Disorders of the Pediatric Chest

Chase, Margaret; Wheeler, Derek S.

doi:10.1007/978-1-84800-925-7_2

Cited by 3 publications

(3 citation statements)

References 137 publications

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“…In the normal host, fluid movement is dependent on both hydrostatic and oncotic pressure (modeled by the Starling equation):

Q_{f} = K_{f} false[false(P_{C} - P_{T} false) - σ false(π_{C} - π_{T} false) false]

where P C −P T gives directionality to hydrostatic pressure and π C −π T gives directionality to oncotic pressure [47]. Under normal conditions fluid stays in the capillary lumen because P C ≃P T and π C > π T .…”

Section: Epidemiology: Aki Ali and Multi-organ Disease Syndromementioning

confidence: 99%

Kidney–lung cross-talk and acute kidney injury

Basu

Wheeler

2013

Pediatr Nephrol

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There is a growing appreciation for the role that acute kidney injury (AKI) plays in the propagation of critical illness. In children, AKI is not only an independent predictor of morbidity and mortality, but is also associated with especially negative outcomes when concurrent with acute lung injury (ALI). Experimental data provide evidence that kidney–lung crosstalk occurs and can be bidirectionally deleterious, although details of the precise molecular mechanisms involved in the AKI–ALI interaction remain incomplete. Clinically, ALI, and the subsequent clinical interventions used to stabilize gas exchange, carry consequences for the homeostasis of kidney function. Meanwhile, AKI negatively affects lung physiology significantly by altering the homeostasis of fluid balance, acid–base balance, and vascular tone. Experimental AKI research supports an “endocrine” role for the kidney, triggering a cascade of extra-renal inflammatory responses affecting lung homeostasis. In this review, we will discuss the pathophysiology of kidney–lung crosstalk, the multiple pathways by which AKI affects kidney–lung homeostasis, and discuss how these phenomena may be unique in critically ill children. Understanding how AKI may affect a “balance of communication” that exists between the kidneys and the lungs is requisite when managing critically ill children, in whom imbalance is the norm.

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“…In the normal host, fluid movement is dependent on both hydrostatic and oncotic pressure (modeled by the Starling equation):

Q_{f} = K_{f} false[false(P_{C} - P_{T} false) - σ false(π_{C} - π_{T} false) false]

Section: Epidemiology: Aki Ali and Multi-organ Disease Syndromementioning

confidence: 99%

Kidney–lung cross-talk and acute kidney injury

Basu

Wheeler

2013

Pediatr Nephrol

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“…Similarly, there are several key developmental differences that predispose children to acute respiratory failure (68–70). Infants and young children have fewer alveoli compared to adults (approximately 20 million alveoli after birth to 300 million alveoli by the age of 8 years) (71–73).…”

Section: The Pediatric Host Response To Sepsismentioning

confidence: 99%

“…This impression of diaphragmatic fatigue and failure has been confirmed through electromyographic measurements of the diaphragms of fatiguing infants who become apneic in the face of increased work of breathing (79–80). Collectively, all of these factors increase the risk of acute respiratory failure in children (69–70, 77). …”

Section: The Pediatric Host Response To Sepsismentioning

confidence: 99%

”Children are not Small Adults!“

Wheeler

Wong²,

Zingarelli³

2011

TOINFJ

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The recognition, diagnosis, and management of sepsis remain among the greatest challenges in pediatric critical care medicine. Sepsis remains among the leading causes of death in both developed and underdeveloped countries and has an incidence that is predicted to increase each year. Unfortunately, promising therapies derived from preclinical models have universally failed to significantly reduce the substantial mortality and morbidity associated with sepsis. There are several key developmental differences in the host response to infection and therapy that clearly delineate pediatric sepsis as a separate, albeit related, entity from adult sepsis. Thus, there remains a critical need for well-designed epidemiologic and mechanistic studies of pediatric sepsis in order to gain a better understanding of these unique developmental differences so that we may provide the appropriate treatment. Herein, we will review the important differences in the pediatric host response to sepsis, highlighting key differences at the whole-organism level, organ system level, and cellular and molecular level.

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