without arrhythmias at the time of pre-anaesthetic examination. Her pulse rate was steady with normal volume. Blood pressure was 117/75 mmHg. Her respiratory rate was 16 breaths per minute. The respiratory system was clear without any rhonchi or rales.  Respiratory system was clear on auscultation with breath holding time (BHT) of 20 seconds. The patient’s jugular venous pulse (JVP) was normal. No hepatomegaly was noted.

Pre-operative management

A 12-lead electrocardiography (ECG) showed normal sinus rhythm (Fig. 1). Her previous 2D- echocardiography showed an intact septae, dilated left ventricle, and generalised hypokinesia of all the walls (Fig. 2). The left ventricular (LV) function was 20%. An enlarged left atrium with mild mitral regurgitation was observed. No pericardial effusion was noted. Post discussion with the nuclear medicine department, an adenosine scan for myocardial perfusion was performed. The adenosine stress test showed a resting heart rate of 71 beats per minute and a blood pressure of 125/68 mmHg. The post injection heart rate was 91 while BP was 112/60 mmHg. Post-injection perfusion defect was not observed. The methoxyisobutylisonitrile (MIBI) tracer uptake was observed in all segments without any perfusion defect. The left ventricular ejection fraction (LVEF) was 44%. Adenosine-induced reversible ischemia was not observed in any of the LV myocardial segments. The routine laboratory investigations were within normal limits. Some of the investigations such as serum sodium, potassium, magnesium, and calcium were within normal limits. A high-risk consent was obtained from the patient. The patient was informed about the plan for general anaesthesia with local infiltration and her coordination was obtained. Premedication was not advised in the wards other than nebulization. As per the American Society of Anaesthesiologists’ (ASA), the patient was classified as ASA III.

On the day of surgery, the patient’s vitals were assessed. Her heart rate was 72 bpm, BP was 127/75 mmHg, and SpO₂ was 96%. The patient was nebulized with budesonide respule in the ward. The patient was monitored using the multipara monitor.

Intra-operative management

Considering the patient’s EF was 44% with no perfusion defects, all invasive monitoring equipment was kept at standby along with a defibrillator. The patient was subject to non-invasive monitoring. Some of the other parameters that were assessed include ECG, oxygen saturation, and end tidal carbon dioxide (ETCO₂). The patient was given intravenous glycopyrolate 0.2 mg, midazolam 1 mg, fentanyl 50 microgram, and ondansetron 4mg. After pre-oxygenation, fentanyl 100 mg, propofol 20 mg and sevoflurane 4% (4 puffs) were administered. I-gel no. 3 was introduced with a confirmation of proper placement with the help of ETCO₂ readings. A neuromuscular-blocking drug (NDMR), rocuronium 30 mg administered in titrated doses with intermittent positive-pressure ventilation (IPPV) using oxygen (50%) nitrous oxide (50%) premix. Sevoflurane mixture at 1.5% was also administered. There was no hypotension or arrhythmias intra-operatively. Intercostal blocks were administered as levels, T3 to T7 mid axillary line using 1.5 % lignocaine (9ml) with bupivacaine 0.125% (15ml).  A total of 3 ml per segment and local incisional infiltration of lignocaine 2% (9 ml) was used. The primary objective of anaesthesia was to avoid negative inotropism, tachycardia, and a sudden increase in afterload. Maintenance of adequate preload was essential. The patient’s Bispectral index (BIS) (using Conox monitoring by FreseniusKabi) was monitored intra-operatively. A level of 50-55 (qCON) was maintained with oxygen and sevoflurane mixture. The patient’s blood loss was minimal, i.e. less than 50 ml. The patient was given 300 ml of ringers lactate solution. Post-surgery the patient was reversed (qCON 80). The extubation process was uneventful. The patient’s vitals remained stable. The patient was awake and fully conscious. Her score as per the visual analogue scale (VAS) was 1, heart rate was 76/minute, and blood pressure was 118/70 mm Hg (Table 3). The patient’s SpO2 was 98% on O₂ 4 lit/min.

Post-operative management

The patient was shifted to the post-operative surgical ICU ward. The patient did not require any inotrope, vasopressor, or ionodilator support. The patient was kept nil-by-mouth (NBM) for four hours while she was given sips of water after four hours. The patient’s perioperative vitals have been stated in Table 1.

 

 

Figure 1 and Figure 1(A): 12-lead electrocardiography (ECG) showed normal sinus rhythm

Figure 2: 2D-Echo: An intact septae, dilated left ventricle, and generalised hypokinesia of all the walls

 

 

Figure 3: Adenosine stress test scan images

 

 

Figure 4: Adenosine scan images showing no filling defect

 

Figure 5: Adenosine scan images of different walls of heart

 

Table 1: Vitals chart

Schedule	HR	BP	Sevoflurane %	O2 Lit/min	N2O Lit/min
Preoperative	72	127/76	0	0.35	0
Induction	78	123/84	4	2	0
Intubation	76	136/80	2	2	0
Post-intubation	78	106/70	1.5	2	2
30-minutes	74	112/60	1.5	0.35	0.35
60-minutes	72	116/70	1.5	0.35	0.35
75-minutes	70	128/66	1.2	0.35	0.35
90- minutes Extubation	78	118/60	0	2	0

