Stress cardiomyopathy following antibiotic-induced anaphylaxis in a 16-month-old child

ABSTRACT

Takotsubo cardiomyopathy (TTC) is a reversible stress-induced myocardial syndrome characterized by transient left ventricular (LV) dysfunction in the absence of coronary artery disease. Pediatric cases are rare, especially in infants and toddlers. We report a 16-month-old female child who developed TTC following severe pneumonia complicated by antibiotic-induced anaphylaxis, cardiopulmonary arrest, and catecholamine exposure during resuscitation. Electrocardiography showed T-wave inversions, and echocardiography demonstrated transient mid and apical LV hypokinesia with preserved basal function. Cardiac troponin-I was markedly elevated. Serial echocardiography documented complete recovery of ventricular function. This case emphasizes the need to consider TTC in young children presenting with myocardial dysfunction following anaphylaxis and resuscitation and highlights the importance of early echocardiographic evaluation.

INTRODUCTION

Takotsubo cardiomyopathy (TTC), also known as stress-induced cardiomyopathy, is characterized by transient regional left ventricular (LV) systolic dysfunction extending beyond a single coronary artery territory, in the absence of obstructive coronary disease.[1] First described by Sato et al., the syndrome derives its name from the resemblance of the LV’s apical ballooning to a Japanese octopus trap.[2]

While TTC is well recognized in adults, pediatric cases remain rare and are likely underdiagnosed. Children often differ from adults in presentation, with equal sex distribution, more frequent nonapical variants, and potentially more severe LV dysfunction.[2] Common pediatric triggers include sepsis, neurological injury, and catecholamine exposure. Reports in infants and toddlers are exceedingly uncommon. We describe a rare case of TTC in a 16-month-old child following antibiotic-induced anaphylaxis and resuscitation.

CASE REPORT

A 16-month-old female child presented with fever and increased work of breathing. On examination, she was in respiratory distress. Chest radiography showed bilateral pneumonia, and a positive sepsis screen prompted initiation of intravenous antibiotics.

Shortly after administration of piperacillin–tazobactam, the child developed sudden generalized cyanosis, breath-holding, floppiness, and cardiovascular collapse, consistent with anaphylaxis and cardiopulmonary arrest. Cardiopulmonary resuscitation was initiated, and adrenaline with a total dose of 1 mg and atropine 0.6 mg were administered, following which return of spontaneous circulation was achieved. Postresuscitation, respiratory distress persisted, and chest radiography demonstrated pulmonary edema in addition to bilateral consolidation.

The child had no prior history of drug allergy and was incompletely immunized. She was admitted to the pediatric intensive care unit and managed with respiratory and inotropic support along with broad-spectrum antibiotics. Arterial blood gas analysis revealed mixed metabolic and respiratory acidosis. Serum lactate was initially elevated at 5.19 mmol/L and normalized to 1.13 mmol/L after stabilization.

Laboratory investigations revealed leukocytosis with neutrophilia and thrombocytosis. Renal and liver function tests were normal. N-terminal pro-B-type natriuretic peptide was 131 pg/mL (within age-appropriate reference range). Cardiac troponin-I was markedly elevated at 158.3 ng/mL.

Electrocardiography showed T-wave inversion in leads I, aVL, V5, and V6. Transthoracic echocardiography demonstrated normal cardiac anatomy with normal coronary origins. There was significant regional wall motion abnormality with hypokinesia of the mid and apical segments of the left ventricle and preserved basal contractility, consistent with the apical variant of TTC [Figure 1].

Figure 1.

Normal basal segment with ballooning of the heart in mid-segment and apical segment of the left ventricle (from top to bottom)

Serial laboratory parameters showed improvement in inflammatory markers, and there was no progression to multiorgan dysfunction. This child was initially started on dobutamine, continued for 24 hours and tapered as the childs’ hemodynamic status improved. Also this child required furosemide for the initial 4-6 hours. Follow-up echocardiography demonstrated complete recovery of LV systolic function, confirming the diagnosis of TTC.

DISCUSSION

TTC is a transient myocardial syndrome precipitated by intense physical or emotional stress, mediated primarily through catecholamine excess.[1] Pediatric TTC is uncommon and has most frequently been reported in association with sepsis, neurological injury, or exposure to high levels of endogenous or exogenous catecholamines.

In this child, severe pneumonia complicated by antibiotic-induced anaphylaxis, cardiopulmonary arrest, and adrenaline administration created a profound catecholamine surge. Excess catecholamines are thought to induce myocardial stunning through direct myocardial toxicity, microvascular dysfunction, and increased afterload, particularly affecting apical myocardial segments where β-adrenergic receptor density is highest.[2]

Diagnostic criteria for TTC include transient LV dysfunction with regional wall motion abnormalities beyond a single coronary territory, absence of coronary artery disease, new electrocardiographic changes or modest elevation of cardiac biomarkers, and exclusion of myocarditis. The clinical course, echocardiographic findings, and complete reversibility of LV dysfunction in this case fulfilled these criteria.[3] The absence of N-terminal pro-B-type natriuretic peptide elevation in our patient may be attributed to the very early timing of sample collection, transient and rapidly reversible ventricular dysfunction.

An important clinical implication is the association between anaphylaxis management and TTC. Several reports describe TTC following epinephrine administration for severe allergic reactions, including antibiotic-induced anaphylaxis. This constellation has been described as part of the adrenaline, takotsubo, anaphylaxis, and Kounis syndrome (“ATAK”) complex.[4] Early echocardiographic assessment in children with shock or myocardial dysfunction following anaphylaxis or catecholamine exposure is therefore essential to guide hemodynamic management and avoid excessive adrenergic stimulation.[5]

CONCLUSION

This case highlights TTC as a rare but important cause of transient myocardial dysfunction in very young children following severe stress and catecholamine exposure. Early recognition with echocardiography and supportive management results in complete recovery. Clinicians should maintain a high index of suspicion for TTC in infants and toddlers presenting with LV dysfunction after anaphylaxis or resuscitation.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that the names and initials will not be published and due efforts will be made to conceal the patient identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.