Neonatal shock: etiology, pathophysiology and management

Cardiovascular compromise in critically ill preterm and term infants initia lly presents with the 'compensated phase' of shock characterized by oliguri a, poor peripheral perfusion and normal blood pressure. As the condition wo rsens, the failure of the neuroendocrine compensatory mechanisms results in the development of hypotension and, in more advanced cases, lactic acidosi s. In this 'uncompensated phase' of shock, the imbalance between tissue oxy gen delivery and oxygen demand leads to gradually advancing cellular damage and organ dysfunction. In clinical practice, neonatal shock is most freque ntly recognized in its uncompensated phase by the presence of hypotension. However, although close to half of the newborns admitted to neonatal intens ive 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 uncompensat ed 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, i n some cases with primary myocardial dysfunction and elevated systemic vasc ular resistance, a more appropriate balance between myocardial contractilit y and afterload may be achieved by the use of dobutamine. Since absolute hy povolemia is a less frequent cause of shock in the newborn, volume administ ration has been shown to be less effective in the immediate postnatal perio d and its extensive use is associated with significant untoward effects, es pecially in preterm infants. During the course of their disease, some of th e sickest hypotensive newborns become unresponsive to volume and presser ad ministration. This phenomenon is caused by the desensitization of the cardi ovascular system to catecholamines by the critical illness and relative or absolute adrenal insufficiency. The findings that steroids rapidly up-regul ate cardiovascular adrenergic receptor expression and serve as hormone subs titution in cases of adrenal insufficiency explain their effectiveness in s tabilizing the cardiovascular status and decreasing the requirement for pre sser support in the critically ill newborn with volume- and presser-resista nt hypotension. Finally, despite recent advances in our understanding of th e pathophysiology and management of neonatal shock, there is little informa tion on the impact of the treatment on organ blood flow and tissue perfusio n and on neonatal morbidity and mortality.