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An unexpected cause of post-operative shock

D.O. McCall, M.S. Spence, L.J. Dixon
DOI: http://dx.doi.org/10.1093/qjmed/hcq027 785-786 First published online: 7 March 2010

A 66-year-old woman, admitted for day-case laser excision of a T1N0 laryngeal squamous cell carcinoma, suddenly became dyspnoeic while in the recovery ward ∼20 min after successful completion of an uneventful procedure.

Arterial blood gas analysis confirmed acute type II respiratory failure which prompted emergency re-intubation, initiation of ventilatory support and transfer to the intensive care unit. A portable chest X-ray showed bilateral alveolar filling defects consistent with severe pulmonary oedema and on 12-lead electrocardiogram (ECG), 1 mm of new ST segment elevation across leads V2–V4 was noted. Progressively worsening hypotension necessitated the initiation of inotropic support.

Although the patient was not known to have ischaemic heart disease, her pro-atherosclerotic risk factors included current cigarette smoking, type 2 diabetes mellitus, hypertension and dyslipidaemia. Accordingly, an acute coronary syndrome (ACS) with consequent cardiogenic shock was suspected.

Urgent transthoracic echocardiocardiography showed severely impaired left ventricular systolic function with an extensive akinetic region extending from the mid-anterior wall to apex to mid-inferior wall, with hyperdynamic basal contraction. Loop diuretic therapy was administered and emergency cardiac catheterization arranged.

Coronary angiography revealed a moderate proximal lesion within the dominant right coronary artery but no obstructive disease elsewhere. Left ventriculography confirmed antero-apical-inferior akinesis with preserved basal function (Figure 1). In the light of persistent hypotension and oliguria despite inotropes, an intra-aortic balloon pump (IABP) was inserted for additional haemodynamic support.

Figure 1.

Left ventriculogram in systole during emergency cardiac catheterization illustrating apical ballooning and preserved basal contraction.

This pattern of left ventricular regional wall motion abnormalities without epicardial coronary artery obstruction was adjudged consistent with the apical ballooning syndrome also known as takotsubo cardiomyopathy. No further intervention was undertaken and the patient returned to intensive care. The serum troponin T concentration measured 12 h later was 0.21 µg/l. Over the next 24 h, ventilatory requirements decreased and haemodynamic status improved permitting extubation, IABP removal and cessation of inotrope infusions on Day 2. A repeat echocardiogram on Day 6 demonstrated normal left ventricular systolic function without evidence of regional wall motion abnormality. Functional assessment of myocardial perfusion by single photon emission computed tomography with adenosine stress was also performed on Day 6 and revealed a mild basal inferior wall defect only.

The patient was discharged from hospital on Day 9 and follow-up cardiac magnetic resonance scan performed 4 weeks later confirmed normal left ventricular systolic function, with no regional wall motion abnormalities or evidence of infarction on delayed contrast enhanced images (Figure 2). At 6-month clinic review, the patient was well and free from cardiovascular symptoms.

Figure 2.

Cardiac magnetic resonance images at 4 weeks with no evidence of late gadolinium enhancement on horizontal long axis view.

First described among five Japanese patients,1 apical ballooning syndrome or takotsubo cardiomyopathy is an important differential diagnosis among individuals presenting with symptoms suggestive of ACS. It is characterized by transient left ventricular regional wall motion abnormalities that extend beyond the distribution of a single epicardial coronary artery, usually affects post-menopausal women and is often associated with an emotionally or physically stressful trigger.2 Systolic left ventricular shape is likened to that of a Japanese octopus-fishing pot or takotsubo, i.e. narrow neck and rounder at the bottom. Additional common features include ST segment elevation and T wave inversion with only minimal biochemical evidence of myocyte necrosis.3 Intractable pulmonary oedema and recurrent ventricular arrhythmias are recognized complications and mortality rates of ∼1% have been reported.4

While the precise aetiology of this syndrome remains unclear, there is a definite association with neurohormonal activation. It is postulated that among oestrogen-deficient women, in particular, catecholamines mediate apical stunning through direct myocyte toxicity and altered microvascular tone.5

This case highlights takotsubo cardiomyopathy as an important diagnostic consideration among patients who decompensate acutely under stressful circumstances including the early post-operative period. While intensive supportive therapy may be required initially, the recovery rates beyond this are excellent.

Conflict of interest: None declared.


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