IngentaConnect Neonatal shock: etiology, pathophysiology and management

Abstract:

Cardiovascular compromise in critically ill preterm and term infants initially presents with the 'compensated phase' of shock characterized by oliguria, poor peripheral perfusion and normal blood pressure. As the condition worsens, the failure of the neuroendocrine compensatory mechanisms results in the development of hypotension and, in more advanced cases, lactic acidosis. In this 'uncompensated phase' of shock, the imbalance between tissue oxygen delivery and oxygen demand leads to gradually advancing cellular damage and organ dysfunction. In clinical practice, neonatal shock is most frequently recognized in its uncompensated phase by the presence of hypotension. However, although close to half of the newborns admitted to neonatal intensive care units receive treatment for hypotension, the normal physiological blood pressure range ensuring appropriate organ perfusion in the newborn is unknown. Therefore, the decision to treat hypotension and thus uncompensated shock in the newborn is based on statistically defined gestational-age- and postnatal-age-dependent normative blood pressure values and physicians' beliefs rather than on data bearing physiological reference. Since, in the majority of newborns, especially in the immediate postnatal period, shock is primarily caused by impaired regulation of peripheral vascular tone with or without myocardial dysfunction, dopamine is the primary drug of choice; it is more effective than dobutamine in raising blood pressure. However, in some cases with primary myocardial dysfunction and elevated systemic vascular resistance, a more appropriate balance between myocardial contractility and afterload may be achieved by the use of dobutamine. Since absolute hypovolemia is a less frequent cause of shock in the newborn, volume administration has been shown to be less effective in the immediate postnatal period and its extensive use is associated with significant untoward effects, especially in preterm infants. During the course of their disease, some of the sickest hypotensive newborns become unresponsive to volume and pressor administration. This phenomenon is caused by the desensitization of the cardiovascular system to catecholamines by the critical illness and relative or absolute adrenal insufficiency. The findings that steroids rapidly up-regulate cardiovascular adrenergic receptor expression and serve as hormone substitution in cases of adrenal insufficiency explain their effectiveness in stabilizing the cardiovascular status and decreasing the requirement for pressor support in the critically ill newborn with volume- and pressor-resistant hypotension. Finally, despite recent advances in our understanding of the pathophysiology and management of neonatal shock, there is little information on the impact of the treatment on organ blood flow and tissue perfusion and on neonatal morbidity and mortality.