Critical care clinics
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Critical care clinics · Apr 2019
ReviewClassic and Nonclassic Renin-Angiotensin Systems in the Critically Ill.
Classic and nonclassic renin-angiotensin systems (RAS) are 2 sides of an ubiquitous endocrine/paracrine cascade regulating blood pressure and homeostasis. Angiotensin II and angiotensin-converting enzyme (ACE) levels are associated with severity of disease in the critically ill, and are central to the physiology and the pathogenesis of circulatory shock. ⋯ The tissue-based RAS has paracrine effects dissociated from those of the circulating RAS. Exogenous angiotensin II or ACE2 may improve the outcome of septic shock and acute respiratory distress syndrome, respectively.
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Critical care clinics · Apr 2019
ReviewDiabetes Insipidus and Syndrome of Inappropriate Antidiuretic Hormone in Critically Ill Patients.
Diabetes insipidus and the syndrome of inappropriate antidiuretic hormone secretion lie at opposite ends of the spectrum of disordered renal handling of water. Whereas renal retention of water insidiously causes hypotonic hyponatremia in syndrome of inappropriate antidiuretic hormone secretion, diabetes insipidus may lead to free water loss, hypernatremia, and volume depletion. ⋯ Moreover, pathologies causing polyuria and hyponatremia in patients in intensive care may be multiple, making diagnosis challenging. We provide an approach to the diagnosis and management of these conditions in intensive care patients.
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The Angiotensin II for the Treatment of Vasodilatory Shock (ATHOS-3) trial demonstrated the vasopressor effects and catecholamine-sparing properties of angiotensin II. As a result, the Food and Drug Administration has approved angiotensin II for the treatment of vasodilatory shock. This review details the goals of treatment of vasodilatory shock in addition to the history, current use, and recent research regarding the use of angiotensin II. An illustrative case of the use of angiotensin II is also incorporated for understanding the clinical utility of the drug.
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Erythropoietin (EPO) is a 34kD pleiotropic cytokine that was first identified as being essential for red blood cell (RBC) production. It is now recognized however that EPO is produced by many tissues. ⋯ Large clinical trials in the critically ill failed to demonstrate a role for EPO as an RBC transfusion sparing agent; however, improved clinical outcomes, attributable to EPO role in tissue protection are observed in critically ill trauma patients. Further research to confirm or refute these observations is required.
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Improved survival after critical illness has led to recognition of impaired recovery following critical illness as a major public health problem. A consistent association between critical illness and accelerated bone loss has been described, including changes in bone turnover markers, bone mineral density, and fragility fracture rate. An association between accelerated bone turnover and increased mortality after critical illness is probable. Assessment of the effect of antifracture agents on fracture rate and mortality in the high-risk population of postmenopausal women with prolonged ventilation is warranted.