Perioperative management of an elderly patient of hypertrophic obstructive cardiomyopathy for knee arthroplasty and the role of peripheral nerve blocks.

This case report exemplifies how the anaesthetic technique of general anesthesia with continuous bilateral femoral nerve block for bilateral knee arthroplasty was well chosen for the management of perioperative complications in an elderly patient with hypertrophic obstructive cardiomyopathy (HOCM). A 69-year-old female patient of HOCM was scheduled for bilateral total knee replacement. Echocardiography revealed severe left ventricular outflow tract obstruction with peak systolic gradient of 56 mmHg. The surgery was conducted under general anaesthesia with invasive monitoring and bilateral continuous femoral nerve blocks for postoperative analgesia. Postoperatively, she developed pulmonary oedema due to the liberal administration of fluids. This complication was successfully managed without interrupting the management of pain. Management of patients with HOCM for noncardiac surgery requires knowledge of variable presentation of two forms of disease. Also, this case report highlights the practical advantage of continuous femoral nerve block (CFNB)s over epidural anaesthesia.

INTRODUCTION

Given the 1:500 prevalence of hypertrophic obstructive cardiomyopathy (HOCM) in the general population, it may present to the anaesthesiologist more often than anticipated.[12] We hereby describe how our anaesthetic technique (general anaesthesia with peripheral nerve blocks) for bilateral knee arthroplasty was well chosen for the perioperative management of such a patient.

CASE REPORT

A 69-year-old female weighing 78 kg, a medically managed (atenolol 25 mg and amlodipine 10 mg once daily) case of HOCM was scheduled for bilateral knee arthroplasty. She had intermittent episodes of dyspnoea and fatigue. There was no history of angina, syncopal attacks, or any sudden death in her family. Systemic examination revealed a regular pulse rate of 68 beats/min , and a grade 3/6 crescendo-decrescendo systolic murmur was heard between the left sternal border and apical area, not radiating to the carotids. Electrocardiography (ECG) showed normal sinus rhythm with nonspecific T wave changes in leads II, III, and aVF with left ventricular hypertrophy and left axis deviation. Chest X-ray showed cardiomegaly with clear lung fields. Echocardiography showed asymmetrical septal hypertrophy, left ventricular outflow tract obstruction (LVOT) with peak systolic gradient (PSG) of 56 mmHg, moderate mitral regurgitation and moderate diastolic dysfunction with ejection fraction of 56%. Computerised tomographic (CT) angiogram showed normal coronaries.

Both cardiac drugs were continued till the morning of surgery along with a premedication of oral ranitidine 150 mg and alprazolam 0.25 mg. In the operating room, baseline blood pressure (BP), heart rate (HR) and respiratory rate (RR) were 160/90 mmHg, 68/minute and 14/minute, respectively. The patient was given injection metoprolol 2 mg, 80 mcg fentanyl and midazolam 2 mg intravenously, before establishing invasive monitoring (left radial blood pressure and right jugular venous pressure), opening central venous pressure (CVP) was 8 mmHg. Bilateral perineural femoral nerve catheters were placed with the help of a nerve stimulator. A bolus of 8 mL of 2% lignocaine with 8 mL of 0.2% ropivacaine was injected in each femoral catheter before the incision of each side, followed by a continuous infusion of ropivacaine 0.2% 8 mL/hour intra and postoperatively. Half an hour later, induction and intubation were accomplished using propofol 100 mg, morphine 8 mg, midazolam 1 mg and vecuronium 8 mg. Mild hypotension occurred with BP falling to 100/50 mmHg, which was managed with a bolus of 200 mL crystalloid and injection phenylephrine 50 μg. To prevent intubation stress, esmolol 30 mg was given intravenously 90 seconds before intubation. Anaesthesia was maintained with 66% nitrous oxide in oxygen and isoflurane 0.2-0.4% (because of its myocardial depressive properties, halothane is an ideal agent in such patients but due to its nonavailability in our institute, isoflurane was used without any adverse haemodynamic changes); the average duration of both tourniquets was 35 to 40 minutes. At the time of both tourniquet deflations, systolic pressures dropped by more than 20% each time which responded to a judicious administration of crystalloid and phenylephrine 100 mcg. CVP remained between 8 and 10 mmHg and urine output was 500 mL with an input of 2.5 L of crystalloids. The surgery lasted for four hours; neuromuscular blockade reversed with neostigmine 3.5 mg and glycopyrrolate 0.6 mg and esmolol 30 mg was given again to prevent exaggerated haemodynamic response at extubation. Post extubation, the patient was haemodynamically stable (BP: 124/62 mmHg, HR: 74/minute) with saturation of 100% on oxygen of 2 L/minute. Postoperatively, the patient was transferred to a special intensive care unit (ICU) for further management.

