A case of “Tako-Tsubo syndrome” with postoperative shock

Abstract

The “Tako-Tsubo syndrome” is a rare, transient, reversible hypokinesia of distal part of left ventricle, with normal coronary arteries. It was recently described and frequently associated with an extreme stressful event in postmenopausal women. We report a case of “Tako-Tsubo syndrome” following elective surgery for oesophageal malignancy with septic shock. Our report highlights the electrocardiographic changes with the progression of this syndrome and the challenges we faced in managing the case.

INTRODUCTION

The “Tako-Tsubo syndrome” (TTS)[1] is newly described, rare, transient, and reversible hypokinesia of the distal part of the left ventricle (inter-ventricular septum and the apex) with normal coronary artery anatomy. It is associated with extreme physical or emotional stress with marked female predilection, especially postmenopausal.[2,3] We herein report a case of TTS in a 61-year-old woman following elective laparoscopic surgery and postoperative septic shock. To the best of our knowledge and literature search, we could not find any case report of TTS with shock. In this report, we have shared electrocardiographic (ECG) changes with the progression of this syndrome and the challenges we faced in managing the case.

CASE REPORT

A 61-year-old female, a diagnosed case of squamous cell carcinoma (stage 1) oesophagus, underwent elective laparoscopic oesophagectomy and gastric pull through operation. Preoperatively, she achieved fitness for operation after proper preoperative assessment by our anesthesia team. Investigations, including left ventricular function and morphology as seen in transthorasic echocardiography (TTE), were within normal limit. In addition, she did not seem to be very anxious during induction and she was given adequate anxiolysis in the form of benzodiazepines pre, intra, and postoperatively. She was induced with fentanyl-propofol, intubated with the help of rocuronium, and maintained with isoflurane with O₂ nitrous and rocuronium. Postoperatively, she was shifted to post-operative intensive care unit (ICU) for few hours of elective ventilation. On postoperative 10^th hour, the patient developed tachycardia (130/min) and hypotension (80/60 mmHg), patient ventilator asynchrony (due to tachypnea) with increased thoracic drain output (bloody in nature). Her central venous pressure (CVP) was low (3 mmHg), 12 lead ECG showed sinus tachycardia [Figure 1]. Her arterial blood gas analysis and cardiac enzymes were within normal limits (except lower pCO2 levels), 1 litre of crystalloid and colloid (1/2 litre each) were infused in view of hypotension. Seeing no improvement, vasopressor (noradrenaline up to 0.05 mcg/kg/h) infusion was taken to improve mean blood pressure. Analgesia and sedation were hiked up with increasing dose of midazolam (2 mg/h) and fentanyl (100 mcg/h). Re-exploration was performed to rule out surgical bleeding as a cause for hypotension. Intraoperatively, no obvious bleeding was found. Drains were, however, repositioned to improve drainage due to probable surgical site oozing. The patient continued to be hemodynamically unstable with persistent need of vasopressor agent. She showed no evidence of fever, leukocytosis, and increase in procalcitonin and her subsequent blood cultures were sterile. Repeat 12 lead ECG after 2 days showed poor progression of r wave in V₁-V₃ [Figure 2]. TTE was performed to show hypokinesia of the distal septum and apex with hyperkinetic basal left ventricle highly suggestive of apical ballooning, with left ventricular peak mid cavity gradient of 65 mmHg, ejection fraction was 40%, with no mitral or aortic regurgitation. Her troponin I and the creatinine kinase (CK) level were normal, however, myoglobin (>500 U) and brain natriuretic peptide (BNP) (3500 U) were high. As TTS was suspected and cardiac troponin was within normal limit cardiologist deferred angiography. Low molecular weight heparin, aspirin, and statins were started. We could not add b-blockers in view of increasing circulatory shock. In view of cardiogenic element low dose dobutamine infusion was added along with nor-adrenaline. Within 12 h interval repeat 12-lead ECG revealed T wave inversion in leads V₃-V₆ and Lead II [Figure 3]. Her troponin I and CK level were still normal, myoglobin level came normal, though BNP was high (1000U). Repeat TTE confirmed previous finding with left ventricular peak mid cavity gradient of 70 mmHg, and further drop of ejection fraction to 30%. In the meantime, the patient developed surgical site sepsis and succumbed to her death on the 7^th ICU day due to multi drug resistant abdominal sepsis and combined cardiogenic and septic shock.

Figure 1.

12 lead ECG showing sinus tachycardia. (10 h post-operative)

Figure 2.

12 lead ECG showing poor progression of r wave in V₁-V₃ (arrowed) (2 days postoperative)

Figure 3.

12-lead ECG revealing T wave inversion in leads V₃-V₆ and lead II (arrowed) (2.5 days post-operative)

DISCUSSION

The pathogenesis of TTS is mostly unclear until today. Excessive catecholamine release during stress leads to epicardial coronary spasm and endothelial abnormalities. Some direct cardiomyocytes modulating effects of catecholamines have been proposed as a pathophysiology of TTS.[2] The apex may be more vulnerable to excessive sympathetic stimulation (especially epinephrine) due to presence of more and more b2 adrenergic receptor in apical region of the heart.[4] One newly proposed transient mid-left ventricular cavity dynamic gradient mechanism[5] was applied in our patient. According to this mechanism, the left ventricle might be arbitrarily divided into two chambers, a proximal normal pressure chamber with normal wall stress and an apical high pressure chamber at with high wall stress. This gradient leads to reduced apical coronary flow. Moreover, elderly women are known to develop abnormal basal/mid-septal thickening (sigmoid septum) and, interestingly, the increased ability to develop a dynamic mid-cavity obstruction during either a dobutamine challenge or when such patients become dehydrated/hypovolemic.[6]

In the available literature, favourable outcomes such as in hospital mortality of 0-8% have been reported in TTS.[2] Usually, the reported patients were conscious, oriented, and complained of chest pain. However, our situation was different. Intubated and mechanically ventilated postoperative patient can present as shock, sinus tachycardia, or patient ventilator asynchrony only. In ICU, if any postmenopausal woman, in a setting of stress, develops an acute reduction of left ventricular ejection function in association with hemodynamic compromise, patient ventilator asynchrony, or ECG evidence of ischemia or infarction, we should think TTS as a differential diagnosis. Inotropes infusion and dehydration may be harmful, causing increase in left ventricular peak systolic gradient. Moreover, therapy to reduce stress (beta blockers) is effective in non-hypotensive patient. However, the question remains as to what will be the treatment approach in patients with TTS and progressively increasing septic shock?