HR= Heart rate; BP= Blood pressure

 

Table 2: Anaesthesia Gas Monitoring (AGM)

Schedule	Oxygen%	Nitrous Oxide %	Sevoflurane %
Preoperative	100	0	0
Induction	100	0	4
Intubation	100	0	2
Post-intubation	50	50	1.5
30 minutes	48	52	1.5
60 minutes	46	54	1.5
75 minutes	51	49	1.2
90 –minutes extubation	100	0	0

 

Table 3: Postoperative course: VAS and vitals

VAS= Visual Analogue Scale; HR= Heart rate; BP= Blood pressure

 

DISCUSSION

Some of the most common perioperative issues in such patients include arrhythmias, precipitation of CCF, and systemic embolism from pre-existing mural thrombi. Mural thrombi may also be present in the LV apex. In our case, the patient was treated with digoxin with METS less than four. The patient had no history of congestive cardiac failure (CHF). As per the adenosine stress scan, her stress-induced ischemia was negative while she had normal hemodynamics without any perfusion defect. The patient was inducted with inhalational agent sevoflurane which is known for its overall hemodynamic stability. Sevoflurane is known for its H- hemodynamically stable, A- airway tolerability, R- rapid elimination and recovery, T- titration (ease of titration), i.e. HART. The choice of supraglotic airway I-gel prevented overall stress response due to invasive endotracheal intubation. It also prevented the use of any beta blocker agent. The BIS monitoring helps in maintaining adequate depth of anaesthesia. The risk of overdose was prevented in our cases. The patient’s airway was secured using the SGAD (I-gel no. 3). The successful insertion in a single attempt was confirmed through ETCO2 and auscultation of air entry as key endpoints. A BIS score of 50-55 was maintained in order to ensure general anaesthesia. Analgesia was provided with the help of infiltration and intercostal blocks T3-T7 in calculated dosages. Midazolam (1mg) was administered to the patient as premedication in the operating room. It provided good anxiolysis. The use of SGAD like I-Gel has been associated with efficient airway control while delivering an anaesthetic agent⁴. It helps in delivering optimal concentrations of both, anaesthetic agent and gas. The use of SGAD was associated with uneventful extubation with minimal stress response. The advent of SGAD has changed the overall management of high-risk patients. In conventional approaches, such high-risk patients have a high-stress response including arrhythmias which may require the use of beta blockers or antiarrhythmic agents. Thus, the need for invasive monitoring is prevented using SGAD, I-Gel. The overall process also reduces overall hospital stay and cost.

 

CONCLUSION

Patients with DCM are a big challenge for the anesthesiologist. Meticulous perioperative training is required for an uneventful surgery. The role of an anaesthetists includes optimal pre-operative workup and consultation. Anaesthetist should be aware of unexpected events. Titration of anaesthetic agents is recommended as it helped in an uneventful perioperative management in our case. In some cases, invasive monitoring is required to avoid catastrophic events. The use of SGAD for breast surgeries along with intercostal blocks and local infiltration can be considered as an ideal choice to reduce overall anaesthetic complications. To conclude, the cause of DCM was unknown in our case. We successfully managed our patient with the help of SGAD posted for breast surgery. However, clinical studies need to be conducted to ascertain the efficiency of SGAD. Clonazipine induced-DCM has also been widely reported^5,6,7. However, we need to investigate if clonazipine was the primary cause of DCM in our patient. This was one of the few cases of successful anaesthetic management of a patient with DCM undergoing breast cancer surgery.

 

ACKNOWLEDGEMENT

We would like to thank Mr. Lyndon Fernandes for his editorial assistance.

 

REFERENCES

• Jefferies JL, Towbin JA. Dilated cardiomyopathy. Lancet. 2010 Feb 27; 375(9716):752-62. doi: 10.1016/S0140-6736(09)62023-7
• Lakdawala NK, Winterfield JR, Funke BH. Dilated Cardiomyopathy. Circulation Arrhythmia and electrophysiology. 2013; 6(1):228-237. doi:10.1161/CIRCEP.111.962050.
• Kaur H, Khetarpal R, Aggarwal S. Dilated Cardiomyopathy: An Anaesthetic Challenge. Journal of Clinical and Diagnostic Research : JCDR. 2013; 7(6):1174-1176. doi:10.7860/JCDR/2013/5390.3069.
• Kannaujia A, Srivastava U, Saraswat N, Mishra A, Kumar A, Saxena S. A Preliminary Study of I-Gel: A New Supraglottic Airway Device. Indian Journal of Anaesthesia. 2009; 53(1):52-56.
• Longhi S, Heres S. Clozapine-induced, dilated cardiomyopathy: a case report. BMC Research Notes. 2017; 10:338. doi:10.1186/s13104-017-2679-5.
• Alawami M, Wasywich C, Cicovic A, Kenedi C. A systematic review of clozapine induced cardiomyopathy. Int J Cardiol. 2014 Sep 20; 176(2):315-20. doi: 10.1016/j.ijcard.2014.07.103.
• Tanner M, Culling W. Clozapine associated dilated cardiomyopathy. Postgraduate Medical Journal. 2003; 79(933):412-413. doi:10.1136/pmj.79.933.412.