Two hours postoperatively, the surgical drains were opened. Four hours later, we noted increase in heart rate upto 94-96 beats/ min; BP was 110/75 mmHg, CVP and RR were10 mmHg and 33/ min respectively and desaturation up to 90% on room air, with bilateral drain loss of about 100 mL each. Her pain assessment on a verbal analogue score was 6 (on a scale of 0-10). Immediately, the oxygen was increased from 2 to 5 L/minute. For pain and tachycardia, a bolus of ropivacaine 0.2%, 8 mL was given through each femoral catheter along with metoprolol 2 mg intravenously, and liberal fluids continued. Also, other parenteral analgesics like diclofenac, paracetamol and tramadol were started on a regular basis, as per our ICU protocol. Six hours postoperatively, dyspnoea persisted with the occurrence of bilateral fine crepts in chest now and CVP increased to 12 mmHg with heart rate and BP being 88-90 beats/min and 108/70 mmHg, respectively. Echocardiography showed a decreased PSG of 45 mmHg. So, furosemide 20 mg and another dose of metoprolol 2 mg were given intravenously. The patient passed about 1200 mL urine over the next three hours; her tachycardia and tachypnoea both settled with an HR of 78/minute and RR of 20/minute and blood pressure increased to 136/67 mmHg. Her daily dose of atenolol was increased from 25 mg once a day to 50 mg orally twice a day. Forty-eight hours later, the patient was shifted from the ICU after removing femoral catheters. The rest of the hospital stay was uneventful.

DISCUSSION

HOCM is marked by asymmetric hypertrophy of the left ventricle (left ventricular wall thickness >15 mm), dynamic LVOT obstruction due to systolic anterior motion of anterior valve leaflet of mitral valve and diastolic dysfunction caused due to impaired relaxation of noncompliant left ventricle.[12]The patient may present from infancy to older than 90 years. Although adverse clinical consequences of the disease, particularly sudden cardiac death, are well documented, a more balanced perspective regarding prognosis has recently evolved in which normal longevity is seen with relatively mild disability.[2] A symptomatic patient may experience progressive heart failure with exertional dyspnoea, fatigue and chest pain, evolution to end-stage phase and atrial fibrillation (AF).[1]

Goals of anaesthetic management should aim at avoiding exacerbation of outflow tract obstruction (due to sympathetic stimulation), maintaining diastolic filling by maintenance of sinus rhythm and preventing fall in preload and afterload.[2] Hence, we chose general anaesthesia with invasive monitoring for our patient. Centroneuraxial blocks, though not absolutely contraindicated, are still best avoided, because of the risk of profound bilateral sympathectomy and hypotension.[3] Adequate filling pressures were guided by CVP. Though isolated measurements of CVP do not provide an accurate guide to left ventricular filling because of poor left ventricular compliance, serial recordings provide a useful trend. Whenever sympathetic shootups were anticipated—establishment of femoral nerve catheter and invasive lines, intubation and extubation—good sedoanalgesia and adequate anaesthetic depth was provided with the beta blocker, esmolol. Vasopressor phenylephrine was used as it increases systemic vascular resistance without ionotropy or chronotropy.

For postoperative analgesia, our choice of continuous femoral nerve blocks (CFNBs) has many advantages over epidural analgesia like lack of hypotension and epidural haematoma associated with the use of anticoagulants, effective pain relief and improved functional recovery.[45] Till date, we have not found much literature on bilateral safe infusion doses of ropivacaine in peripheral nerve block for prolonged durations. Our limitation is that we did not do serum values of ropivacaine because of lack of this facility in our institute. However, no signs or symptoms of toxicity were seen with our doses and patient satisfaction was good.

According to standard teaching, sudden cardiac death is the most feared complication in perioperative setup, but Maron et al. proposed two forms of disease, early onset and late onset.[6] HOCM in the elderly is less severe and has a more benign course, unlike the early onset of the disease in young adults, where more lethal complications like sudden cardiac death is seen.[7] Haering et al. found congestive heart failure (CHF) to be the predominant complication in elderly patients in the perioperative setup. This is related to diastolic dysfunction in HOCM which causes increased diastolic filling pressures, pulmonary congestion and dyspnoea which is seen in 90% of the patients of HOCM.[8] The chief complaint of our patient, who was elderly, was also dyspnoea. Focusing only on the LVOT gradient and providing fluids aggressively may very well surpass the limits of cardiac compensation and precipitate CHF.[8] In our patient also, initial attempts to decrease ventricular gradient were fruitful to some extent by using beta blockers and local anaesthetic boluses for pain, but liberal fluids and diastolic dysfunction tipped the balance towards failure (desaturation and tachypnoea), which finally responded to the diuretic. At this stage, if epidural boluses had been given instead of femoral, the resulting hypotension and tachycardia would have complicated the picture. Hence, our choice of postoperative analgesia was well chosen.

CONCLUSION

In conclusion, we do need to understand HOCM pathophysiology and prevent exacerbation of LVOT obstruction, but recent literature shifts our focus from catastrophic obstructive complications like perioperative sudden cardiac death in young HOCM to more benign anaesthetic course in elderly HOCM.