Correspondence (reply): In Reply

The fact that an otherwise healthy, young patient’s cardiopulmonary system decompensates in such a manner owing to unilateral impairment is indeed surprising. The literature cited with our article, however, reports several such instances. The pathophysiological examination remains unclear—the shift of larger volumes of intravascular fluids into the thorax (interstitial and intra-alveolar) has been discussed as a possible mechanism (1). The need for catecholamines in the patient in our case report existed for a short period of time only, before sedation was stepped down, and the required dosage was low.

The suggested differential diagnosis of stress associated takotsubo cardiomyopathy is an interesting one. Unfortunately, we cannot refer to valid parameters in the sense of valid diagnostic tests as neither electrocardiography nor echocardiography were undertaken, nor were the respective laboratory results available. Repeated work-up of the documentation, however, does not hint at such an entity. The clinical symptoms described for takotsubo cardiomyopathy, similar to those of cardiac ischemia, were not present before intubation, after extubation, and retrospectively in the patient’s further inpatient and outpatient progress (2). Isolated unilateral pulmonary edema as a result of a transient cardiac pump failure owing to the "myocardial stunning" described in the context of this disorder seems to us rather untypical. Also, female patients of an older age are regarded as having a higher risk (3). Without objective findings, takotsubo cardiomyopathy can certainly not be excluded, but to us it seems rather unlikely. If any clinical signs are present then this differential diagnosis should probably be excluded by means of suitable diagnostic tests.