Head-tilt maneuver assists with achieving airway patency during resuscitation. However, the relationship between angle of head-tilt and airway patency has not been defined. Our objective was to define an optimal head-tilt position for airway patency in neonates (age: 0–28 days) and young infants (age: 29 days–4 months). We performed a retrospective study of head and neck magnetic resonance imaging (MRI) of neonates and infants to define the angle of head-tilt for airway patency. We excluded those with an artificial airway or an airway malformation. We defined head-tilt angle a priori as the angle between occipito-ophisthion line and ophisthion-C7 spinous process line on the sagittal MR images. We evaluated medical records for Hypoxic Ischemic Encephalopathy (HIE) and exposure to sedation during MRI. We analyzed MRI of head and neck regions of 63 children (53 neonates and 10 young infants). Of these 63 children, 17 had evidence of airway obstruction and 46 had a patent airway on MRI. Also, 16/63 had underlying HIE and 47/63 newborn infants had exposure to sedative medications during MRI. In spontaneously breathing and neurologically depressed newborn infants, the head-tilt angle (median ± SD) associated with patent airway (125.3° ± 11.9°) was significantly different from that of blocked airway (108.2° ± 17.1°) (Mann Whitney U-test, p = 0.0045). The logistic regression analysis showed that the proportion of patent airways progressively increased with an increasing head-tilt angle, with > 95% probability of a patent airway at head-tilt angle 144–150°.

We describe an 83-year-old woman who presented to the emergency department with extreme thirst. Diagnostic testing revealed Takotsubo cardiomyopathy. Following symptomatic improvement and discharge, she returned to the emergency department with exudative pericardial effusion and elevated intrapericardial pressures. This case illustrates the importance of close follow-up of Takotsubo patients in whom complications such as pericardial effusion may lead to cardiac tamponade and hemodynamic instability if not managed properly.

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Late-stage heart failure and renal dysfunction are often seen in conjunction. Cardiorenal syndrome (CRS) describes the complex interaction between the two disease states. Early literature described the pathophysiology of CRS as related only to reduced cardiac output and decreased renal perfusion. Recent literature suggests a more multifaceted mechanism. Left ventricular assist devices (LVAD), used as bridge-to-transplant and destination therapy in patients with heart failure, impact not only cardiac function but also renal function, especially in those patients with preoperative renal dysfunction. The mechanism by which LVAD implantation affects renal function is complex and understated in early literature. In this review, we discuss the pathogenesis of CRS, the impact of preoperative renal dysfunction in patients undergoing LVAD implantation, and the effect of LVAD implantation on postoperative renal function.

We describe a 39-year-old man referred for surgical aortic valve replacement for severe symptomatic aortic stenosis. Intraoperative inspection was unexpectedly consistent with marantic endocarditis. Pathology confirmed nonbacterial thrombotic endocarditis. We present high-resolution intraoperative, diagnostic, and pathology images of nonbacterial thrombotic endocarditis in a patient with antiphospholipid syndrome with atypical presentation.