Cot death

Since antiquity, cot death was explained as accidental suffocation, overlaying, or smothering. Parents were blamed for neglect or drunkenness, and a cage called arcuccio was invented around 1570 to protect the sleeping infant. Up to the 19th century, accidents were registered as natural causes of death. From 1830, accidental suffocation became unacceptable for physicians and legislators, and ‘natural’ explanations for the catastrophe were sought, with parents being consoled rather than blamed. Prone sleeping originated in the 1930s and from 1944 was associated with cot death. However, from the 1960s many authors recommended prone sleeping for infants, and many countries adopted the advice. A worldwide epidemic followed, peaking at 2% in England and Wales and 5% in New Zealand in the 1980s. Although epidemiological evidence was available by 1970, the first intervention was initiated in the Netherlands in 1989. Cot death disappeared almost entirely wherever prone sleeping was avoided. This strongly supports the assumption that prone sleeping has the greatest influence on the disorder, and that the epidemic resulted from wrong advice.

Case report of an atrial septal defect with negative transthoracic echocardiography, a diagnostic challenge in a middle-aged female with marked dyspnoea

A 39-year-old G3P3 female presented with abrupt onset dyspnoea of one month duration. She was markedly symptomatic when lying supine and resorted to prone sleeping. Chest X-ray reported as cardiomegaly. Transthoracic echocardiography was unremarkable twice. Computed tomography chest showed a dilated pulmonary artery. Transesophageal echocardiography identified a 12-mm ostium secundum atrial septal defect with mild pulmonary hypertension. The defect was closed with a cocoon device and rendered her symptom free. This case highlights the importance of timely organization of transesophageal echocardiography when transthoracic echocardiography is negative. It also illustrates marked dyspnoea could be a presentation of undiagnosed atrial septal defect with mild pulmonary hypertension.