Neonatal intensive care units have continually grown in number and complexity in their short history. The care given to infants and families in these units is done, in large part, by nursing. This article discusses the development of a scale that will explore the perceptions of this care by both consumers and providers. The perceptions of each group will be compared to determine if care that is thought and intended to be caring for providers is indeed perceived as such by consumers. This is of significant importance to the developing body of knowledge related to caring in nursing, and it will also promote care that is family centered.

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Retinopathy of prematurity (ROP) is a common disease of premature infants. It is characterized by an abnormal proliferation of blood vessels in the developing retina and is the leading cause of childhood blindness in developed countries. This article describes a systematic approach to prospectively reduce the incidence of ROP in a newborn intensive care unit (NICU). We realized the need for improvement when we reviewed comparative data indicating that our rates of ROP were higher than those in NICUs in our local area, across the United States, and around the world. After informal efforts appeared successful in significantly reducing ROP, we designed and implemented a more structured approach to ROP prevention that included improvements in practice related to oxygen administration and monitoring. An evidence-based guideline was developed, and education was provided to all direct care providers. We also standardized bedside oxygen delivery equipment and implemented new parameters related to nasal cannula weaning. Rates of ROP, severe ROP, and ROP requiring surgical intervention were reduced by more than 50% during the first year and more than 75% by the end of the second year after implementation of our unit-based program.

Observations of a patient with botulism requiring mechanical ventilatory support for 59 days and hospitalization for approximately 3 months are reported. During the time of greatest muscular paralysis, urinary urea nitrogen excretion exceeded 20 g per day. This degree of azoturia was thought to be due to obligate loss of lean body tissue secondary to paralysis and not to stress or starvation related demands. A contributing factor to the magnitude of azoturia was the presence of a large premorbid body frame and muscle mass. The nutritional goal was not to achieve nitrogen balance but to maintain visceral protein stores. As the patient improved neurologically, the azoturia decreased allowing a positive nitrogen balance with a rebuilding of skeletal muscle.

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